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http://www.ncbi.nlm.nih.gov/pubmed/11117200,http://www.ncbi.nlm.nih.gov/pubmed/22986150,http://www.ncbi.nlm.nih.gov/pubmed/20658515,http://www.ncbi.nlm.nih.gov/pubmed/24113777,http://www.ncbi.nlm.nih.gov/pubmed/6290538,http://www.ncbi.nlm.nih.gov/pubmed/22945636,http://www.ncbi.nlm.nih.gov/pubmed/169249,http://www.ncbi.nlm.nih.gov/pubmed/18329679,http://www.ncbi.nlm.nih.gov/pubmed/227209,http://www.ncbi.nlm.nih.gov/pubmed/23137442,http://www.ncbi.nlm.nih.gov/pubmed/23926648,http://www.ncbi.nlm.nih.gov/pubmed/19900468,http://www.ncbi.nlm.nih.gov/pubmed/22414628,http://www.ncbi.nlm.nih.gov/pubmed/6093898,http://www.ncbi.nlm.nih.gov/pubmed/17570630,http://www.ncbi.nlm.nih.gov/pubmed/23021374,http://www.ncbi.nlm.nih.gov/pubmed/20051527,http://www.ncbi.nlm.nih.gov/pubmed/12165107,http://www.ncbi.nlm.nih.gov/pubmed/17983645,http://www.ncbi.nlm.nih.gov/pubmed/2534509,http://www.ncbi.nlm.nih.gov/pubmed/23943159,http://www.ncbi.nlm.nih.gov/pubmed/19755667,http://www.ncbi.nlm.nih.gov/pubmed/8936679,http://www.ncbi.nlm.nih.gov/pubmed/1747413,http://www.ncbi.nlm.nih.gov/pubmed/6312037,http://www.ncbi.nlm.nih.gov/pubmed/20232113
Are there plasma membrane receptors for thyroid hormones?
Receptors for thyroid hormones are present on plasma membrane of cells; in particular thyroid hormones bind integrin that is a heterodimeric component of plasma membrane
http://www.ncbi.nlm.nih.gov/pubmed/25219355,http://www.ncbi.nlm.nih.gov/pubmed/21275980,http://www.ncbi.nlm.nih.gov/pubmed/23667118,http://www.ncbi.nlm.nih.gov/pubmed/24743217,http://www.ncbi.nlm.nih.gov/pubmed/17535679,http://www.ncbi.nlm.nih.gov/pubmed/22642611,http://www.ncbi.nlm.nih.gov/pubmed/25296541,http://www.ncbi.nlm.nih.gov/pubmed/23899121,http://www.ncbi.nlm.nih.gov/pubmed/25601060,http://www.ncbi.nlm.nih.gov/pubmed/20618424,http://www.ncbi.nlm.nih.gov/pubmed/23551067,http://www.ncbi.nlm.nih.gov/pubmed/22844307,http://www.ncbi.nlm.nih.gov/pubmed/24649461,http://www.ncbi.nlm.nih.gov/pubmed/15965699,http://www.ncbi.nlm.nih.gov/pubmed/22510082
Which disorder is rated by Palmini classification?
Palmini classification system is used for classification of focal cortical dysplasia.
http://www.ncbi.nlm.nih.gov/pubmed/22649318,http://www.ncbi.nlm.nih.gov/pubmed/17576662,http://www.ncbi.nlm.nih.gov/pubmed/21258568,http://www.ncbi.nlm.nih.gov/pubmed/16717399,http://www.ncbi.nlm.nih.gov/pubmed/16814664,http://www.ncbi.nlm.nih.gov/pubmed/17239026,http://www.ncbi.nlm.nih.gov/pubmed/22318706,http://www.ncbi.nlm.nih.gov/pubmed/19092364,http://www.ncbi.nlm.nih.gov/pubmed/23137502,http://www.ncbi.nlm.nih.gov/pubmed/15992646,http://www.ncbi.nlm.nih.gov/pubmed/17106196,http://www.ncbi.nlm.nih.gov/pubmed/20849606,http://www.ncbi.nlm.nih.gov/pubmed/19449462,http://www.ncbi.nlm.nih.gov/pubmed/22595018,http://www.ncbi.nlm.nih.gov/pubmed/18827024,http://www.ncbi.nlm.nih.gov/pubmed/18510486,http://www.ncbi.nlm.nih.gov/pubmed/18397963
what is the role of erythropoietin in cardiac regeneration after myocardial infarction?
In preclinical studies, erythropoietin improved cardiac function and perfusion by angiomyogenesis and protection of cardiomyocytes in myocardial infarction indicating that erythropoietin may play a role in the stimulation of cell regeneration under normal physiologic conditions and in patients with myocardial injury. Epo overexpression was found to enhance the cellular regenerative properties of MSCs by both autocrine and paracrine pathways. However, results from recent clinical trials did not support beneficial effects of cytokine therapy with erythropoietin in patients with myocardial infarction.
http://www.ncbi.nlm.nih.gov/pubmed/25300486
Does Rad9 interact with Aft1 in S.cerevisiae?
Yes. Rad9 functions together with Aft1 on DNA damage-prone chromatin to facilitate genome surveillance, thereby ensuring rapid and effective response to possible DNA damage events.
http://www.ncbi.nlm.nih.gov/pubmed/18033728,http://www.ncbi.nlm.nih.gov/pubmed/19026658,http://www.ncbi.nlm.nih.gov/pubmed/1694790,http://www.ncbi.nlm.nih.gov/pubmed/20171226,http://www.ncbi.nlm.nih.gov/pubmed/10929203,http://www.ncbi.nlm.nih.gov/pubmed/7460905,http://www.ncbi.nlm.nih.gov/pubmed/12529857,http://www.ncbi.nlm.nih.gov/pubmed/2659540,http://www.ncbi.nlm.nih.gov/pubmed/8752741
Are there any desmins present in plants?
No. Desmins are type III intermediate filament (IF) proteins that have been identified to date only in metazoa (human, Danio rerio, bovine). Desmins are also associated with severe forms of skeletal, cardiac and myofibrillar myopathies.
http://www.ncbi.nlm.nih.gov/pubmed/18422033,http://www.ncbi.nlm.nih.gov/pubmed/19138419,http://www.ncbi.nlm.nih.gov/pubmed/20960165,http://www.ncbi.nlm.nih.gov/pubmed/11109652,http://www.ncbi.nlm.nih.gov/pubmed/23227861,http://www.ncbi.nlm.nih.gov/pubmed/22819125,http://www.ncbi.nlm.nih.gov/pubmed/19627727,http://www.ncbi.nlm.nih.gov/pubmed/20671410,http://www.ncbi.nlm.nih.gov/pubmed/22527824,http://www.ncbi.nlm.nih.gov/pubmed/1856259,http://www.ncbi.nlm.nih.gov/pubmed/1691523,http://www.ncbi.nlm.nih.gov/pubmed/18421188,http://www.ncbi.nlm.nih.gov/pubmed/12608662,http://www.ncbi.nlm.nih.gov/pubmed/22459018,http://www.ncbi.nlm.nih.gov/pubmed/20886354,http://www.ncbi.nlm.nih.gov/pubmed/9790279,http://www.ncbi.nlm.nih.gov/pubmed/10971829,http://www.ncbi.nlm.nih.gov/pubmed/4936649,http://www.ncbi.nlm.nih.gov/pubmed/10525005,http://www.ncbi.nlm.nih.gov/pubmed/22136271,http://www.ncbi.nlm.nih.gov/pubmed/15332726,http://www.ncbi.nlm.nih.gov/pubmed/16279854,http://www.ncbi.nlm.nih.gov/pubmed/9915102
Are viruses involved in the etiology of human subacute thyroiditis?
Subacute thyroiditis (SAT) is an inflammatory disorder of the thyroid caused probably by viruses The principal classes of viruses involed in SAT include Epstein Barr and Retroviridae
http://www.ncbi.nlm.nih.gov/pubmed/24919398,http://www.ncbi.nlm.nih.gov/pubmed/24378737,http://www.ncbi.nlm.nih.gov/pubmed/25045881,http://www.ncbi.nlm.nih.gov/pubmed/25013953,http://www.ncbi.nlm.nih.gov/pubmed/24454829,http://www.ncbi.nlm.nih.gov/pubmed/25888034,http://www.ncbi.nlm.nih.gov/pubmed/26131842,http://www.ncbi.nlm.nih.gov/pubmed/25025868
List core circadian clock genes.
The core circadian clock genes are CLOCK, BMAL1, Per, and Cry.
http://www.ncbi.nlm.nih.gov/pubmed/20582309,http://www.ncbi.nlm.nih.gov/pubmed/15082788,http://www.ncbi.nlm.nih.gov/pubmed/12884740,http://www.ncbi.nlm.nih.gov/pubmed/15651351,http://www.ncbi.nlm.nih.gov/pubmed/12872253,http://www.ncbi.nlm.nih.gov/pubmed/16541790,http://www.ncbi.nlm.nih.gov/pubmed/23996628,http://www.ncbi.nlm.nih.gov/pubmed/21303696
Which peripheral neuropathy has been associated with NDRG1 mutations?
Charcot-Marie-Tooth (CMT) 4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1).CMT4D disease is a severe autosomal recessive demyelinating neuropathy with extensive axonal loss leading to early disability, caused by mutations in the N-myc downstream regulated gene 1 (NDRG1)
http://www.ncbi.nlm.nih.gov/pubmed/21157109,http://www.ncbi.nlm.nih.gov/pubmed/23465244
Is miR-126 involved in heart failure?
Yes, miR-126 is associated with heart failure.
http://www.ncbi.nlm.nih.gov/pubmed/22926332,http://www.ncbi.nlm.nih.gov/pubmed/22473781,http://www.ncbi.nlm.nih.gov/pubmed/20869962,http://www.ncbi.nlm.nih.gov/pubmed/23274061,http://www.ncbi.nlm.nih.gov/pubmed/18853243,http://www.ncbi.nlm.nih.gov/pubmed/19370079,http://www.ncbi.nlm.nih.gov/pubmed/18310510,http://www.ncbi.nlm.nih.gov/pubmed/16198371,http://www.ncbi.nlm.nih.gov/pubmed/18356487,http://www.ncbi.nlm.nih.gov/pubmed/20874677,http://www.ncbi.nlm.nih.gov/pubmed/20491649,http://www.ncbi.nlm.nih.gov/pubmed/22050707,http://www.ncbi.nlm.nih.gov/pubmed/12679191,http://www.ncbi.nlm.nih.gov/pubmed/18639559,http://www.ncbi.nlm.nih.gov/pubmed/20675566,http://www.ncbi.nlm.nih.gov/pubmed/19460403,http://www.ncbi.nlm.nih.gov/pubmed/19370081,http://www.ncbi.nlm.nih.gov/pubmed/20429690,http://www.ncbi.nlm.nih.gov/pubmed/21352470,http://www.ncbi.nlm.nih.gov/pubmed/17488730,http://www.ncbi.nlm.nih.gov/pubmed/20008278,http://www.ncbi.nlm.nih.gov/pubmed/19942861,http://www.ncbi.nlm.nih.gov/pubmed/19959541,http://www.ncbi.nlm.nih.gov/pubmed/18562309,http://www.ncbi.nlm.nih.gov/pubmed/21054406,http://www.ncbi.nlm.nih.gov/pubmed/17875610,http://www.ncbi.nlm.nih.gov/pubmed/22245452,http://www.ncbi.nlm.nih.gov/pubmed/22768138,http://www.ncbi.nlm.nih.gov/pubmed/15498824,http://www.ncbi.nlm.nih.gov/pubmed/23784505,http://www.ncbi.nlm.nih.gov/pubmed/24289075,http://www.ncbi.nlm.nih.gov/pubmed/22229508,http://www.ncbi.nlm.nih.gov/pubmed/20716127
Does resveratrol reduce cardiac remodeling?
Resveratrol attenuates left ventricular remodeling. Resveratrol is a beneficial pharmacological tool that augments autophagy to bring about reverse remodeling in the postinfarction heart. Resveratrol administration improved cardiac environment by reducing inflammatory state and decreased unfavorable ventricular remodeling of the diabetic heart, leading to a marked recovery of ventricular function. Resveratrol can constitute an adjuvant therapeutic option in prevention of dilated cardiomyopathy.Most of the evidence shows that Resveratrol supresses cardiac remodeling.
http://www.ncbi.nlm.nih.gov/pubmed/18635949,http://www.ncbi.nlm.nih.gov/pubmed/22331875,http://www.ncbi.nlm.nih.gov/pubmed/15331765,http://www.ncbi.nlm.nih.gov/pubmed/22426402,http://www.ncbi.nlm.nih.gov/pubmed/11208145,http://www.ncbi.nlm.nih.gov/pubmed/11082038,http://www.ncbi.nlm.nih.gov/pubmed/22809326,http://www.ncbi.nlm.nih.gov/pubmed/19117012,http://www.ncbi.nlm.nih.gov/pubmed/18644871,http://www.ncbi.nlm.nih.gov/pubmed/21429245,http://www.ncbi.nlm.nih.gov/pubmed/23070014,http://www.ncbi.nlm.nih.gov/pubmed/23404999,http://www.ncbi.nlm.nih.gov/pubmed/21966475,http://www.ncbi.nlm.nih.gov/pubmed/12505983,http://www.ncbi.nlm.nih.gov/pubmed/18927485,http://www.ncbi.nlm.nih.gov/pubmed/19433452,http://www.ncbi.nlm.nih.gov/pubmed/21514572,http://www.ncbi.nlm.nih.gov/pubmed/15325583,http://www.ncbi.nlm.nih.gov/pubmed/18550537,http://www.ncbi.nlm.nih.gov/pubmed/17284523,http://www.ncbi.nlm.nih.gov/pubmed/16585521,http://www.ncbi.nlm.nih.gov/pubmed/10806201,http://www.ncbi.nlm.nih.gov/pubmed/22227450,http://www.ncbi.nlm.nih.gov/pubmed/22363588,http://www.ncbi.nlm.nih.gov/pubmed/22653298
Which is the receptor for substrates of Chaperone Mediated Autophagy?
Chaperone-mediated autophagy (CMA) is a lysosomal pathway for selective removal of damaged cytosolic proteins. The LAMP2A (Lysosome-associated membrane protein 2 isoform A) functions as a receptor for cytosolic proteins and also as essential component of the CMA translocation complex [28]. Cytosolic substrate proteins bind to monomers of LAMP-2A, which then multimerizes to form the complex required for substrate transmembrane import.
http://www.ncbi.nlm.nih.gov/pubmed/12691636,http://www.ncbi.nlm.nih.gov/pubmed/7777669,http://www.ncbi.nlm.nih.gov/pubmed/22707076,http://www.ncbi.nlm.nih.gov/pubmed/17922627,http://www.ncbi.nlm.nih.gov/pubmed/19808348,http://www.ncbi.nlm.nih.gov/pubmed/1357906,http://www.ncbi.nlm.nih.gov/pubmed/2936238,http://www.ncbi.nlm.nih.gov/pubmed/9519348,http://www.ncbi.nlm.nih.gov/pubmed/11930867
What are the hallmarks of congestive heart failure?
Congestive heart failure (HF) is a clinical syndrome, with hallmarks of fatigue and dyspnea, that continues to be highly prevalent and morbid. Common pathophysiologic features of HF include changes in left ventricle structure, function, and neurohormonal activation. Disturbed myocardial calcium handling is also one of the pathophysiologic hallmarks of congestive heart failure. One of the hallmarks of chronic congestive heart failure is an increase in sympathetic tone to the peripheral circulation and to the heart. It has been proposed that the activation of neurohormonal pathways and the formation of oxygen free radicals ultimately lead to the activation of a family of transcription factors that are involved in cardiac and vascular remodelling which are hallmarks of congestive heart failure. Myocardial failure ultimately leads to exaggerated neurohumoral compensatory mechanisms and derangements of the peripheral circulation, which are the hallmarks of congestive heart failure. Two additional hallmarks of this syndrome are sodium and water retention. Accumulation of oxidized matrix between the endothelium and cardiac muscle, and endocardial endothelial dysfunction, are also hallmarks of congestive heart failure.
http://www.ncbi.nlm.nih.gov/pubmed/19829181,http://www.ncbi.nlm.nih.gov/pubmed/16812977,http://www.ncbi.nlm.nih.gov/pubmed/19482666
What is the mode of inheritance of short QT syndrome?
The short QT syndrome has an autosomal dominant mode of inheritance.
http://www.ncbi.nlm.nih.gov/pubmed/20808697,http://www.ncbi.nlm.nih.gov/pubmed/17703631,http://www.ncbi.nlm.nih.gov/pubmed/18053204,http://www.ncbi.nlm.nih.gov/pubmed/16172968,http://www.ncbi.nlm.nih.gov/pubmed/21947244,http://www.ncbi.nlm.nih.gov/pubmed/19329361,http://www.ncbi.nlm.nih.gov/pubmed/23621600,http://www.ncbi.nlm.nih.gov/pubmed/23607065,http://www.ncbi.nlm.nih.gov/pubmed/21898188,http://www.ncbi.nlm.nih.gov/pubmed/16139655,http://www.ncbi.nlm.nih.gov/pubmed/23049642,http://www.ncbi.nlm.nih.gov/pubmed/23964263,http://www.ncbi.nlm.nih.gov/pubmed/12414200,http://www.ncbi.nlm.nih.gov/pubmed/21696651,http://www.ncbi.nlm.nih.gov/pubmed/20165722,http://www.ncbi.nlm.nih.gov/pubmed/23210044
List clinical trials that have directly compared microsurgical clipping with endovascular coiling for treatment of ruptured brain aneurysms?
Barrow Ruptured Aneurysm Trial (BRAT) and international subarachnoid aneurysmal trial (ISAT) have directly compared microsurgical clipping with endovascular coiling for treatment of ruptured brain aneurysms. FIAT study, a clinical care trial aiming to compare angiographic and clinical outcomes following treatment with a Flow-Diverter or with the best conventional treatment option (including clipping) is underway.
http://www.ncbi.nlm.nih.gov/pubmed/21866560,http://www.ncbi.nlm.nih.gov/pubmed/23486871,http://www.ncbi.nlm.nih.gov/pubmed/24048081,http://www.ncbi.nlm.nih.gov/pubmed/23884811,http://www.ncbi.nlm.nih.gov/pubmed/21963829,http://www.ncbi.nlm.nih.gov/pubmed/21676420,http://www.ncbi.nlm.nih.gov/pubmed/22530521,http://www.ncbi.nlm.nih.gov/pubmed/22213222
What is the reason for the narcolepsy cases developed after H1N1 influenza vaccination?
The proposed mechanism for postvaccination narcolepsy is one in which an environmental trigger causes or enhances an antibody-mediated autoimmune response in patients with a preexisting genetic susceptibility.
http://www.ncbi.nlm.nih.gov/pubmed/22982358,http://www.ncbi.nlm.nih.gov/pubmed/23966249,http://www.ncbi.nlm.nih.gov/pubmed/23624169,http://www.ncbi.nlm.nih.gov/pubmed/23882370,http://www.ncbi.nlm.nih.gov/pubmed/20580647,http://www.ncbi.nlm.nih.gov/pubmed/24166579,http://www.ncbi.nlm.nih.gov/pubmed/23527322,http://www.ncbi.nlm.nih.gov/pubmed/24194552,http://www.ncbi.nlm.nih.gov/pubmed/21683932,http://www.ncbi.nlm.nih.gov/pubmed/24199960,http://www.ncbi.nlm.nih.gov/pubmed/17182990,http://www.ncbi.nlm.nih.gov/pubmed/21624562,http://www.ncbi.nlm.nih.gov/pubmed/23966257,http://www.ncbi.nlm.nih.gov/pubmed/23420460,http://www.ncbi.nlm.nih.gov/pubmed/18620875,http://www.ncbi.nlm.nih.gov/pubmed/18191617,http://www.ncbi.nlm.nih.gov/pubmed/15783264,http://www.ncbi.nlm.nih.gov/pubmed/23597030,http://www.ncbi.nlm.nih.gov/pubmed/23178035,http://www.ncbi.nlm.nih.gov/pubmed/23995816,http://www.ncbi.nlm.nih.gov/pubmed/16712496,http://www.ncbi.nlm.nih.gov/pubmed/21764791,http://www.ncbi.nlm.nih.gov/pubmed/24132372,http://www.ncbi.nlm.nih.gov/pubmed/23536396,http://www.ncbi.nlm.nih.gov/pubmed/19142702,http://www.ncbi.nlm.nih.gov/pubmed/19164222,http://www.ncbi.nlm.nih.gov/pubmed/23053137
Which are the biotracers used for detection of Alzheimer's disease using PET?
Pittsburgh compound B (PIB) was the first radiotracer capable of highlighting deposits of beta-amyloid—one pathological hallmark of Alzheimer's disease—in living individuals during a PET scan. The Alzheimer's Association helped fund early PIB development. The Association in 2006 also awarded a $2.1 million grant to the Alzheimer's Disease Neuroimaging Initiative (ADNI) to expand this long-term, nationwide study to include PIB-PET imaging. 18F flutemetamol (flute), another radiotracer that highlights beta-amyloid in a PET scan, is structurally identical to PIB except for one fluorine atom in place of a carbon atom. That small chemical change enables flutemetamol to remain stable significantly longer than does PIB, potentially increasing its usefulness outside research settings. In phase II study results reported in the Annals of Neurology, flutemetamol performed similarly to PIB. Additional testing is under way. Florbetapir F 18 (18F-AV-45) is also a radiotracer that highlights brain beta-amyloid during a PET scan. At the 2010 Alzheimer's Association International Conference on Alzheimer's Disease (AAICAD), florbetapir's developer first reported data, later published in the JAMA, showing nearly perfect correlation between brain amyloid levels detected by florbetapir PET scans in study volunteers and levels found in autopsies of the same individuals a few months later. The developer has sought Food and Drug Administration (FDA) approval to market florbetapir under the brand name Amyvid. The FDA has said it will withhold approval until the developer establishes a professional training program to ensure accuracy and consistency in reading and interpreting Amyvid scans. Florbetaben (BAY 94-9172) is another radiotracer designed to detect beta-amyloid during a PET scan. Phase II study results and other florbetaben data were reported at the 2010 Alzheimer's Association International Conference on Alzheimer's Disease (AAICAD). Phase II data were also later published in Lancet Neurology. Further studies are now under way.
http://www.ncbi.nlm.nih.gov/pubmed/16683036,http://www.ncbi.nlm.nih.gov/pubmed/20428234,http://www.ncbi.nlm.nih.gov/pubmed/16381948
What was the purpose of the FANTOM3 project?
The FANTOM3 annotation system, consisting of automated computational prediction, manual curation, and final expert curation, facilitated the comprehensive characterization of the mouse transcriptome, and could be applied to the transcriptomes of other speciesFunctional Annotation Of Mouse 3 (FANTOM3), an international collaboration research project focusing on expanding the transcriptome and subsequent analyses. The FANTOM3 annotation system, consisting of automated computational prediction, manual curation, and final expert curation, facilitated the comprehensive characterization of the mouse transcriptome, and could be applied to the transcriptomes of other species.
http://www.ncbi.nlm.nih.gov/pubmed/8828040,http://www.ncbi.nlm.nih.gov/pubmed/19543403,http://www.ncbi.nlm.nih.gov/pubmed/9931467,http://www.ncbi.nlm.nih.gov/pubmed/15871047,http://www.ncbi.nlm.nih.gov/pubmed/22057813,http://www.ncbi.nlm.nih.gov/pubmed/11591470,http://www.ncbi.nlm.nih.gov/pubmed/6572942,http://www.ncbi.nlm.nih.gov/pubmed/7723057
In which isochores are Alu elements enriched?
Alu elements are enriched in high GC% isochores due to reduced Alu loss by recombination in these regions. The frequency of Alu sequences increases with increasing GC, but attains a maximum in H2 isochores.
http://www.ncbi.nlm.nih.gov/pubmed/21295813,http://www.ncbi.nlm.nih.gov/pubmed/23821183,http://www.ncbi.nlm.nih.gov/pubmed/16925274,http://www.ncbi.nlm.nih.gov/pubmed/18701613,http://www.ncbi.nlm.nih.gov/pubmed/18501812,http://www.ncbi.nlm.nih.gov/pubmed/9689695,http://www.ncbi.nlm.nih.gov/pubmed/23024163,http://www.ncbi.nlm.nih.gov/pubmed/20566568,http://www.ncbi.nlm.nih.gov/pubmed/19762051,http://www.ncbi.nlm.nih.gov/pubmed/19013593,http://www.ncbi.nlm.nih.gov/pubmed/2218396,http://www.ncbi.nlm.nih.gov/pubmed/16217311,http://www.ncbi.nlm.nih.gov/pubmed/17222634,http://www.ncbi.nlm.nih.gov/pubmed/22554593,http://www.ncbi.nlm.nih.gov/pubmed/2669121
Is oxalate renal excretion increased after bariatric surgery?
Bariatric surgery is associated with a significant risk of nephrolithiasis. Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy must be considered with the other risks of bariatric surgery Hyperoxaluria in patients treated with bariatric surgery was found to be a result of hyperabsorption of oxalateUrinary oxalate increases after bariatric surgery
http://www.ncbi.nlm.nih.gov/pubmed/23074403,http://www.ncbi.nlm.nih.gov/pubmed/19430299,http://www.ncbi.nlm.nih.gov/pubmed/16458330,http://www.ncbi.nlm.nih.gov/pubmed/22006429,http://www.ncbi.nlm.nih.gov/pubmed/23536897,http://www.ncbi.nlm.nih.gov/pubmed/21199003,http://www.ncbi.nlm.nih.gov/pubmed/11403720,http://www.ncbi.nlm.nih.gov/pubmed/16434186,http://www.ncbi.nlm.nih.gov/pubmed/21266528,http://www.ncbi.nlm.nih.gov/pubmed/12650907,http://www.ncbi.nlm.nih.gov/pubmed/10768832,http://www.ncbi.nlm.nih.gov/pubmed/14534542,http://www.ncbi.nlm.nih.gov/pubmed/12941809,http://www.ncbi.nlm.nih.gov/pubmed/17638058
Which are the mutational hotspots of the human KRAS oncogene?
The KRAS oncogene has four main mutational hotspots located at codons 12, 13, 61 and 146.The mutational hotspots for the K-ras oncogene are codons 12 and 13
http://www.ncbi.nlm.nih.gov/pubmed/24140113,http://www.ncbi.nlm.nih.gov/pubmed/25205765,http://www.ncbi.nlm.nih.gov/pubmed/25470043,http://www.ncbi.nlm.nih.gov/pubmed/24183451
Which intraflagellar transport (IFT) motor protein has been linked to human skeletal ciliopathies?
Cytoplasmic dynein-2 (dynein-2) performs intraflagellar transport and is associated with human skeletal ciliopathiesIntraflagellar transport (IFT) depends on two evolutionarily conserved modules, subcomplexes A (IFT-A) and B (IFT-B), to drive ciliary assembly and maintenance. All six IFT-A components and their motor protein, DYNC2H1, have been linked to human skeletal ciliopathies, including asphyxiating thoracic dystrophy (ATD; also known as Jeune syndrome), Sensenbrenner syndrome, and Mainzer-Saldino syndrome (MZSDS).
http://www.ncbi.nlm.nih.gov/pubmed/24579720,http://www.ncbi.nlm.nih.gov/pubmed/23609782,http://www.ncbi.nlm.nih.gov/pubmed/24494635,http://www.ncbi.nlm.nih.gov/pubmed/24928997,http://www.ncbi.nlm.nih.gov/pubmed/24444048,http://www.ncbi.nlm.nih.gov/pubmed/23448220,http://www.ncbi.nlm.nih.gov/pubmed/24832354,http://www.ncbi.nlm.nih.gov/pubmed/18951300,http://www.ncbi.nlm.nih.gov/pubmed/24090587,http://www.ncbi.nlm.nih.gov/pubmed/22047971,http://www.ncbi.nlm.nih.gov/pubmed/22766059,http://www.ncbi.nlm.nih.gov/pubmed/24251808,http://www.ncbi.nlm.nih.gov/pubmed/25732947,http://www.ncbi.nlm.nih.gov/pubmed/24707333,http://www.ncbi.nlm.nih.gov/pubmed/24032475,http://www.ncbi.nlm.nih.gov/pubmed/22229582,http://www.ncbi.nlm.nih.gov/pubmed/22171583,http://www.ncbi.nlm.nih.gov/pubmed/24001305,http://www.ncbi.nlm.nih.gov/pubmed/23208729,http://www.ncbi.nlm.nih.gov/pubmed/25296871
What is the mechanism of action of ocrelizumab for treatment of multiple sclerosis?
Ocrelizumab is a cytolytic monoclonal antibody that binds CD20 antigen present of B cells. It is approved for treatment of multiple sclerosis.
http://www.ncbi.nlm.nih.gov/pubmed/23500724
What is the link between Nonidet-40 (NP-40) and biotinylation?
0.5% of the non-ionic detergent Nonidet-40 (NP-40) during cell lysis and nuclei isolation is sufficient to practically eliminate contamination by endogenous biotinylated carboxylases during purification of biotin tagged nuclear proteins.NP-40 reduces contamination by endogenous biotinylated carboxylases during purification of biotin tagged nuclear proteins.
http://www.ncbi.nlm.nih.gov/pubmed/23847260,http://www.ncbi.nlm.nih.gov/pubmed/24040022,http://www.ncbi.nlm.nih.gov/pubmed/21094887,http://www.ncbi.nlm.nih.gov/pubmed/22065773,http://www.ncbi.nlm.nih.gov/pubmed/12952890,http://www.ncbi.nlm.nih.gov/pubmed/21660507,http://www.ncbi.nlm.nih.gov/pubmed/21471966,http://www.ncbi.nlm.nih.gov/pubmed/23535403,http://www.ncbi.nlm.nih.gov/pubmed/16679409,http://www.ncbi.nlm.nih.gov/pubmed/9678349,http://www.ncbi.nlm.nih.gov/pubmed/16507360,http://www.ncbi.nlm.nih.gov/pubmed/9487391,http://www.ncbi.nlm.nih.gov/pubmed/7536936,http://www.ncbi.nlm.nih.gov/pubmed/8353487,http://www.ncbi.nlm.nih.gov/pubmed/9024780,http://www.ncbi.nlm.nih.gov/pubmed/11751274,http://www.ncbi.nlm.nih.gov/pubmed/12667455,http://www.ncbi.nlm.nih.gov/pubmed/22925639,http://www.ncbi.nlm.nih.gov/pubmed/16107314,http://www.ncbi.nlm.nih.gov/pubmed/21364561,http://www.ncbi.nlm.nih.gov/pubmed/21947263,http://www.ncbi.nlm.nih.gov/pubmed/22889989,http://www.ncbi.nlm.nih.gov/pubmed/17333537,http://www.ncbi.nlm.nih.gov/pubmed/23122604,http://www.ncbi.nlm.nih.gov/pubmed/23166390,http://www.ncbi.nlm.nih.gov/pubmed/15015744,http://www.ncbi.nlm.nih.gov/pubmed/9099757,http://www.ncbi.nlm.nih.gov/pubmed/19013827,http://www.ncbi.nlm.nih.gov/pubmed/10359800,http://www.ncbi.nlm.nih.gov/pubmed/9074937,http://www.ncbi.nlm.nih.gov/pubmed/10026129,http://www.ncbi.nlm.nih.gov/pubmed/20043281,http://www.ncbi.nlm.nih.gov/pubmed/21820484,http://www.ncbi.nlm.nih.gov/pubmed/23093590,http://www.ncbi.nlm.nih.gov/pubmed/11774371
Which is the transcript responsible for X-chromosome inactivation?
The long non- coding RNA Xist (X inactive specific transcript)
http://www.ncbi.nlm.nih.gov/pubmed/23283335,http://www.ncbi.nlm.nih.gov/pubmed/21041318,http://www.ncbi.nlm.nih.gov/pubmed/25352792,http://www.ncbi.nlm.nih.gov/pubmed/24647936,http://www.ncbi.nlm.nih.gov/pubmed/22341326,http://www.ncbi.nlm.nih.gov/pubmed/23724838,http://www.ncbi.nlm.nih.gov/pubmed/23217739,http://www.ncbi.nlm.nih.gov/pubmed/25070340,http://www.ncbi.nlm.nih.gov/pubmed/23877069,http://www.ncbi.nlm.nih.gov/pubmed/24572099,http://www.ncbi.nlm.nih.gov/pubmed/23088961,http://www.ncbi.nlm.nih.gov/pubmed/25954011,http://www.ncbi.nlm.nih.gov/pubmed/21278729,http://www.ncbi.nlm.nih.gov/pubmed/24001071,http://www.ncbi.nlm.nih.gov/pubmed/23044043,http://www.ncbi.nlm.nih.gov/pubmed/21373649,http://www.ncbi.nlm.nih.gov/pubmed/22341319,http://www.ncbi.nlm.nih.gov/pubmed/22890236,http://www.ncbi.nlm.nih.gov/pubmed/24285886,http://www.ncbi.nlm.nih.gov/pubmed/24048849,http://www.ncbi.nlm.nih.gov/pubmed/25741722,http://www.ncbi.nlm.nih.gov/pubmed/25759964,http://www.ncbi.nlm.nih.gov/pubmed/21782903
What are viral vectors used for in optogenetics?
Viral vectors are used to express optogenetic constructs in selected cells.
http://www.ncbi.nlm.nih.gov/pubmed/24842888,http://www.ncbi.nlm.nih.gov/pubmed/20356930,http://www.ncbi.nlm.nih.gov/pubmed/10521526,http://www.ncbi.nlm.nih.gov/pubmed/22454397,http://www.ncbi.nlm.nih.gov/pubmed/22065782,http://www.ncbi.nlm.nih.gov/pubmed/23629963,http://www.ncbi.nlm.nih.gov/pubmed/24920338,http://www.ncbi.nlm.nih.gov/pubmed/21327870,http://www.ncbi.nlm.nih.gov/pubmed/25002999,http://www.ncbi.nlm.nih.gov/pubmed/22445064,http://www.ncbi.nlm.nih.gov/pubmed/24262168,http://www.ncbi.nlm.nih.gov/pubmed/21844169,http://www.ncbi.nlm.nih.gov/pubmed/22563080,http://www.ncbi.nlm.nih.gov/pubmed/20720006
Which domain allowing self-association do exist in TDP-43 and FUS proteins?
PRION PROTEINSMutations in related RNA-binding proteins TDP-43, FUS/TLS and TAF15 have been connected to ALS. These three proteins share several features, including the presence of a bioinformatics-predicted prion domain, aggregation-prone nature in vitro and in vivo and toxic effects when expressed in multiple model systems. TDP-43, FUS and TAF15 share similar properties, including aggregation-prone behavior in vitro and ability to confer neurodegeneration in Drosophila. For TDP-43, both the RRM1 and the C-terminal glycine-rich domain are required for SG localization. Moreover, two RNA-binding proteins, FUS and TDP-43, which form cytoplasmic aggregates in amyotrophic lateral sclerosis, harbor a 'prion domain' similar to those found in several yeast prion proteinScouring the human genome with this algorithm enriches a select group of RNA-binding proteins harboring a canonical RNA recognition motif (RRM) and a putative prion domain. Moreover, two RNA-binding proteins, FUS and TDP-43, which form cytoplasmic aggregates in amyotrophic lateral sclerosis, harbor a 'prion domain' similar to those found in several yeast prion proteins. PrLDs are over-represented in human RNA-binding proteins and mediate phase transitions underpinning RNP granule assembly. For example, TDP-43 and FUS form cytoplasmic inclusions in amyotrophic lateral sclerosis (ALS) and mutations in TDP-43 and FUS can cause ALS.Two RNA-binding proteins, FUS and TDP-43, which form cytoplasmic aggregates in amyotrophic lateral sclerosis, harbor a 'prion domain' similar to those found in several yeast prion proteins.
http://www.ncbi.nlm.nih.gov/pubmed/24003126,http://www.ncbi.nlm.nih.gov/pubmed/24166911,http://www.ncbi.nlm.nih.gov/pubmed/16500976,http://www.ncbi.nlm.nih.gov/pubmed/21880598,http://www.ncbi.nlm.nih.gov/pubmed/19506577,http://www.ncbi.nlm.nih.gov/pubmed/17913488,http://www.ncbi.nlm.nih.gov/pubmed/20074071
Is there a role for transcription factories in genome organization?
The mammalian nucleus is a highly complex structure that carries out a diverse range of functions such as DNA replication, cell division, RNA processing, and nuclear export/import. Many of these activities occur at discrete subcompartments that intersect with specific regions of the genome. Over the past few decades, evidence has accumulated to suggest that RNA transcription also occurs in specialized sites, called transcription factories, that may influence how the genome is organized. There may be certain efficiency benefits to cluster transcriptional activity in this way. However, the clustering of genes at transcription factories may have consequences for genome stability, and increase the susceptibility to recurrent chromosomal translocations that lead to cancer Yes. The mammalian nucleus is a highly complex structure that carries out a diverse range of functions such as DNA replication, cell division, RNA processing, and nuclear export/import. Many of these activities occur at discrete subcompartments that intersect with specific regions of the genome. Over the past few decades, evidence has accumulated to suggest that RNA transcription also occurs in specialized sites, called transcription factories, that may influence how the genome is organized. Those active chromatin hubs and transcription factories also involve long-range interactions. Thus, it seems that the second law of thermodynamics acts through nonspecific entropic forces between engaged polymerases to drive the self-organization of genomes into loops containing several thousands (and sometimes millions) of basepairs.
http://www.ncbi.nlm.nih.gov/pubmed/22170717,http://www.ncbi.nlm.nih.gov/pubmed/19204208
Which are the Chompret criteria for Li-Fraumeni syndrome?
1) According to the Chompret criteria for LFS, any patient with adrenocortical cancer (ACC), irrespective of age and family history, is at high risk for a TP53 germline mutation. 2) All families with a p53 mutation must have at least one family member with a sarcoma, breast, brain, or adrenocortical carcinoma (ACC).
http://www.ncbi.nlm.nih.gov/pubmed/24675041,http://www.ncbi.nlm.nih.gov/pubmed/24891360,http://www.ncbi.nlm.nih.gov/pubmed/25945060,http://www.ncbi.nlm.nih.gov/pubmed/25101329,http://www.ncbi.nlm.nih.gov/pubmed/26366094,http://www.ncbi.nlm.nih.gov/pubmed/24856155,http://www.ncbi.nlm.nih.gov/pubmed/24670165,http://www.ncbi.nlm.nih.gov/pubmed/25458559,http://www.ncbi.nlm.nih.gov/pubmed/25258420
When ceritinib used instead of crizotinib?
Ceritinib is approved for the treatment of ALK-positive metastatic NSCLC patients that are crizotinib-resistant and crizotinib-naïve.
http://www.ncbi.nlm.nih.gov/pubmed/12943237,http://www.ncbi.nlm.nih.gov/pubmed/17522089,http://www.ncbi.nlm.nih.gov/pubmed/18479207,http://www.ncbi.nlm.nih.gov/pubmed/22989627,http://www.ncbi.nlm.nih.gov/pubmed/19969073,http://www.ncbi.nlm.nih.gov/pubmed/21248284,http://www.ncbi.nlm.nih.gov/pubmed/21902453,http://www.ncbi.nlm.nih.gov/pubmed/20646000,http://www.ncbi.nlm.nih.gov/pubmed/23889121,http://www.ncbi.nlm.nih.gov/pubmed/23749642,http://www.ncbi.nlm.nih.gov/pubmed/21083423,http://www.ncbi.nlm.nih.gov/pubmed/18222042,http://www.ncbi.nlm.nih.gov/pubmed/22916248,http://www.ncbi.nlm.nih.gov/pubmed/19812325,http://www.ncbi.nlm.nih.gov/pubmed/17105810,http://www.ncbi.nlm.nih.gov/pubmed/19375361
What type of enzyme is peroxiredoxin 2 (PRDX2)?
Peroxiredoxin 2 (PRDX2) is an antioxidant enzyme that uses cysteine residues to decompose peroxides. Peroxiredoxin-2 (PRDX2), an enzyme reducing hydrogen peroxide and lipid peroxides Peroxiredoxin 2 (Prx2) is a thiol-dependent peroxidase.
http://www.ncbi.nlm.nih.gov/pubmed/20970105
Is the length of the poly(A) tail involved in human disease?
Yes. Severely truncated poly(A) tails of mitochondrial mRNAs were found to be involved in an autosomal recessive spastic ataxia with optic atrophy.
http://www.ncbi.nlm.nih.gov/pubmed/23391255,http://www.ncbi.nlm.nih.gov/pubmed/22759575,http://www.ncbi.nlm.nih.gov/pubmed/18061402,http://www.ncbi.nlm.nih.gov/pubmed/20715052,http://www.ncbi.nlm.nih.gov/pubmed/18070356,http://www.ncbi.nlm.nih.gov/pubmed/22537298,http://www.ncbi.nlm.nih.gov/pubmed/21357575,http://www.ncbi.nlm.nih.gov/pubmed/22149859,http://www.ncbi.nlm.nih.gov/pubmed/23281733,http://www.ncbi.nlm.nih.gov/pubmed/20589122,http://www.ncbi.nlm.nih.gov/pubmed/20357844
Why graphics processing units (GPU) are more suitable for biological tasks than central processing units (CPU)?
Traditional central processing unist (CPUs) are reaching their limit in processing power and are not designed primarily for multithreaded applications. Graphics processing units (GPUs) on the other hand are affordable, scalable computer powerhouses that, thanks to the ever increasing demand for higher quality graphics, have yet to reach their limit. Typically high-end CPUs have 8-16 cores, whereas GPUs can have more than 2,500 cores. GPUs are also, by design, highly parallel, multicore and multithreaded, able of handling thousands of threads doing the same calculation on different subsets of a large data set. This ability is what makes them perfectly suited for biological analysis tasks. Lately this potential has been realized by many bioinformatics researches and a huge variety of tools and algorithms have been ported to GPUs, or designed from the ground up to maximize the usage of available cores.
http://www.ncbi.nlm.nih.gov/pubmed/18954857,http://www.ncbi.nlm.nih.gov/pubmed/20187783,http://www.ncbi.nlm.nih.gov/pubmed/22947347,http://www.ncbi.nlm.nih.gov/pubmed/7608251,http://www.ncbi.nlm.nih.gov/pubmed/18080776,http://www.ncbi.nlm.nih.gov/pubmed/16384862,http://www.ncbi.nlm.nih.gov/pubmed/19903697,http://www.ncbi.nlm.nih.gov/pubmed/23970761,http://www.ncbi.nlm.nih.gov/pubmed/1193013,http://www.ncbi.nlm.nih.gov/pubmed/23307789,http://www.ncbi.nlm.nih.gov/pubmed/22123068,http://www.ncbi.nlm.nih.gov/pubmed/3730832,http://www.ncbi.nlm.nih.gov/pubmed/9001190,http://www.ncbi.nlm.nih.gov/pubmed/23298477,http://www.ncbi.nlm.nih.gov/pubmed/18386142,http://www.ncbi.nlm.nih.gov/pubmed/23565368,http://www.ncbi.nlm.nih.gov/pubmed/21896621
Which are the thyroid hormone analogs utilized in human studies?
TRIAC and TETRAC are two different thyroid hormone analogs utilized in human studies
http://www.ncbi.nlm.nih.gov/pubmed/17597390,http://www.ncbi.nlm.nih.gov/pubmed/22738784,http://www.ncbi.nlm.nih.gov/pubmed/12535830
Are patients with marfan syndrome at increased risk of arrhythmias?
Patients with marfan syndrome carry increased risk for arrhythmias
http://www.ncbi.nlm.nih.gov/pubmed/16857109,http://www.ncbi.nlm.nih.gov/pubmed/19097381,http://www.ncbi.nlm.nih.gov/pubmed/18958964,http://www.ncbi.nlm.nih.gov/pubmed/15508453,http://www.ncbi.nlm.nih.gov/pubmed/16739060,http://www.ncbi.nlm.nih.gov/pubmed/15655606,http://www.ncbi.nlm.nih.gov/pubmed/12394270,http://www.ncbi.nlm.nih.gov/pubmed/17954092,http://www.ncbi.nlm.nih.gov/pubmed/15672765,http://www.ncbi.nlm.nih.gov/pubmed/17643218,http://www.ncbi.nlm.nih.gov/pubmed/15221987,http://www.ncbi.nlm.nih.gov/pubmed/17229322,http://www.ncbi.nlm.nih.gov/pubmed/16136600,http://www.ncbi.nlm.nih.gov/pubmed/15245670,http://www.ncbi.nlm.nih.gov/pubmed/16566359,http://www.ncbi.nlm.nih.gov/pubmed/11126742,http://www.ncbi.nlm.nih.gov/pubmed/18082353,http://www.ncbi.nlm.nih.gov/pubmed/16437936,http://www.ncbi.nlm.nih.gov/pubmed/17470686,http://www.ncbi.nlm.nih.gov/pubmed/14753595,http://www.ncbi.nlm.nih.gov/pubmed/19829995,http://www.ncbi.nlm.nih.gov/pubmed/19343179,http://www.ncbi.nlm.nih.gov/pubmed/16821517,http://www.ncbi.nlm.nih.gov/pubmed/22678007,http://www.ncbi.nlm.nih.gov/pubmed/18180842,http://www.ncbi.nlm.nih.gov/pubmed/15993051,http://www.ncbi.nlm.nih.gov/pubmed/24325620
What are the treatments of choice for GIST (gastrointestinal stromal tumor)?
The surgical resection is a treatment of choice for gastrointestinal stromal tumors. It has been shown that adequate surgical resection correlates with high 5-years survival rates for patients with gastric GIST. When they are localized, the treatment of choice is surgical excision, but advanced tumors have a limited response to chemo or radiotherapy. Imatinib (STI571 or Glivec) is a selective inhibitor or tyrosine kinase proteins that has been used successfully in the treatment of advanced GIST. Approximately 80% of patients with metastatic GIST benefit from imatinib, although acquired resistance to the agent may develop. For patients with primary GIST, surgery remains the treatment of choice, and whether outcome is improved by adjuvant imatinib is currently under broad investigation.
http://www.ncbi.nlm.nih.gov/pubmed/25207108,http://www.ncbi.nlm.nih.gov/pubmed/19529061,http://www.ncbi.nlm.nih.gov/pubmed/6984375,http://www.ncbi.nlm.nih.gov/pubmed/17725169,http://www.ncbi.nlm.nih.gov/pubmed/16940490,http://www.ncbi.nlm.nih.gov/pubmed/24019633,http://www.ncbi.nlm.nih.gov/pubmed/24730627,http://www.ncbi.nlm.nih.gov/pubmed/20550487,http://www.ncbi.nlm.nih.gov/pubmed/15025618,http://www.ncbi.nlm.nih.gov/pubmed/22966723,http://www.ncbi.nlm.nih.gov/pubmed/17408950,http://www.ncbi.nlm.nih.gov/pubmed/8290523,http://www.ncbi.nlm.nih.gov/pubmed/313731,http://www.ncbi.nlm.nih.gov/pubmed/8080604,http://www.ncbi.nlm.nih.gov/pubmed/14551758,http://www.ncbi.nlm.nih.gov/pubmed/9927835,http://www.ncbi.nlm.nih.gov/pubmed/9018261
List Kartagener Syndrome Triad.
The triad of situs inversus, bronchiectasis and sinusitis is known as Kartagener syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/24232919,http://www.ncbi.nlm.nih.gov/pubmed/21484336,http://www.ncbi.nlm.nih.gov/pubmed/21951698,http://www.ncbi.nlm.nih.gov/pubmed/23966205,http://www.ncbi.nlm.nih.gov/pubmed/22718021,http://www.ncbi.nlm.nih.gov/pubmed/19829708,http://www.ncbi.nlm.nih.gov/pubmed/23777630,http://www.ncbi.nlm.nih.gov/pubmed/24075187,http://www.ncbi.nlm.nih.gov/pubmed/22536400,http://www.ncbi.nlm.nih.gov/pubmed/21288772,http://www.ncbi.nlm.nih.gov/pubmed/23593020,http://www.ncbi.nlm.nih.gov/pubmed/22798623,http://www.ncbi.nlm.nih.gov/pubmed/17984056,http://www.ncbi.nlm.nih.gov/pubmed/22892954,http://www.ncbi.nlm.nih.gov/pubmed/24030947,http://www.ncbi.nlm.nih.gov/pubmed/23108159,http://www.ncbi.nlm.nih.gov/pubmed/23644600,http://www.ncbi.nlm.nih.gov/pubmed/21529284,http://www.ncbi.nlm.nih.gov/pubmed/23143600
Which disease is associated with the ectopic expression of the protein encoded by the gene DUX4?
Facioscapulohumeral dystrophy (FSHD) is a progressive muscular dystrophy caused by decreased epigenetic repression of the D4Z4 macrosatellite repeats and ectopic expression of DUX4, a retrogene encoding a germline transcription factor encoded in each repeat.
http://www.ncbi.nlm.nih.gov/pubmed/11709084,http://www.ncbi.nlm.nih.gov/pubmed/19801976,http://www.ncbi.nlm.nih.gov/pubmed/24265417,http://www.ncbi.nlm.nih.gov/pubmed/9301423,http://www.ncbi.nlm.nih.gov/pubmed/11230698
Which G protein is essential in the formation and function of lamellipodia?
Recruitment of the small G-protein Rac1 to the plasma membrane is essential in inducing the local formation of specialized cellular processes termed lamellipodia.
http://www.ncbi.nlm.nih.gov/pubmed/22915799,http://www.ncbi.nlm.nih.gov/pubmed/15466872,http://www.ncbi.nlm.nih.gov/pubmed/17439959,http://www.ncbi.nlm.nih.gov/pubmed/21966267,http://www.ncbi.nlm.nih.gov/pubmed/22720156,http://www.ncbi.nlm.nih.gov/pubmed/22203821,http://www.ncbi.nlm.nih.gov/pubmed/15994766,http://www.ncbi.nlm.nih.gov/pubmed/16557012
Which are the main functions of the APOBEC3 family of proteins?
The APOBEC3 family of cytidine deaminases play a critical role in host-mediated defense against exogenous viruses, most notably, human immunodeficiency virus type-1 (HIV-1), and endogenous transposable elements, such as LINE-1 and Alu retrotransposons.
http://www.ncbi.nlm.nih.gov/pubmed/17710556,http://www.ncbi.nlm.nih.gov/pubmed/11850619,http://www.ncbi.nlm.nih.gov/pubmed/11356363,http://www.ncbi.nlm.nih.gov/pubmed/16705169,http://www.ncbi.nlm.nih.gov/pubmed/18004385,http://www.ncbi.nlm.nih.gov/pubmed/20599948,http://www.ncbi.nlm.nih.gov/pubmed/22572731,http://www.ncbi.nlm.nih.gov/pubmed/14506132,http://www.ncbi.nlm.nih.gov/pubmed/18987983,http://www.ncbi.nlm.nih.gov/pubmed/19786836,http://www.ncbi.nlm.nih.gov/pubmed/15368356,http://www.ncbi.nlm.nih.gov/pubmed/20562223,http://www.ncbi.nlm.nih.gov/pubmed/21267468,http://www.ncbi.nlm.nih.gov/pubmed/12581305,http://www.ncbi.nlm.nih.gov/pubmed/21803857
Which histone modifications are associated with constitutive heterochromatin?
Strong methylation at H3 lysine 9 occurred preferentially in heterochromatic chromocenters of Arabidopsis nuclei. In general, heterochromatin has been linked to trimethylation of H3 at lysine 9 and parsimony analysis reveal that histone H3K9 methylation is, next to histone deacetylation, the evolutionary most stable heterochromatic mark. Classical histone modifications associated with heterochromatin also include H3K27me1 and H3K27me2. H3K36me3 function is not restricted to actively transcribed regions only and may contribute to the composition of heterochromatin. Other histone methylation marks usually found in constitutive heterochromatin are H4K20me3, H3K9me3, and H3K79me3. H3S10P is a good marker of pericentromeric heterochromatin.H3K9 methylation H3S10 phosphorylation H3K79 and H4K20 methylation
http://www.ncbi.nlm.nih.gov/pubmed/23227840,http://www.ncbi.nlm.nih.gov/pubmed/23322582,http://www.ncbi.nlm.nih.gov/pubmed/22261725,http://www.ncbi.nlm.nih.gov/pubmed/23811049
What is the main application of SWATH-MS in proteomics?
Using the method called SWATH-MS one might ask sample sets for the presence and quantity of essentially any protein of interest.
http://www.ncbi.nlm.nih.gov/pubmed/19074884,http://www.ncbi.nlm.nih.gov/pubmed/15875088,http://www.ncbi.nlm.nih.gov/pubmed/19690186,http://www.ncbi.nlm.nih.gov/pubmed/20852007,http://www.ncbi.nlm.nih.gov/pubmed/20424130,http://www.ncbi.nlm.nih.gov/pubmed/22072582,http://www.ncbi.nlm.nih.gov/pubmed/19299660,http://www.ncbi.nlm.nih.gov/pubmed/23133653,http://www.ncbi.nlm.nih.gov/pubmed/16690748,http://www.ncbi.nlm.nih.gov/pubmed/17160069
Do selenoproteins and selenium play a role in prostate cancer prevention?
No, although initial epidemiological studies on humans and on animal and cell- based models indicated that selenoproteins may be protecting against prostate cancer, more research is needed to improve the understanding of selenium metabolism and requirements for optimal health.
http://www.ncbi.nlm.nih.gov/pubmed/19302373,http://www.ncbi.nlm.nih.gov/pubmed/19052641,http://www.ncbi.nlm.nih.gov/pubmed/17049789,http://www.ncbi.nlm.nih.gov/pubmed/16687936,http://www.ncbi.nlm.nih.gov/pubmed/16164422
What can Nothobranchius furzeri be used as a model system for?
N. furzeri an interesting model system to investigate the effects of experimental manipulations on longevity and age-related pathologies. N. furzeri could represent a model system for studying the genetic control of life-history traits in natural populations. N. furzeri could be a very useful model for comparative genomics of aging. It can be employed to test the effects of experimental manipulation on aging and apharmacological research.
http://www.ncbi.nlm.nih.gov/pubmed/22624882,http://www.ncbi.nlm.nih.gov/pubmed/23027955,http://www.ncbi.nlm.nih.gov/pubmed/23000899,http://www.ncbi.nlm.nih.gov/pubmed/23555929
What is the function of TALENs?
These chimeric enzymes can be used to introduce a double strand break at a specific genomic site which then can become the substrate for error-prone non-homologous end joining (NHEJ), generating mutations at the site of cleavage. Artificial transcription activator-like effector nucleases (TALENs) provide a powerful new approach for targeted zebrafish genome editing and functional genomic applications. Transcription Activator-Like Effector Nucleases (TALENs) consist of a nuclease domain fused to a DNA binding domain which is engineered to bind to any genomic sequence. Transcription activator-like effector nucleases (TALENs) are programmable nucleases that join FokI endonuclease with the modular DNA-binding domain of TALEs.Transcription Activator-Like Effector Nucleases (TALENs) consist of a nuclease domain fused to a DNA binding domain which is engineered to bind to any genomic sequence. These chimeric enzymes can be used to introduce a double strand break at a specific genomic site which then can become the substrate for error-prone non-homologous end joining (NHEJ), generating mutations at the site of cleavage. TALENs provide a powerful new approach for targeted genome editing and functional genomic applications.
http://www.ncbi.nlm.nih.gov/pubmed/24498912,http://www.ncbi.nlm.nih.gov/pubmed/25182207,http://www.ncbi.nlm.nih.gov/pubmed/25475141,http://www.ncbi.nlm.nih.gov/pubmed/24763532,http://www.ncbi.nlm.nih.gov/pubmed/24724574,http://www.ncbi.nlm.nih.gov/pubmed/25116951,http://www.ncbi.nlm.nih.gov/pubmed/24823363,http://www.ncbi.nlm.nih.gov/pubmed/25520183,http://www.ncbi.nlm.nih.gov/pubmed/25515746,http://www.ncbi.nlm.nih.gov/pubmed/24782594,http://www.ncbi.nlm.nih.gov/pubmed/25355199,http://www.ncbi.nlm.nih.gov/pubmed/24497204
Has protein citrullination been implicated in rheumatoid arthritis?
Yes, protein citrullination been implicated in rheumatoid arthritis.
http://www.ncbi.nlm.nih.gov/pubmed/24092417,http://www.ncbi.nlm.nih.gov/pubmed/21328299,http://www.ncbi.nlm.nih.gov/pubmed/22165979,http://www.ncbi.nlm.nih.gov/pubmed/21047485
Show results of randomised controlled trials for certolizumab pegol.
Improvement of clinical results (ACR50, 28 joint disease activity score (DAS-28) remission and HAQ scores) with certolizumab pegol. Adverse events were more frequent with certolizumab; there was a statistically significant increase in the number of serious adverse events, infections and hypertension. Randomised controlled trials (RCTs) of CZP have demonstrated rapid improvements in workplace and home productivity.
http://www.ncbi.nlm.nih.gov/pubmed/24196352,http://www.ncbi.nlm.nih.gov/pubmed/24051958,http://www.ncbi.nlm.nih.gov/pubmed/24142993,http://www.ncbi.nlm.nih.gov/pubmed/24167568,http://www.ncbi.nlm.nih.gov/pubmed/24251111,http://www.ncbi.nlm.nih.gov/pubmed/23682733,http://www.ncbi.nlm.nih.gov/pubmed/23707720
Which is the mass-tag that reveal the ubiquitination of a lysine residue?
Lys-ɛ-Gly-Gly (K-ɛ-GG) is the remnant produced by trypsin digestion of proteins having ubiquitinated lysine side chains.
http://www.ncbi.nlm.nih.gov/pubmed/19788051,http://www.ncbi.nlm.nih.gov/pubmed/22664156,http://www.ncbi.nlm.nih.gov/pubmed/17854869,http://www.ncbi.nlm.nih.gov/pubmed/21038489,http://www.ncbi.nlm.nih.gov/pubmed/19539236,http://www.ncbi.nlm.nih.gov/pubmed/19018300,http://www.ncbi.nlm.nih.gov/pubmed/20224942,http://www.ncbi.nlm.nih.gov/pubmed/17726918,http://www.ncbi.nlm.nih.gov/pubmed/18313300,http://www.ncbi.nlm.nih.gov/pubmed/17622327,http://www.ncbi.nlm.nih.gov/pubmed/21702048,http://www.ncbi.nlm.nih.gov/pubmed/17996090,http://www.ncbi.nlm.nih.gov/pubmed/19255248,http://www.ncbi.nlm.nih.gov/pubmed/22878905,http://www.ncbi.nlm.nih.gov/pubmed/23308019
Which gene is involved in CADASIL?
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), the most common form of familial vascular dementia, is caused by mutations of the NOTCH3 gene.
http://www.ncbi.nlm.nih.gov/pubmed/22147010,http://www.ncbi.nlm.nih.gov/pubmed/12869545,http://www.ncbi.nlm.nih.gov/pubmed/20529852
What is the role of thyroid hormone receptor alpha1 in insulin secretion?
Liganded TR(alpha) plays a critical role in beta-cell replication and in expansion of the beta-cell mass. the TRalpha P398H mutation which cannot bind T3, is associated with insulin resistance. Loss of Thra protects mice from high-fat diet-induced hepatic and peripheral insulin resistance.
http://www.ncbi.nlm.nih.gov/pubmed/15569610,http://www.ncbi.nlm.nih.gov/pubmed/7774596,http://www.ncbi.nlm.nih.gov/pubmed/10082645,http://www.ncbi.nlm.nih.gov/pubmed/21191184,http://www.ncbi.nlm.nih.gov/pubmed/25569209,http://www.ncbi.nlm.nih.gov/pubmed/9119223,http://www.ncbi.nlm.nih.gov/pubmed/21979917,http://www.ncbi.nlm.nih.gov/pubmed/9009281,http://www.ncbi.nlm.nih.gov/pubmed/22195969,http://www.ncbi.nlm.nih.gov/pubmed/20495385,http://www.ncbi.nlm.nih.gov/pubmed/21129203,http://www.ncbi.nlm.nih.gov/pubmed/9150892,http://www.ncbi.nlm.nih.gov/pubmed/22965135,http://www.ncbi.nlm.nih.gov/pubmed/25487262,http://www.ncbi.nlm.nih.gov/pubmed/25972891,http://www.ncbi.nlm.nih.gov/pubmed/19841062,http://www.ncbi.nlm.nih.gov/pubmed/22464441,http://www.ncbi.nlm.nih.gov/pubmed/8798672
Do R-loops tend to form at sites of DNA replication?
R-loops co-localize with the ORC within the same CpG island region in a significant fraction of these efficient replication origins. Physiological R-loop formation at CpG island promoters can contribute to DNA replication origin specification at these regions, the most efficient replication initiation sites in mammalian cells. One mechanism may be that downstream of a replication block, RNA at R-loops is extended by DNA polymerase I, opening up the DNA duplex and leading to the recruitment of the replisome. This would allow replication to proceed while the original block is repaired or bypassed. Thus, the organized structure of the R-loop is critical for primer RNA function in vivo with important implications for the RNA processing and DNA replication machinery.We found that overproduction of RecG protein drastically decreased copy numbers of ColE1-type plasmids, which require R-loop formation between the template DNA and a primer RNA transcript (RNA II) for the initiation of replication. ColE1 plasmid origins of replication and oriK sites initiate primosome assembly by an RNA-DNA hybrid structure known as R-loop. We propose that downstream of a replication block, RNA at R-loops is extended by DNA polymerase I, opening up the DNA duplex and leading to the recruitment of the replisome. We review evidence suggesting that R-loops are frequent during normal cell growth and that R-loops are critical for the maintenance of genome integrity.
http://www.ncbi.nlm.nih.gov/pubmed/19198095,http://www.ncbi.nlm.nih.gov/pubmed/10733264,http://www.ncbi.nlm.nih.gov/pubmed/11147512,http://www.ncbi.nlm.nih.gov/pubmed/11147511,http://www.ncbi.nlm.nih.gov/pubmed/12588639,http://www.ncbi.nlm.nih.gov/pubmed/21164341,http://www.ncbi.nlm.nih.gov/pubmed/19589043,http://www.ncbi.nlm.nih.gov/pubmed/15372589,http://www.ncbi.nlm.nih.gov/pubmed/12952501,http://www.ncbi.nlm.nih.gov/pubmed/8784230,http://www.ncbi.nlm.nih.gov/pubmed/1933685,http://www.ncbi.nlm.nih.gov/pubmed/14741081,http://www.ncbi.nlm.nih.gov/pubmed/10651109,http://www.ncbi.nlm.nih.gov/pubmed/15853578
Which two catechol-O-methyl transferase (COMT) inhibitors can be used for treatment of Parkinson disease?
Tolcapone (central and peripheral) and entacapone (peripheral) are catechol-O-methyl transferase inhibitors that are used for treatment of Parkinson disease.
http://www.ncbi.nlm.nih.gov/pubmed/22502568,http://www.ncbi.nlm.nih.gov/pubmed/21721843,http://www.ncbi.nlm.nih.gov/pubmed/22585043,http://www.ncbi.nlm.nih.gov/pubmed/23396250,http://www.ncbi.nlm.nih.gov/pubmed/22963508,http://www.ncbi.nlm.nih.gov/pubmed/22168818,http://www.ncbi.nlm.nih.gov/pubmed/21945137,http://www.ncbi.nlm.nih.gov/pubmed/23331681,http://www.ncbi.nlm.nih.gov/pubmed/22238362,http://www.ncbi.nlm.nih.gov/pubmed/22250786,http://www.ncbi.nlm.nih.gov/pubmed/21844209,http://www.ncbi.nlm.nih.gov/pubmed/22507538
What are the structures formed when keratin molecules come together?
Keratins form the intermediate filaments of the cytoskeleton and provide scaffold structures within cells.
http://www.ncbi.nlm.nih.gov/pubmed/16330914,http://www.ncbi.nlm.nih.gov/pubmed/19609889,http://www.ncbi.nlm.nih.gov/pubmed/11747849,http://www.ncbi.nlm.nih.gov/pubmed/23124142,http://www.ncbi.nlm.nih.gov/pubmed/23990180
Which is the prognostic impact of hypothyroidism in patients with acute myocardial infarction?
Thyroid dysfunction, particularly low T3 syndrome, is a strong predictor of short-term and long-term poor prognoses in patients with acute myocardial infarctions.
http://www.ncbi.nlm.nih.gov/pubmed/13129802,http://www.ncbi.nlm.nih.gov/pubmed/25173930,http://www.ncbi.nlm.nih.gov/pubmed/24360741,http://www.ncbi.nlm.nih.gov/pubmed/16808883,http://www.ncbi.nlm.nih.gov/pubmed/24115583,http://www.ncbi.nlm.nih.gov/pubmed/24355598,http://www.ncbi.nlm.nih.gov/pubmed/24920614,http://www.ncbi.nlm.nih.gov/pubmed/25888396
Which are the main features of CREST and other ALS-linked proteins?
CREST and certain other ALS-linked proteins share several features implicated in ALS pathogenesis, namely the ability to aggregate, be recruited to stress granules and alter paraspeckle integrity.Similar to several proteins implicated in ALS, CREST contains a prion-like domain and was reported to be a component of paraspeckles. Like several other ALS-associated proteins, CREST is recruited to induced stress granules. Our data indicate that CREST and certain other ALS-linked proteins share several features implicated in ALS pathogenesis, namely the ability to aggregate, be recruited to stress granules and alter paraspeckle integrity.Like several other ALS-associated proteins, CREST is recruited to induced stress granules.
http://www.ncbi.nlm.nih.gov/pubmed/20301466,http://www.ncbi.nlm.nih.gov/pubmed/22422768,http://www.ncbi.nlm.nih.gov/pubmed/24370574,http://www.ncbi.nlm.nih.gov/pubmed/23595086,http://www.ncbi.nlm.nih.gov/pubmed/20807279,http://www.ncbi.nlm.nih.gov/pubmed/22787013,http://www.ncbi.nlm.nih.gov/pubmed/22589293,http://www.ncbi.nlm.nih.gov/pubmed/16601229,http://www.ncbi.nlm.nih.gov/pubmed/25480325,http://www.ncbi.nlm.nih.gov/pubmed/23908839
Mutations of which genes have been associated with Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)?
Mutations in five genes – ryanodine receptor 2 (RYR2), calsequestrin 2(CASQ2), triadic (TRDN), calmodulin 1 (CALM1) and potassium channel, inwardly rectifying subfamily J, member 2 (KCNJ2) – have been found to be associated with CPVT
http://www.ncbi.nlm.nih.gov/pubmed/20808788,http://www.ncbi.nlm.nih.gov/pubmed/15862762,http://www.ncbi.nlm.nih.gov/pubmed/21289049,http://www.ncbi.nlm.nih.gov/pubmed/19687145,http://www.ncbi.nlm.nih.gov/pubmed/19684599,http://www.ncbi.nlm.nih.gov/pubmed/20097656,http://www.ncbi.nlm.nih.gov/pubmed/21859475,http://www.ncbi.nlm.nih.gov/pubmed/22683623,http://www.ncbi.nlm.nih.gov/pubmed/22954214,http://www.ncbi.nlm.nih.gov/pubmed/19823040,http://www.ncbi.nlm.nih.gov/pubmed/8918932,http://www.ncbi.nlm.nih.gov/pubmed/9461388,http://www.ncbi.nlm.nih.gov/pubmed/11724736
What is the relationship between nucleosomes and exons?
Nucleosomes are preferentially located within exons compared to nearby intronic sequences. Preferential positioning within the exons is indepedent of gene expression levels, stronger in exons with weak splice sites and conserved through metazoan evolution.
http://www.ncbi.nlm.nih.gov/pubmed/20499259,http://www.ncbi.nlm.nih.gov/pubmed/20045317,http://www.ncbi.nlm.nih.gov/pubmed/22272142,http://www.ncbi.nlm.nih.gov/pubmed/22779800,http://www.ncbi.nlm.nih.gov/pubmed/19691298,http://www.ncbi.nlm.nih.gov/pubmed/23140189,http://www.ncbi.nlm.nih.gov/pubmed/22553386,http://www.ncbi.nlm.nih.gov/pubmed/21955456,http://www.ncbi.nlm.nih.gov/pubmed/18763758,http://www.ncbi.nlm.nih.gov/pubmed/23202316,http://www.ncbi.nlm.nih.gov/pubmed/21342558,http://www.ncbi.nlm.nih.gov/pubmed/21138791,http://www.ncbi.nlm.nih.gov/pubmed/20055175,http://www.ncbi.nlm.nih.gov/pubmed/21179343,http://www.ncbi.nlm.nih.gov/pubmed/22435086,http://www.ncbi.nlm.nih.gov/pubmed/17477520,http://www.ncbi.nlm.nih.gov/pubmed/20116902,http://www.ncbi.nlm.nih.gov/pubmed/22587766,http://www.ncbi.nlm.nih.gov/pubmed/9651155,http://www.ncbi.nlm.nih.gov/pubmed/21143043,http://www.ncbi.nlm.nih.gov/pubmed/20621485,http://www.ncbi.nlm.nih.gov/pubmed/20427100,http://www.ncbi.nlm.nih.gov/pubmed/21284830,http://www.ncbi.nlm.nih.gov/pubmed/17668276,http://www.ncbi.nlm.nih.gov/pubmed/20085380,http://www.ncbi.nlm.nih.gov/pubmed/22546667
List programs suitable for pharmacophore modelling
A pharmacophore is an abstract description of molecular features which are necessary for molecular recognition of a ligand by a biological macromolecule. The IUPAC defines a pharmacophore to be "an ensemble of steric and electronic features that is necessary to ensure the optimal supramolecular interactions with a specific biological target and to trigger (or block) its biological response". A pharmacophore model explains how structurally diverse ligands can bind to a common receptor site. Furthermore pharmacophore models can be used to identify through denovo design or virtual screening novel ligands that will bind to the same receptor. Nowadays there are many programs suitable for pharmacophore modelling such as LigandScout, Discovery Studio, Catalyst, PharmaGist, Genetic Algorithm Similarity and Molecular Operating Environment.
http://www.ncbi.nlm.nih.gov/pubmed/15132715,http://www.ncbi.nlm.nih.gov/pubmed/22009156,http://www.ncbi.nlm.nih.gov/pubmed/20810577,http://www.ncbi.nlm.nih.gov/pubmed/21896670,http://www.ncbi.nlm.nih.gov/pubmed/23448365,http://www.ncbi.nlm.nih.gov/pubmed/19034261,http://www.ncbi.nlm.nih.gov/pubmed/11932302,http://www.ncbi.nlm.nih.gov/pubmed/17160166,http://www.ncbi.nlm.nih.gov/pubmed/23565426,http://www.ncbi.nlm.nih.gov/pubmed/23786024
Is selenium deficiency involved in autoimmune thyroid disease?
Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interactionIn areas with severe selenium deficiency higher incidence of thyroiditis has been reported due to a decreased activity of selenium-dependent glutathione peroxidase enzyme within thyroid cellsThe essential trace element selenium was recently recognized as being incorporated as selenocysteine in all three deiodinases of the thyroid gland. This has decisively confirmed the clear-cut link between selenium and thyroid function. Additionally, it has been established that the thyroid contains more selenium than any other tissue, and that selenium deficiency aggravates the manifestation of autoimmune thyroid disease.The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease
http://www.ncbi.nlm.nih.gov/pubmed/24126373,http://www.ncbi.nlm.nih.gov/pubmed/16885236,http://www.ncbi.nlm.nih.gov/pubmed/8090716,http://www.ncbi.nlm.nih.gov/pubmed/7654063,http://www.ncbi.nlm.nih.gov/pubmed/22970697,http://www.ncbi.nlm.nih.gov/pubmed/16044424,http://www.ncbi.nlm.nih.gov/pubmed/23847141
List disorders that are caused by mutations in the mitochondrial MTND6 gene.
Mitochondrial MTND6 gene mutations are the cause of Leigh syndrome and Leber's hereditary optic neuropathy and/or dystonia.
http://www.ncbi.nlm.nih.gov/pubmed/25220802,http://www.ncbi.nlm.nih.gov/pubmed/26539452,http://www.ncbi.nlm.nih.gov/pubmed/24705333,http://www.ncbi.nlm.nih.gov/pubmed/25489581,http://www.ncbi.nlm.nih.gov/pubmed/20970979
Which are the most common methods for ctDNA (circulating tumour DNA) detection?
Recently, nanoplasmonics has emerged as a platform for one-step dual detection with high sensitivity and specificity. The practice of "liquid biopsy" as a diagnostic, prognostic and theranostic tool in non-small cell lung cancer (NSCLC) patients is an appealing approach, at least in theory, since it is noninvasive and easily repeated. Cancer personalized profiling by deep sequencing (CAPP-Seq), an economical and ultrasensitive method for quantifying ctDNA. A new DNA sensor using a nickel(II) phenanthroline complex ([Ni(phen)(2)PHPIP]·2ClO(4)) as the electrochemical probe was developed. The sensor is very sensitive and selective for calf thymus DNA (ctDNA) detection in aqueous medium.A new DNA sensor using a nickel(II) phenanthroline complex ([Ni(phen)(2)PHPIP]·2ClO(4)) as the electrochemical probe was developed. The calculated dynamics parameters of the electrode process indicate that there are obvious interactions between the probe and the ctDNA in aqueous solution. Under constant potential conditions, the redox current peak of the probe (Ni-complex) decreases obviously as the probe interacts/binds with ctDNAs. These results demonstrate that the sensor can simultaneously detect the hot-spot mutation and epigenetic changes on the ctDNA.
http://www.ncbi.nlm.nih.gov/pubmed/15241680,http://www.ncbi.nlm.nih.gov/pubmed/17036334,http://www.ncbi.nlm.nih.gov/pubmed/19449410,http://www.ncbi.nlm.nih.gov/pubmed/17103449,http://www.ncbi.nlm.nih.gov/pubmed/12794698,http://www.ncbi.nlm.nih.gov/pubmed/19215249,http://www.ncbi.nlm.nih.gov/pubmed/17414289,http://www.ncbi.nlm.nih.gov/pubmed/22622662,http://www.ncbi.nlm.nih.gov/pubmed/19755431,http://www.ncbi.nlm.nih.gov/pubmed/24168007,http://www.ncbi.nlm.nih.gov/pubmed/21403557,http://www.ncbi.nlm.nih.gov/pubmed/20592905,http://www.ncbi.nlm.nih.gov/pubmed/18000976,http://www.ncbi.nlm.nih.gov/pubmed/14963686,http://www.ncbi.nlm.nih.gov/pubmed/23044018,http://www.ncbi.nlm.nih.gov/pubmed/19086028,http://www.ncbi.nlm.nih.gov/pubmed/23378035
Which gene is associated with Muenke syndrome?
Muenke syndrome has been related to a mutation on the Fibroblast Growth Factor Receptor (FGFR3) gene.
http://www.ncbi.nlm.nih.gov/pubmed/21120498,http://www.ncbi.nlm.nih.gov/pubmed/21346578,http://www.ncbi.nlm.nih.gov/pubmed/18504282,http://www.ncbi.nlm.nih.gov/pubmed/23292481,http://www.ncbi.nlm.nih.gov/pubmed/19506586,http://www.ncbi.nlm.nih.gov/pubmed/18819772,http://www.ncbi.nlm.nih.gov/pubmed/22772888,http://www.ncbi.nlm.nih.gov/pubmed/21985166
Is it safe to use Abatacept during pregnancy?
It is not safe to use the drug abatacept during pregnancy, since there is very limited experience/knowledge yet. Additionally, it is recommended to withdraw the drug before pregnancy.Prophylactic withdrawal of drugs before pregnancy is mandatory for abatacept.
http://www.ncbi.nlm.nih.gov/pubmed/19074369,http://www.ncbi.nlm.nih.gov/pubmed/20967606
What is DeepCAGE?
The cap analysis of gene expression (CAGE) technology has been established to detect transcriptional starting sites (TSSs) and expression levels by utilizing 5' cDNA tags and PCR. It has been reported that the amount of templates is proportional to the amplification efficiency of PCR. CAGE has been used as a key technique for analyzing promoter activity and finding new transcripts including alternative spliced products and noncoding transcripts. DeepCAGE can be utilized for high-throughput next-generation sequencing technology. DeepCAGE can produce much deeper transcriptome datasets and can reveal more details of the regulatory network.
http://www.ncbi.nlm.nih.gov/pubmed/23221979,http://www.ncbi.nlm.nih.gov/pubmed/23084476
Is STAT3 involved in EIF2AK2-dependent suppression of autophagy?
STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagyPharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. On the other hand, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy. Therefore, STAT3 may act as a competitive inhibitor of EIF2AK2 to suppress autophagy.
http://www.ncbi.nlm.nih.gov/pubmed/25913272,http://www.ncbi.nlm.nih.gov/pubmed/25007730,http://www.ncbi.nlm.nih.gov/pubmed/21782519,http://www.ncbi.nlm.nih.gov/pubmed/24468190,http://www.ncbi.nlm.nih.gov/pubmed/23787092,http://www.ncbi.nlm.nih.gov/pubmed/25024381,http://www.ncbi.nlm.nih.gov/pubmed/23454164,http://www.ncbi.nlm.nih.gov/pubmed/21816030,http://www.ncbi.nlm.nih.gov/pubmed/21816031,http://www.ncbi.nlm.nih.gov/pubmed/22739688,http://www.ncbi.nlm.nih.gov/pubmed/19806009,http://www.ncbi.nlm.nih.gov/pubmed/21604980,http://www.ncbi.nlm.nih.gov/pubmed/19859560,http://www.ncbi.nlm.nih.gov/pubmed/21073995,http://www.ncbi.nlm.nih.gov/pubmed/20735271,http://www.ncbi.nlm.nih.gov/pubmed/21816032,http://www.ncbi.nlm.nih.gov/pubmed/25077418,http://www.ncbi.nlm.nih.gov/pubmed/24292709,http://www.ncbi.nlm.nih.gov/pubmed/25072396
RTS S AS01 vaccine was developed to prevent which disease?
RTS,S/AS01 vaccine was developed for prevention of malaria.
http://www.ncbi.nlm.nih.gov/pubmed/25274727,http://www.ncbi.nlm.nih.gov/pubmed/22495300,http://www.ncbi.nlm.nih.gov/pubmed/25409831
What are the Topological Domains (TADs)?
Topolological domains or TADs are megabase-sized local chromatin interaction domains which are a pervasive structural feature of the genome organization. These domains correlate with regions of the genome that constrain the spread of heterochromatin. The domains are stable across different cell types and highly conserved across species, indicating that topological domains are an inherent property of mammalian genomes. The boundaries of topological domains are enriched for the insulator binding protein CTCF, housekeeping genes, transfer RNAs and short interspersed element (SINE) retrotransposons, indicating that these factors may have a role in establishing the topological domain structure of the genome.
http://www.ncbi.nlm.nih.gov/pubmed/8985605,http://www.ncbi.nlm.nih.gov/pubmed/25901328
What is the vibrational theory of olfaction?
The vibrational theory of olfaction assumes that electron transfer occurs across odorants at the active sites of odorant receptors (ORs), serving as a sensitive measure of odorant vibrational frequencies, ultimately leading to olfactory perception. The theory proposes that olfactory receptors respond not to the shape of the molecules but to their vibrations. It differs from previous vibrational theories (Dyson, Wright) in providing a detailed and plausible mechanism for biological transduction of molecular vibrations: inelastic electron tunnelling. Thus, the authors, that have proposed this theory, suggest that olfaction, like colour vision and hearing, is a spectral sense.
http://www.ncbi.nlm.nih.gov/pubmed/16140943,http://www.ncbi.nlm.nih.gov/pubmed/17962299,http://www.ncbi.nlm.nih.gov/pubmed/16140944,http://www.ncbi.nlm.nih.gov/pubmed/21811597,http://www.ncbi.nlm.nih.gov/pubmed/21465478,http://www.ncbi.nlm.nih.gov/pubmed/24657531,http://www.ncbi.nlm.nih.gov/pubmed/23390377,http://www.ncbi.nlm.nih.gov/pubmed/12191639
Are CTCF and BORIS involved in genome regulation and cancer?
Yes. CTCF is ubiquitously expressed and plays diverse roles in gene regulation, imprinting, insulation, intra/interchromosomal interactions, nuclear compartmentalisation, and alternative splicing. CTCF has a single paralogue, the testes-specific CTCF-like gene (CTCFL)/BORIS. CTCF and BORIS can be deregulated in cancer. The tumour suppressor gene CTCF can be mutated or deleted in cancer, or CTCF DNA binding can be altered by epigenetic changes. BORIS is aberrantly expressed frequently in cancer, leading some to propose a pro-tumourigenic role for BORIS. However, BORIS can inhibit cell proliferation, and is mutated in cancer similarly to CTCF suggesting BORIS activation in cancer may be due to global genetic or epigenetic changes typical of malignant transformation.
http://www.ncbi.nlm.nih.gov/pubmed/21089077
What is the application of the ASSET algorithm in C.elegans?
ASSET (Algorithm for the Segmentation and the Standardization of C. elegans Time-lapse recordings) is a robust algorithm for the automated segmentation and standardization of early Caenorhabditis elegans embryos. It gathers quantitative information with subcellular precision in the early Caenorhabditis elegans embryo, which is an attractive model to investigate evolutionarily conserved cellular mechanisms. ASSET automatically detects the eggshell and the cell cortex from DIC time-lapse recordings of live one-cell-stage embryos and can also track subcellular structures using fluorescent time-lapse microscopy. Importantly, ASSET standardizes the data into an absolute coordinate system to allow robust quantitative comparisons between embryos.The early Caenorhabditis elegans embryo is an attractive model to investigate evolutionarily conserved cellular mechanisms. In summary, we establish ASSET as a novel tool for the efficient quantification and standardization of images from early C. elegans embryos.
http://www.ncbi.nlm.nih.gov/pubmed/15703275,http://www.ncbi.nlm.nih.gov/pubmed/18216854
Are Sidekick proteins members of the immunoglobulin superfamily?
Yes, sidekick are cell adhesion molecules of the immunoglobulin superfamily.
http://www.ncbi.nlm.nih.gov/pubmed/16751093,http://www.ncbi.nlm.nih.gov/pubmed/19229130,http://www.ncbi.nlm.nih.gov/pubmed/16636294,http://www.ncbi.nlm.nih.gov/pubmed/19452047
What are the pyknons?
Using an unsupervised pattern-discovery method, the human intergenic and intronic regions were processed and all variable-length patterns with identically conserved copies and multiplicities above what is expected by chance were catalogued. Among the millions of discovered patterns, a subset of 127,998 patterns was found, termed pyknons, which have additional nonoverlapping instances in the untranslated and protein-coding regions of 30,675 transcripts from 20,059 human genes. The pyknons arrange combinatorially in the untranslated and coding regions of numerous human genes where they form mosaics. Pyknons might represent a biologically important link between coding and non-coding DNA.
http://www.ncbi.nlm.nih.gov/pubmed/22294745,http://www.ncbi.nlm.nih.gov/pubmed/16728541,http://www.ncbi.nlm.nih.gov/pubmed/8663170,http://www.ncbi.nlm.nih.gov/pubmed/7768329,http://www.ncbi.nlm.nih.gov/pubmed/10426574,http://www.ncbi.nlm.nih.gov/pubmed/22719854,http://www.ncbi.nlm.nih.gov/pubmed/1417847,http://www.ncbi.nlm.nih.gov/pubmed/8444882,http://www.ncbi.nlm.nih.gov/pubmed/15062548,http://www.ncbi.nlm.nih.gov/pubmed/12072404
Which deiodinases are best known to be present in brain?
All the 3 deiodinases (Type 1, Type 2 and Type 3 deiodinase) are present in the "brain" but Type 1 deiodinase is only found in neurohypophysis that cannot be actually considered true "brain tissue".
http://www.ncbi.nlm.nih.gov/pubmed/15647112,http://www.ncbi.nlm.nih.gov/pubmed/16844989,http://www.ncbi.nlm.nih.gov/pubmed/23530628,http://www.ncbi.nlm.nih.gov/pubmed/15980447,http://www.ncbi.nlm.nih.gov/pubmed/15162482,http://www.ncbi.nlm.nih.gov/pubmed/19153681,http://www.ncbi.nlm.nih.gov/pubmed/22148174,http://www.ncbi.nlm.nih.gov/pubmed/12798041,http://www.ncbi.nlm.nih.gov/pubmed/19429691,http://www.ncbi.nlm.nih.gov/pubmed/21328706,http://www.ncbi.nlm.nih.gov/pubmed/17520325,http://www.ncbi.nlm.nih.gov/pubmed/23297037,http://www.ncbi.nlm.nih.gov/pubmed/22540951,http://www.ncbi.nlm.nih.gov/pubmed/18989393,http://www.ncbi.nlm.nih.gov/pubmed/19622743,http://www.ncbi.nlm.nih.gov/pubmed/18006547,http://www.ncbi.nlm.nih.gov/pubmed/12192075,http://www.ncbi.nlm.nih.gov/pubmed/21935968,http://www.ncbi.nlm.nih.gov/pubmed/21426944,http://www.ncbi.nlm.nih.gov/pubmed/12169530,http://www.ncbi.nlm.nih.gov/pubmed/19470175,http://www.ncbi.nlm.nih.gov/pubmed/12070338,http://www.ncbi.nlm.nih.gov/pubmed/18218108,http://www.ncbi.nlm.nih.gov/pubmed/21967762,http://www.ncbi.nlm.nih.gov/pubmed/15141026,http://www.ncbi.nlm.nih.gov/pubmed/18467177,http://www.ncbi.nlm.nih.gov/pubmed/19421989,http://www.ncbi.nlm.nih.gov/pubmed/15215418,http://www.ncbi.nlm.nih.gov/pubmed/22987359,http://www.ncbi.nlm.nih.gov/pubmed/15070403,http://www.ncbi.nlm.nih.gov/pubmed/15769290,http://www.ncbi.nlm.nih.gov/pubmed/17597890,http://www.ncbi.nlm.nih.gov/pubmed/21064129,http://www.ncbi.nlm.nih.gov/pubmed/17597895,http://www.ncbi.nlm.nih.gov/pubmed/15215419,http://www.ncbi.nlm.nih.gov/pubmed/22031179,http://www.ncbi.nlm.nih.gov/pubmed/16858668,http://www.ncbi.nlm.nih.gov/pubmed/21531175,http://www.ncbi.nlm.nih.gov/pubmed/17088282,http://www.ncbi.nlm.nih.gov/pubmed/16225682,http://www.ncbi.nlm.nih.gov/pubmed/16674095,http://www.ncbi.nlm.nih.gov/pubmed/18312695,http://www.ncbi.nlm.nih.gov/pubmed/10698111,http://www.ncbi.nlm.nih.gov/pubmed/16597327,http://www.ncbi.nlm.nih.gov/pubmed/22247276,http://www.ncbi.nlm.nih.gov/pubmed/20488436,http://www.ncbi.nlm.nih.gov/pubmed/11274469,http://www.ncbi.nlm.nih.gov/pubmed/17958348,http://www.ncbi.nlm.nih.gov/pubmed/18355838
What are the computational methods for the prediction of beta-barrel transmembrane proteins?
Computational tools have been developed for beta-barrel transmembrane protein discrimination, topology prediction and prediction of their structural features. Initial methods developed for the prediction of the transmembrane beta strands were based on hydrophobicity analysis, using sliding windows along the sequence, in order to capture the alternating patterns of hydrophobic-hydrophilic residues of the transmembrane strands, or using generalized secondary structure prediction methods. Other approaches included the construction of special empirical rules using amino-acid propensities and prior knowledge of the structural nature of the proteins, and the development of Neural Network-based predictors to predict the location of alpha-carbon atoms with respect to the membrane. During the last few years, other more refined methods, appeared, including: Neural Networks, Hidden Markov Models, Support Vector Machines, k-Nearest Neighbors, Radial Basis Functions, Bayesian Networks, Genetic Algorithms, Mahalanobis Discriminant Functions, Cellular Automata, N-to-1 Extreme Learning Machines. Hidden Markov Model-based methods are among the most successful in topology prediction, being able to capture the unique architecture of beta-barrel transmembrane proteins. Consensus methods, as well as pipelines of several related tools (e.g. subcellular localization prediciton, alpha-helical transmembrane protein prediction, signal-peptide/lipoprotein prediction) have also used for discriminating beta-barrel transmembrane proteins. Recently, a number of methods for predicting more detailed structural features (e.g. surface accessibility, residue contacts, even detailed atomic 3D models) tailored to beta-barrel transmembrane proteins have been developed, based on knowledge-based potential functions, graph theoretic models, physical models and multi-tape S-attribute grammars. Methods/tools falling in the aforementioned classes are (listed in alphabetical order): BBF (beta-barrel finder), BETAWARE, BOCTOPUS, BOMP, BTMX (Beta barrel TransMembrane eXposure), HHomp, HMM-B2TMR, OMBBpred, PROFtmb, PRED-TMBB, TMB-Hunt, TBBPred, TMBETAPRED-RBF, TMBHMM, TransFold, TMBpro, TMBKNN, Wimley
http://www.ncbi.nlm.nih.gov/pubmed/12824356
Describe what is the usage of the Theatre software tool for genomic analysis.
Theatre is a web-based computing system designed for the comparative analysis of genomic sequences, especially with respect to motifs likely to be involved in the regulation of gene expression. Theatre is an interface to commonly used sequence analysis tools and biological sequence databases to determine or predict the positions of coding regions, repetitive sequences and transcription factor binding sites in families of DNA sequences. The information is displayed in a manner that can be easily understood and can reveal patterns that might not otherwise have been noticed. In addition to web-based output, Theatre can produce publication quality colour hardcopies showing predicted features in aligned genomic sequences.Theatre is a web-based computing system designed for the comparative analysis of genomic sequences, especially with respect to motifs likely to be involved in the regulation of gene expression. The information is displayed in a manner that can be easily understood and can reveal patterns that might not otherwise have been noticed. Theatre can be accessed at http://www.hgmp.mrc.ac.uk/Registered/Webapp/theatre/.
http://www.ncbi.nlm.nih.gov/pubmed/25268582,http://www.ncbi.nlm.nih.gov/pubmed/17711474,http://www.ncbi.nlm.nih.gov/pubmed/14534164,http://www.ncbi.nlm.nih.gov/pubmed/15757364,http://www.ncbi.nlm.nih.gov/pubmed/15883375,http://www.ncbi.nlm.nih.gov/pubmed/25442502,http://www.ncbi.nlm.nih.gov/pubmed/19660565,http://www.ncbi.nlm.nih.gov/pubmed/19820186,http://www.ncbi.nlm.nih.gov/pubmed/15215390,http://www.ncbi.nlm.nih.gov/pubmed/22877946,http://www.ncbi.nlm.nih.gov/pubmed/23409927,http://www.ncbi.nlm.nih.gov/pubmed/15677727,http://www.ncbi.nlm.nih.gov/pubmed/16980320,http://www.ncbi.nlm.nih.gov/pubmed/22492356,http://www.ncbi.nlm.nih.gov/pubmed/21152003
How are CRM (cis-regulatory modules) defined?
Eukaryotic genes are often regulated by several transcription factors whose binding sites are tightly clustered and form cis-regulatory modules.In many species, especially higher eukaryotes, transcription factor binding sites tend to occur as homotypic or heterotypic clusters, also known as cis-regulatory modules. Several tools allow to detect significant co-occurrences of closely located binding sites (cis-regulatory modules, CRMs).Several tools allow to detect significant co-occurrences of closely located binding sites (cis-regulatory modules, CRMs). CisMiner can be queried for the results presented in this work and can also perform a customized cis-regulatory module prediction on a query set of transcription factor binding sites provided by the user. In many species, especially higher eukaryotes, transcription factor binding sites tend to occur as homotypic or heterotypic clusters, also known as cis-regulatory modules. Eukaryotic genes are often regulated by several transcription factors whose binding sites are tightly clustered and form cis-regulatory modules. Our web server is available at http://creme.dcode.org.
http://www.ncbi.nlm.nih.gov/pubmed/23710633,http://www.ncbi.nlm.nih.gov/pubmed/25451386,http://www.ncbi.nlm.nih.gov/pubmed/19112098,http://www.ncbi.nlm.nih.gov/pubmed/18971376,http://www.ncbi.nlm.nih.gov/pubmed/10555147,http://www.ncbi.nlm.nih.gov/pubmed/19948724,http://www.ncbi.nlm.nih.gov/pubmed/21266500,http://www.ncbi.nlm.nih.gov/pubmed/18415121,http://www.ncbi.nlm.nih.gov/pubmed/18508637,http://www.ncbi.nlm.nih.gov/pubmed/11371203,http://www.ncbi.nlm.nih.gov/pubmed/15598648
Which is the main regulatory molecule of SERCA2A function in the cardiac muscle?
SERCA2a activity is regulated by phosphorylation of another SR protein, Phospholamban (PLN). Phospholamban (PLB) inhibits the activity of SERCA2a, the Ca(2+)-ATPase in cardiac sarcoplasmic reticulum, by decreasing the apparent affinity of the enzyme for Ca(2+).
http://www.ncbi.nlm.nih.gov/pubmed/15908750,http://www.ncbi.nlm.nih.gov/pubmed/21336163,http://www.ncbi.nlm.nih.gov/pubmed/24282181,http://www.ncbi.nlm.nih.gov/pubmed/19842203,http://www.ncbi.nlm.nih.gov/pubmed/17932455,http://www.ncbi.nlm.nih.gov/pubmed/24092421,http://www.ncbi.nlm.nih.gov/pubmed/17203459,http://www.ncbi.nlm.nih.gov/pubmed/23523603,http://www.ncbi.nlm.nih.gov/pubmed/16688751,http://www.ncbi.nlm.nih.gov/pubmed/24029077,http://www.ncbi.nlm.nih.gov/pubmed/17103451,http://www.ncbi.nlm.nih.gov/pubmed/11891681,http://www.ncbi.nlm.nih.gov/pubmed/23466526,http://www.ncbi.nlm.nih.gov/pubmed/20125191,http://www.ncbi.nlm.nih.gov/pubmed/15006694,http://www.ncbi.nlm.nih.gov/pubmed/14681759,http://www.ncbi.nlm.nih.gov/pubmed/23427518,http://www.ncbi.nlm.nih.gov/pubmed/17478475
Which gene is responsible for the development of the Mowat-Wilson syndrome?
Mowat-Wilson syndrome is a genetic disease caused by heterozygous mutations or deletions of the zinc finger E-box-binding homeobox 2 (ZEB2) gene.Nonsense mutations of the ZFHX1B gene in two Japanese girls with Mowat-Wilson syndromezfhz1b is the causative gene for Mowat-Wilson syndrome, in which patients demonstrate developmental delay and Hirschsprung disease, as well as other anomalies.Mowat-Wilson syndrome (MWS) is a multiple congenital anomaly-mental retardation complex caused by mutations in the Zinc Finger Homeobox 1 B gene (ZFHX1B, also known as ZEB2 or SIP-1).zfhz1b is the causative gene for Mowat-Wilson syndrome, in which patients demonstrate developmental delay and Hirschsprung disease, as well as other anomalies. Intrahepatic biliary anomalies in a patient with Mowat-Wilson syndrome uncover a role for the zinc finger homeobox gene zfhx1b in vertebrate biliary development
http://www.ncbi.nlm.nih.gov/pubmed/23925142,http://www.ncbi.nlm.nih.gov/pubmed/22223483,http://www.ncbi.nlm.nih.gov/pubmed/18571757,http://www.ncbi.nlm.nih.gov/pubmed/7989542,http://www.ncbi.nlm.nih.gov/pubmed/23518650,http://www.ncbi.nlm.nih.gov/pubmed/16318699,http://www.ncbi.nlm.nih.gov/pubmed/23181535,http://www.ncbi.nlm.nih.gov/pubmed/23239357,http://www.ncbi.nlm.nih.gov/pubmed/16614251
How is active neurotoxin of Clostridium botulinum detected?
Active neurotoxin of Clostridium botulinum can be detected by: mouse lethality assay by mass spectrometry bioassay differentiated cell models peptide cleavage assay FDC (functional dual coating) microtitre plate immuno-biochemical assay endopeptidase activity monitored via UV-Visible spectroscopy
http://www.ncbi.nlm.nih.gov/pubmed/23704573
Which factor interacts with Treslin/TICRR throughout the cell cycle of human cells?
MDM two binding protein (MTBP) is a factor that interacts with Treslin/TICRR throughout the cell cycle. MTBP depletion by means of small interfering RNA inhibits DNA replication by preventing assembly of the CMG (Cdc45-MCM-GINS) holohelicase during origin firing. Although MTBP has been implicated in the function of the p53 tumor suppressor, it is required for DNA replication irrespective of a cell's p53 status. MTBP is proposed to act with Treslin/TICRR to integrate signals from cell cycle and DNA damage response pathways to control the initiation of DNA replication in human cells.
http://www.ncbi.nlm.nih.gov/pubmed/24915039,http://www.ncbi.nlm.nih.gov/pubmed/24471924,http://www.ncbi.nlm.nih.gov/pubmed/22763387,http://www.ncbi.nlm.nih.gov/pubmed/24712303,http://www.ncbi.nlm.nih.gov/pubmed/24135407,http://www.ncbi.nlm.nih.gov/pubmed/22929803,http://www.ncbi.nlm.nih.gov/pubmed/24103732,http://www.ncbi.nlm.nih.gov/pubmed/24239172,http://www.ncbi.nlm.nih.gov/pubmed/25935605,http://www.ncbi.nlm.nih.gov/pubmed/25005844,http://www.ncbi.nlm.nih.gov/pubmed/22995770
What is oprozomib?
Oprozomib is a second-generation, highly-selective, orally administered proteasome inhibitor with promising activity against multiple myeloma. Oprozomib directly inhibited OC formation and bone resorption in vitro, while enhancing osteogenic differentiation and matrix mineralization. Oprozomib increased trabecular bone volume, decreased bone resorption and enhanced bone formation in non-tumor bearing mice. Consequently, oprozomib seems to be able to effectively shift the bone microenvironment from a catabolic to an anabolic state and, similar to bortezomib, may decrease skeletal complications of MM. Oprozomib effectively decreases multiple myeloma cell viability. Oprozomib potently inhibit cell survival and induce apoptosis in HNSCC cell lines via upregulation of pro-apoptotic Bik. Upregulation of Mcl-1 by these agents served to dampen their efficacies. Oprozomib also induced autophagy, mediated, in part, by activation of the UPR pathway involving upregulation of ATF4 transcription factor. Autophagy induction served a prosurvival role. Oral administration of ONX 0912 inhibited the growth of HNSCC xenograft tumors in a dose-dependent manner. Oprozomib inhibited NF-κB expression.
http://www.ncbi.nlm.nih.gov/pubmed/19230141,http://www.ncbi.nlm.nih.gov/pubmed/22025663,http://www.ncbi.nlm.nih.gov/pubmed/24257462,http://www.ncbi.nlm.nih.gov/pubmed/19448693,http://www.ncbi.nlm.nih.gov/pubmed/11162129,http://www.ncbi.nlm.nih.gov/pubmed/19398037
Is there a relationship between junctin and ryanodine receptors?
Yes, junctin binds to ryanodine receptors within the junctional sarcoplasmic reticulum of calcium release units, and normally acts as an activator of RyR channels at low luminal [Ca(2+)], and as an inhibitor at high luminal [Ca(2+)].
http://www.ncbi.nlm.nih.gov/pubmed/9562190,http://www.ncbi.nlm.nih.gov/pubmed/8907145,http://www.ncbi.nlm.nih.gov/pubmed/11130352,http://www.ncbi.nlm.nih.gov/pubmed/11015242,http://www.ncbi.nlm.nih.gov/pubmed/1470965,http://www.ncbi.nlm.nih.gov/pubmed/21044832,http://www.ncbi.nlm.nih.gov/pubmed/17849242
Which medication should be administered when managing patients with suspected acute opioid overdose?
Naloxone is opioid anagonist that should be administered for all patients with suspected acute opioid overdose. Intravenous naltrexone hydrochloride is usually administered, however, other formulations, including enteral methylnaltrexone, nebulized naloxone and subcutaneous naloxone, are under investigation and can be used under certain circumstances.
http://www.ncbi.nlm.nih.gov/pubmed/23834025,http://www.ncbi.nlm.nih.gov/pubmed/16254244,http://www.ncbi.nlm.nih.gov/pubmed/12432450,http://www.ncbi.nlm.nih.gov/pubmed/22251972,http://www.ncbi.nlm.nih.gov/pubmed/20026667,http://www.ncbi.nlm.nih.gov/pubmed/21283637,http://www.ncbi.nlm.nih.gov/pubmed/19889207,http://www.ncbi.nlm.nih.gov/pubmed/15564378
In which nuclear compartments is heterochromatin located?
This compartment localizes into three main regions: the peripheral heterochromatin, perinucleolar heterochromatin, and pericentromeric heterochromatin. Silencing appears to be associated with histone H3 lysine 9 trimethylation (H3K9me3), DNA methylation and the localization of the silenced gene to a specific nuclear compartment enriched in these modification
http://www.ncbi.nlm.nih.gov/pubmed/17958891,http://www.ncbi.nlm.nih.gov/pubmed/19842203,http://www.ncbi.nlm.nih.gov/pubmed/17203459,http://www.ncbi.nlm.nih.gov/pubmed/23523603,http://www.ncbi.nlm.nih.gov/pubmed/23243526,http://www.ncbi.nlm.nih.gov/pubmed/24029077,http://www.ncbi.nlm.nih.gov/pubmed/16150342,http://www.ncbi.nlm.nih.gov/pubmed/18445050,http://www.ncbi.nlm.nih.gov/pubmed/23427518,http://www.ncbi.nlm.nih.gov/pubmed/23322667,http://www.ncbi.nlm.nih.gov/pubmed/16053902,http://www.ncbi.nlm.nih.gov/pubmed/22486326,http://www.ncbi.nlm.nih.gov/pubmed/19215041,http://www.ncbi.nlm.nih.gov/pubmed/16688751,http://www.ncbi.nlm.nih.gov/pubmed/23001561,http://www.ncbi.nlm.nih.gov/pubmed/22246645,http://www.ncbi.nlm.nih.gov/pubmed/20428734,http://www.ncbi.nlm.nih.gov/pubmed/23152852,http://www.ncbi.nlm.nih.gov/pubmed/24282181,http://www.ncbi.nlm.nih.gov/pubmed/17932455,http://www.ncbi.nlm.nih.gov/pubmed/20093881,http://www.ncbi.nlm.nih.gov/pubmed/18259761,http://www.ncbi.nlm.nih.gov/pubmed/15006694,http://www.ncbi.nlm.nih.gov/pubmed/14681759,http://www.ncbi.nlm.nih.gov/pubmed/15908750,http://www.ncbi.nlm.nih.gov/pubmed/21893004,http://www.ncbi.nlm.nih.gov/pubmed/23312518,http://www.ncbi.nlm.nih.gov/pubmed/18230842,http://www.ncbi.nlm.nih.gov/pubmed/12746390,http://www.ncbi.nlm.nih.gov/pubmed/23466526,http://www.ncbi.nlm.nih.gov/pubmed/20125191,http://www.ncbi.nlm.nih.gov/pubmed/16088920,http://www.ncbi.nlm.nih.gov/pubmed/17223398,http://www.ncbi.nlm.nih.gov/pubmed/20145308,http://www.ncbi.nlm.nih.gov/pubmed/16532472,http://www.ncbi.nlm.nih.gov/pubmed/19236961
Have mutations in the ZEB2 gene been found in any human syndrome?
Yes, the Mowat-Wilson syndrome
http://www.ncbi.nlm.nih.gov/pubmed/20004108,http://www.ncbi.nlm.nih.gov/pubmed/19617358,http://www.ncbi.nlm.nih.gov/pubmed/19933360,http://www.ncbi.nlm.nih.gov/pubmed/24290807,http://www.ncbi.nlm.nih.gov/pubmed/23963890,http://www.ncbi.nlm.nih.gov/pubmed/23245695,http://www.ncbi.nlm.nih.gov/pubmed/21145481,http://www.ncbi.nlm.nih.gov/pubmed/19762288,http://www.ncbi.nlm.nih.gov/pubmed/22559785,http://www.ncbi.nlm.nih.gov/pubmed/25463394
Which enzymes are involved in global genome nucleotide excision repair (GG-NER) in bacteria?
Nucleotide excision repair (NER) is universally used to recognize and remove many types of DNA damage. In eubacteria, the NER system typically consists of UvrA, UvrB, UvrC, the UvrD helicase, DNA polymerase I, and ligase. Damage recognition during bacterial NER depends upon UvrA, which binds to the damage and loads UvrB onto the DNA. Subsequently, UvrA, UvrB and UvrC form the excinuclease protein UvrABC endonuclease, a multi-enzymatic complex which carries out repair of damaged DNA in sequential manner. In some cases, Cho may be the effective nuclease for NER, rather than UvrC. UvrC nuclease and the short oligonucleotide that contains the DNA lesion are removed from the post-incision complex by UvrD, a superfamily 1A helicase. In gram-positive organisms, PcrA helicase can also displace UvrC and the excised oligonucleotide from a post-incision NER complex.
http://www.ncbi.nlm.nih.gov/pubmed/20581784,http://www.ncbi.nlm.nih.gov/pubmed/15584870,http://www.ncbi.nlm.nih.gov/pubmed/16825580,http://www.ncbi.nlm.nih.gov/pubmed/21291389,http://www.ncbi.nlm.nih.gov/pubmed/22001562,http://www.ncbi.nlm.nih.gov/pubmed/23144205,http://www.ncbi.nlm.nih.gov/pubmed/22563249,http://www.ncbi.nlm.nih.gov/pubmed/20080988,http://www.ncbi.nlm.nih.gov/pubmed/17644079,http://www.ncbi.nlm.nih.gov/pubmed/15073377,http://www.ncbi.nlm.nih.gov/pubmed/17994112,http://www.ncbi.nlm.nih.gov/pubmed/11090108,http://www.ncbi.nlm.nih.gov/pubmed/12890053,http://www.ncbi.nlm.nih.gov/pubmed/16672364,http://www.ncbi.nlm.nih.gov/pubmed/16185151
Is JTV519 (K201) a potential drug for the prevention of arrhythmias?
Yes, JTV519 has antiarrhythmic properties.
http://www.ncbi.nlm.nih.gov/pubmed/23087084,http://www.ncbi.nlm.nih.gov/pubmed/22293089,http://www.ncbi.nlm.nih.gov/pubmed/23509776,http://www.ncbi.nlm.nih.gov/pubmed/22303357,http://www.ncbi.nlm.nih.gov/pubmed/18700954,http://www.ncbi.nlm.nih.gov/pubmed/19664288,http://www.ncbi.nlm.nih.gov/pubmed/19912656,http://www.ncbi.nlm.nih.gov/pubmed/19440243,http://www.ncbi.nlm.nih.gov/pubmed/23071542,http://www.ncbi.nlm.nih.gov/pubmed/22912875,http://www.ncbi.nlm.nih.gov/pubmed/22898998,http://www.ncbi.nlm.nih.gov/pubmed/23293655,http://www.ncbi.nlm.nih.gov/pubmed/22583478,http://www.ncbi.nlm.nih.gov/pubmed/23074383,http://www.ncbi.nlm.nih.gov/pubmed/23064433,http://www.ncbi.nlm.nih.gov/pubmed/18040713,http://www.ncbi.nlm.nih.gov/pubmed/21418558,http://www.ncbi.nlm.nih.gov/pubmed/21284896,http://www.ncbi.nlm.nih.gov/pubmed/21559780,http://www.ncbi.nlm.nih.gov/pubmed/22417299,http://www.ncbi.nlm.nih.gov/pubmed/20842113,http://www.ncbi.nlm.nih.gov/pubmed/21799879,http://www.ncbi.nlm.nih.gov/pubmed/22312290,http://www.ncbi.nlm.nih.gov/pubmed/22303318,http://www.ncbi.nlm.nih.gov/pubmed/23276969,http://www.ncbi.nlm.nih.gov/pubmed/23016435,http://www.ncbi.nlm.nih.gov/pubmed/21971665,http://www.ncbi.nlm.nih.gov/pubmed/23431261,http://www.ncbi.nlm.nih.gov/pubmed/23158014,http://www.ncbi.nlm.nih.gov/pubmed/19521961,http://www.ncbi.nlm.nih.gov/pubmed/23250910,http://www.ncbi.nlm.nih.gov/pubmed/23554741,http://www.ncbi.nlm.nih.gov/pubmed/18927107,http://www.ncbi.nlm.nih.gov/pubmed/22392644,http://www.ncbi.nlm.nih.gov/pubmed/21903334,http://www.ncbi.nlm.nih.gov/pubmed/22666523,http://www.ncbi.nlm.nih.gov/pubmed/22194833,http://www.ncbi.nlm.nih.gov/pubmed/22616882,http://www.ncbi.nlm.nih.gov/pubmed/20716340,http://www.ncbi.nlm.nih.gov/pubmed/22056881,http://www.ncbi.nlm.nih.gov/pubmed/23251295,http://www.ncbi.nlm.nih.gov/pubmed/21811665,http://www.ncbi.nlm.nih.gov/pubmed/19721809,http://www.ncbi.nlm.nih.gov/pubmed/21962230,http://www.ncbi.nlm.nih.gov/pubmed/18442408,http://www.ncbi.nlm.nih.gov/pubmed/20221895,http://www.ncbi.nlm.nih.gov/pubmed/22384020,http://www.ncbi.nlm.nih.gov/pubmed/21102580,http://www.ncbi.nlm.nih.gov/pubmed/22469780,http://www.ncbi.nlm.nih.gov/pubmed/21712563,http://www.ncbi.nlm.nih.gov/pubmed/22938091,http://www.ncbi.nlm.nih.gov/pubmed/17700064,http://www.ncbi.nlm.nih.gov/pubmed/21931505,http://www.ncbi.nlm.nih.gov/pubmed/22666228,http://www.ncbi.nlm.nih.gov/pubmed/23175432,http://www.ncbi.nlm.nih.gov/pubmed/23024649,http://www.ncbi.nlm.nih.gov/pubmed/19712461,http://www.ncbi.nlm.nih.gov/pubmed/21029445,http://www.ncbi.nlm.nih.gov/pubmed/21860412,http://www.ncbi.nlm.nih.gov/pubmed/23391324,http://www.ncbi.nlm.nih.gov/pubmed/16854228,http://www.ncbi.nlm.nih.gov/pubmed/23407615,http://www.ncbi.nlm.nih.gov/pubmed/21461395,http://www.ncbi.nlm.nih.gov/pubmed/18036240,http://www.ncbi.nlm.nih.gov/pubmed/22126155,http://www.ncbi.nlm.nih.gov/pubmed/23125218,http://www.ncbi.nlm.nih.gov/pubmed/22408395,http://www.ncbi.nlm.nih.gov/pubmed/20925959,http://www.ncbi.nlm.nih.gov/pubmed/22548175,http://www.ncbi.nlm.nih.gov/pubmed/23209884,http://www.ncbi.nlm.nih.gov/pubmed/19638982,http://www.ncbi.nlm.nih.gov/pubmed/22968430
What is the mechanism of microRNA deregulation in carcinogenesis?
MicroRNAs (miRNAs) are endogenous non-protein coding single-stranded RNAs (19–25 nucleotides in length) generated from cleavage of larger non-coding RNAs by the ribonuclease III enzyme Dicer. They become part of the RNA-induced silencing complex and negatively regulate gene expression by binding to homologous 3'-UTR region of target protein-coding mRNAs as an imperfect match, causing translational repression or degradation. Approximately one-third of the protein-coding genes are susceptible to miRNA regulation. Accumulating evidence indicates that deregulated miRNA expression is associated with the onset and progression of a number of human cancers. Therefore, cancer-associated miRNAs (CA-miRNAs) could regulate target genes by acting either as "oncogenes" or "tumor suppressor miRNA (TS-miRNAs)". In line with this, numerous cancers (e.g. breast, lung, oesophageal, prostate, pancreatic, gastric and colon cancer) have been classified based on their unique miRNA expression profile.
http://www.ncbi.nlm.nih.gov/pubmed/24698685,http://www.ncbi.nlm.nih.gov/pubmed/25263562,http://www.ncbi.nlm.nih.gov/pubmed/24081491,http://www.ncbi.nlm.nih.gov/pubmed/22424946,http://www.ncbi.nlm.nih.gov/pubmed/24337580,http://www.ncbi.nlm.nih.gov/pubmed/24095279,http://www.ncbi.nlm.nih.gov/pubmed/25567907,http://www.ncbi.nlm.nih.gov/pubmed/25567906,http://www.ncbi.nlm.nih.gov/pubmed/23863162,http://www.ncbi.nlm.nih.gov/pubmed/25936802,http://www.ncbi.nlm.nih.gov/pubmed/21981924
Which type of GTPases is required for amino acid-dependent activation of mTORC1?
Heterodimeric Rag GTPases are required for amino-acid-mediated mTORC1 activation at the lysosomeAmino acids act through the heterodimeric Rag GTPases (RagA or RagB bound to RagC or RagD) in order to promote the translocation of mTORC1 to the lysosomal surface, its site of activation.
http://www.ncbi.nlm.nih.gov/pubmed/2716062,http://www.ncbi.nlm.nih.gov/pubmed/12777511,http://www.ncbi.nlm.nih.gov/pubmed/6165649,http://www.ncbi.nlm.nih.gov/pubmed/23420552,http://www.ncbi.nlm.nih.gov/pubmed/12832639,http://www.ncbi.nlm.nih.gov/pubmed/11884141
In which genomic regions are Alu enriched?
There are regions such as the four homeobox gene clusters, which are nearly devoid of these repeats that contrast with repeat dense regions in other transcriptionally active regions of the genome. Alu elements are more clustered in genes which are involved in metabolism, transport, and signaling processes. In contrast, they are significantly fewer in genes coding for information pathway components as well as structural proteins. This bias in Alu distribution is independent of the effect of Alu density of the flanking genomic region and is also not affected by the GC content of the gene and its upstream and downstream regions.There are regions such as the four homeobox gene clusters, which are nearly devoid of these repeats that contrast with repeat dense regions in other transcriptionally active regions of the genome.
http://www.ncbi.nlm.nih.gov/pubmed/12465067,http://www.ncbi.nlm.nih.gov/pubmed/8041372,http://www.ncbi.nlm.nih.gov/pubmed/1672807,http://www.ncbi.nlm.nih.gov/pubmed/21047175,http://www.ncbi.nlm.nih.gov/pubmed/23614923,http://www.ncbi.nlm.nih.gov/pubmed/18609312,http://www.ncbi.nlm.nih.gov/pubmed/17579361,http://www.ncbi.nlm.nih.gov/pubmed/12471465,http://www.ncbi.nlm.nih.gov/pubmed/15390042,http://www.ncbi.nlm.nih.gov/pubmed/25004170,http://www.ncbi.nlm.nih.gov/pubmed/8351010,http://www.ncbi.nlm.nih.gov/pubmed/8338342,http://www.ncbi.nlm.nih.gov/pubmed/15465396,http://www.ncbi.nlm.nih.gov/pubmed/20694531,http://www.ncbi.nlm.nih.gov/pubmed/16242937,http://www.ncbi.nlm.nih.gov/pubmed/15596620,http://www.ncbi.nlm.nih.gov/pubmed/8341310,http://www.ncbi.nlm.nih.gov/pubmed/23184149
What is the synonym of the lubag disease?
Lubag disease is also known as X-linked dystonia-parkinsonism (XDP). This disease is characterized by dystonia and parkinsonism, and afflicts Filipino men, and rarely, women originating principally from the Panay Island.
http://www.ncbi.nlm.nih.gov/pubmed/23869191,http://www.ncbi.nlm.nih.gov/pubmed/15215653,http://www.ncbi.nlm.nih.gov/pubmed/16864444,http://www.ncbi.nlm.nih.gov/pubmed/22711363,http://www.ncbi.nlm.nih.gov/pubmed/15684474,http://www.ncbi.nlm.nih.gov/pubmed/21505988
Dracorhodin perchlorate was tested for treatment of which cancers?
Dracorhodin perchlorate induce apoptosis in prostate cancer, gastric tumor, melanoma and premyelocytic leukemia.
http://www.ncbi.nlm.nih.gov/pubmed/22687168,http://www.ncbi.nlm.nih.gov/pubmed/21059535,http://www.ncbi.nlm.nih.gov/pubmed/23563645,http://www.ncbi.nlm.nih.gov/pubmed/21803799,http://www.ncbi.nlm.nih.gov/pubmed/21487978,http://www.ncbi.nlm.nih.gov/pubmed/21856578,http://www.ncbi.nlm.nih.gov/pubmed/22496109,http://www.ncbi.nlm.nih.gov/pubmed/22088659,http://www.ncbi.nlm.nih.gov/pubmed/22311713,http://www.ncbi.nlm.nih.gov/pubmed/23691321,http://www.ncbi.nlm.nih.gov/pubmed/21679067,http://www.ncbi.nlm.nih.gov/pubmed/20351673,http://www.ncbi.nlm.nih.gov/pubmed/22577160,http://www.ncbi.nlm.nih.gov/pubmed/23202144,http://www.ncbi.nlm.nih.gov/pubmed/20351675,http://www.ncbi.nlm.nih.gov/pubmed/22640501,http://www.ncbi.nlm.nih.gov/pubmed/23701076,http://www.ncbi.nlm.nih.gov/pubmed/23493652,http://www.ncbi.nlm.nih.gov/pubmed/23660636,http://www.ncbi.nlm.nih.gov/pubmed/23523158,http://www.ncbi.nlm.nih.gov/pubmed/21839654,http://www.ncbi.nlm.nih.gov/pubmed/23809937,http://www.ncbi.nlm.nih.gov/pubmed/23948669,http://www.ncbi.nlm.nih.gov/pubmed/23235683,http://www.ncbi.nlm.nih.gov/pubmed/22648477,http://www.ncbi.nlm.nih.gov/pubmed/21876515,http://www.ncbi.nlm.nih.gov/pubmed/22569567,http://www.ncbi.nlm.nih.gov/pubmed/23034121,http://www.ncbi.nlm.nih.gov/pubmed/22987234,http://www.ncbi.nlm.nih.gov/pubmed/20373339,http://www.ncbi.nlm.nih.gov/pubmed/23249660,http://www.ncbi.nlm.nih.gov/pubmed/22951366,http://www.ncbi.nlm.nih.gov/pubmed/24255092,http://www.ncbi.nlm.nih.gov/pubmed/23419569,http://www.ncbi.nlm.nih.gov/pubmed/21106999,http://www.ncbi.nlm.nih.gov/pubmed/23953830,http://www.ncbi.nlm.nih.gov/pubmed/24975855,http://www.ncbi.nlm.nih.gov/pubmed/23781006,http://www.ncbi.nlm.nih.gov/pubmed/19958985,http://www.ncbi.nlm.nih.gov/pubmed/23402260,http://www.ncbi.nlm.nih.gov/pubmed/21107001,http://www.ncbi.nlm.nih.gov/pubmed/21808631,http://www.ncbi.nlm.nih.gov/pubmed/22155803,http://www.ncbi.nlm.nih.gov/pubmed/23301864,http://www.ncbi.nlm.nih.gov/pubmed/23443168
What is the role of venous angioplasty in multiple sclerosis?
Chronic cerebrospinal venous insufficiency (CCSVI) may be an important factor in the pathogenesis of multiple sclerosis (MS). The proposed treatment for CCSVI is percutaneous transluminal angioplasty, also known as the 'liberation procedure', which is claimed to improve the blood flow in the brain, thereby alleviating some of the symptoms of MS. There have been reports to suggest that venous angioplasty in MS patients is a feasible and safe procedure and is associated with improved disease symptom severity, quality of life, and corrects blood pressure deviation, improves CSF dynamics. Open venous reconstruction of the internal jugular vein has also been tried with good results. However, some authors have failed to document beneficial value of venous angioplasty in MS patients and systematic review has suggested that there is currently no high level evidence to support or refute the efficacy or safety of percutaneous transluminal angioplasty for treatment of CCSVI in people with MS.
http://www.ncbi.nlm.nih.gov/pubmed/23333482,http://www.ncbi.nlm.nih.gov/pubmed/15611632,http://www.ncbi.nlm.nih.gov/pubmed/20407210,http://www.ncbi.nlm.nih.gov/pubmed/11157805,http://www.ncbi.nlm.nih.gov/pubmed/10088637,http://www.ncbi.nlm.nih.gov/pubmed/21557222,http://www.ncbi.nlm.nih.gov/pubmed/17387268
Are the Fanconi anemia genes a part of the same signalling pathway?
The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNAMutations in at least 14 different genes have been shown to cause FAMutations in at least 14 different genes have been shown to cause FA. The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA. The Fanconi anemia genes code for proteins that act in complexes to coordinate the repair of damaged DNA.The FA genes code for proteins that act in complexes to coordinate the repair of damaged DNA. Mutations in at least 14 different genes have been shown to cause FA.
http://www.ncbi.nlm.nih.gov/pubmed/23746978,http://www.ncbi.nlm.nih.gov/pubmed/25858066,http://www.ncbi.nlm.nih.gov/pubmed/25984329,http://www.ncbi.nlm.nih.gov/pubmed/19804333,http://www.ncbi.nlm.nih.gov/pubmed/25169179,http://www.ncbi.nlm.nih.gov/pubmed/23773460,http://www.ncbi.nlm.nih.gov/pubmed/17198039,http://www.ncbi.nlm.nih.gov/pubmed/20560035,http://www.ncbi.nlm.nih.gov/pubmed/20680811,http://www.ncbi.nlm.nih.gov/pubmed/19907881,http://www.ncbi.nlm.nih.gov/pubmed/17888423,http://www.ncbi.nlm.nih.gov/pubmed/14647535,http://www.ncbi.nlm.nih.gov/pubmed/19022705,http://www.ncbi.nlm.nih.gov/pubmed/22405796,http://www.ncbi.nlm.nih.gov/pubmed/15030272,http://www.ncbi.nlm.nih.gov/pubmed/16969166,http://www.ncbi.nlm.nih.gov/pubmed/19857353,http://www.ncbi.nlm.nih.gov/pubmed/25205213,http://www.ncbi.nlm.nih.gov/pubmed/21749886,http://www.ncbi.nlm.nih.gov/pubmed/22943934,http://www.ncbi.nlm.nih.gov/pubmed/19627664,http://www.ncbi.nlm.nih.gov/pubmed/15692093,http://www.ncbi.nlm.nih.gov/pubmed/25145464,http://www.ncbi.nlm.nih.gov/pubmed/18543793,http://www.ncbi.nlm.nih.gov/pubmed/21526485,http://www.ncbi.nlm.nih.gov/pubmed/26259288
Are there clinical trials using stem cells for the treatment of cardiac disease?
Yes, there exists clinical trials for cardiac stem cell based treatment.Yes, there are several clinical trials on the use of stem cells for the treatment of cardiac (heart) disease.
http://www.ncbi.nlm.nih.gov/pubmed/25512710,http://www.ncbi.nlm.nih.gov/pubmed/23604474,http://www.ncbi.nlm.nih.gov/pubmed/25534027,http://www.ncbi.nlm.nih.gov/pubmed/22359296,http://www.ncbi.nlm.nih.gov/pubmed/22078060,http://www.ncbi.nlm.nih.gov/pubmed/25437055,http://www.ncbi.nlm.nih.gov/pubmed/25531272,http://www.ncbi.nlm.nih.gov/pubmed/22922032,http://www.ncbi.nlm.nih.gov/pubmed/25514241,http://www.ncbi.nlm.nih.gov/pubmed/22992936
Is DNA methylation an epigenetic modification of chromatin related to gene expression?
Epigenetic changes such as DNA methylation alter gene expression at the level of transcription by upregulating, downregulating, or silencing genes completely.
http://www.ncbi.nlm.nih.gov/pubmed/23308270,http://www.ncbi.nlm.nih.gov/pubmed/22699452,http://www.ncbi.nlm.nih.gov/pubmed/14530176,http://www.ncbi.nlm.nih.gov/pubmed/19773260,http://www.ncbi.nlm.nih.gov/pubmed/19958752,http://www.ncbi.nlm.nih.gov/pubmed/12351384,http://www.ncbi.nlm.nih.gov/pubmed/24800817,http://www.ncbi.nlm.nih.gov/pubmed/18224412,http://www.ncbi.nlm.nih.gov/pubmed/20124515,http://www.ncbi.nlm.nih.gov/pubmed/22668850,http://www.ncbi.nlm.nih.gov/pubmed/17707228,http://www.ncbi.nlm.nih.gov/pubmed/21606163,http://www.ncbi.nlm.nih.gov/pubmed/11825872,http://www.ncbi.nlm.nih.gov/pubmed/22960038,http://www.ncbi.nlm.nih.gov/pubmed/21732494,http://www.ncbi.nlm.nih.gov/pubmed/16397623,http://www.ncbi.nlm.nih.gov/pubmed/21170035,http://www.ncbi.nlm.nih.gov/pubmed/22885124,http://www.ncbi.nlm.nih.gov/pubmed/15507521,http://www.ncbi.nlm.nih.gov/pubmed/20143233,http://www.ncbi.nlm.nih.gov/pubmed/16177182,http://www.ncbi.nlm.nih.gov/pubmed/20861919,http://www.ncbi.nlm.nih.gov/pubmed/17095621,http://www.ncbi.nlm.nih.gov/pubmed/20826720,http://www.ncbi.nlm.nih.gov/pubmed/22399799
Is Growth factor independence 1b (GFI1B) important for hematopoiesis?
Yes. Gfi-1B is a transcriptional repressor essential for the regulation of erythropoiesis and megakaryopoiesis. Gfi-1b(-/-) embryonic stem cells fail to contribute to red cells of adult chimeras. Gfi-1b(-/-) embryos exhibit delayed maturation of primitive erythrocytes and subsequently die with failure to produce definitive enucleated erythrocytes.
http://www.ncbi.nlm.nih.gov/pubmed/25188481,http://www.ncbi.nlm.nih.gov/pubmed/17996589,http://www.ncbi.nlm.nih.gov/pubmed/25188483,http://www.ncbi.nlm.nih.gov/pubmed/23545923,http://www.ncbi.nlm.nih.gov/pubmed/17076650,http://www.ncbi.nlm.nih.gov/pubmed/17076653,http://www.ncbi.nlm.nih.gov/pubmed/20425391,http://www.ncbi.nlm.nih.gov/pubmed/17242661,http://www.ncbi.nlm.nih.gov/pubmed/18922829,http://www.ncbi.nlm.nih.gov/pubmed/22650376,http://www.ncbi.nlm.nih.gov/pubmed/17020458,http://www.ncbi.nlm.nih.gov/pubmed/20359632
Has Revlimid been approved by the US Food and Drug Administration?
Yes, Revlimid has been approved by the US Food and Drug Administration for treatment of multiple myeloma.
http://www.ncbi.nlm.nih.gov/pubmed/16522182,http://www.ncbi.nlm.nih.gov/pubmed/14668231,http://www.ncbi.nlm.nih.gov/pubmed/12804086,http://www.ncbi.nlm.nih.gov/pubmed/11301301,http://www.ncbi.nlm.nih.gov/pubmed/9021270,http://www.ncbi.nlm.nih.gov/pubmed/1774068,http://www.ncbi.nlm.nih.gov/pubmed/20370891,http://www.ncbi.nlm.nih.gov/pubmed/21714130
Which is the execution time (complexity) of the Smith-Waterman algorithm for the alignment of two sequences
The complexity of the Smith-Waterman dynamic programming algorithm is quadratic, that is, it runs in time proportional to the product of lengths of the sequences being aligned.
http://www.ncbi.nlm.nih.gov/pubmed/23861251,http://www.ncbi.nlm.nih.gov/pubmed/25258341,http://www.ncbi.nlm.nih.gov/pubmed/24325358,http://www.ncbi.nlm.nih.gov/pubmed/21765413,http://www.ncbi.nlm.nih.gov/pubmed/21765412,http://www.ncbi.nlm.nih.gov/pubmed/23100277
List mutations that are implicated in the Gray Platelet Syndrome.
GFI1B and NBEAL2 mutations are implicated in the Gray Platelet Syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/24336569,http://www.ncbi.nlm.nih.gov/pubmed/23873081,http://www.ncbi.nlm.nih.gov/pubmed/25122746,http://www.ncbi.nlm.nih.gov/pubmed/25048165,http://www.ncbi.nlm.nih.gov/pubmed/24136345,http://www.ncbi.nlm.nih.gov/pubmed/24870050,http://www.ncbi.nlm.nih.gov/pubmed/24770324,http://www.ncbi.nlm.nih.gov/pubmed/23907171,http://www.ncbi.nlm.nih.gov/pubmed/23940360,http://www.ncbi.nlm.nih.gov/pubmed/23999092,http://www.ncbi.nlm.nih.gov/pubmed/25759096
Has single guide RNA been used on human cells?
Yes, sgRNA has been used in human cell lines.