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http://www.ncbi.nlm.nih.gov/pubmed/21971724,http://www.ncbi.nlm.nih.gov/pubmed/17620463,http://www.ncbi.nlm.nih.gov/pubmed/6481730,http://www.ncbi.nlm.nih.gov/pubmed/20686061,http://www.ncbi.nlm.nih.gov/pubmed/19726741 | Which are the musculoskeletal manifestations of Marfan syndrome? | Musculoskeletal manifestations of Marfan syndrome include scoliosis, dural ectasia, pectus excavatum and carinatum, arachnodactyly, otto pelvis (protrusio acetabuli), dolichostenomelia and ligamentous laxity. |
http://www.ncbi.nlm.nih.gov/pubmed/25225357 | What is the "Proteomic ruler"? | The MS signal of histones can be used as a "proteomic ruler" because it is proportional to the amount of DNA in the sample, which in turn depends on the number of cells. As a result, our proteomic ruler approach adds an absolute scale to the MS readout and allows estimation of the copy numbers of individual proteins per cell. |
http://www.ncbi.nlm.nih.gov/pubmed/21725586,http://www.ncbi.nlm.nih.gov/pubmed/23689841,http://www.ncbi.nlm.nih.gov/pubmed/23707381,http://www.ncbi.nlm.nih.gov/pubmed/23316055,http://www.ncbi.nlm.nih.gov/pubmed/24189052,http://www.ncbi.nlm.nih.gov/pubmed/22728817,http://www.ncbi.nlm.nih.gov/pubmed/19887642,http://www.ncbi.nlm.nih.gov/pubmed/20147392 | What is the mechanism by which HIV-1-encoded Vif protein allows virus replication? | The HIV-1 Vif protein counteracts the antiviral activity of the APOBEC3 family by targeting the proteins for degradation through the ubiquitin-proteasome pathway. More specifically, Vif, serving as a substrate receptor, facilitates ubiquitination of APOBEC3 proteins by forming a Cullin5-based E3 ubiquitin ligase complex, which targets APOBEC3 proteins for rapid proteasomal degradation. |
http://www.ncbi.nlm.nih.gov/pubmed/24107108,http://www.ncbi.nlm.nih.gov/pubmed/22720195,http://www.ncbi.nlm.nih.gov/pubmed/19622861,http://www.ncbi.nlm.nih.gov/pubmed/18256287,http://www.ncbi.nlm.nih.gov/pubmed/18641461,http://www.ncbi.nlm.nih.gov/pubmed/14522818,http://www.ncbi.nlm.nih.gov/pubmed/22175015,http://www.ncbi.nlm.nih.gov/pubmed/16022178,http://www.ncbi.nlm.nih.gov/pubmed/9430721,http://www.ncbi.nlm.nih.gov/pubmed/19251701,http://www.ncbi.nlm.nih.gov/pubmed/23722928,http://www.ncbi.nlm.nih.gov/pubmed/23878395,http://www.ncbi.nlm.nih.gov/pubmed/17088247,http://www.ncbi.nlm.nih.gov/pubmed/17591882,http://www.ncbi.nlm.nih.gov/pubmed/17855341,http://www.ncbi.nlm.nih.gov/pubmed/17241234 | Which proteins are the different isoforms of the p38 MAP kinase? | The p38 Mitogen-Activated Protein (MAP) kinase, a serine/threonine kinase, is one of the best characterized kinases in the inflammatory process. There are four isoforms of the enzyme (p38alpha, p38beta, p38gamma and p38delta), which differ in tissue distribution, regulation of kinase activation and subsequent phosphorylation of downstream substrates. Among the four identified p38 isoforms (p38α, p38β, p38γ, and p38δ), the α-form is the most fully studied.The mammalian p38 mitogen-activated protein kinases (MAPKs) family is composed of four members (p38α, p38β, p38γ, and p38δ), which are very similar in amino acid sequence but differ in their expression patterns.The mitogen-activated protein kinase (MAPK) p38 is a Ser/Thr kinase, originally isolated from lipopolysaccharide-stimulated monocytes. There are four isoforms of the enzyme (p38alpha, p38beta, p38gamma and p38delta), which differ in tissue distribution, regulation of kinase activation and subsequent phosphorylation of downstream substrates. The p38 Mitogen-Activated Protein (MAP) kinase, a serine/threonine kinase, is one of the best characterized kinases in the inflammatory process. Among the four identified p38 isoforms (p38α, p38β, p38γ, and p38δ), the α-form is the most fully studied and plays a central role in the biosynthesis of the proinflammatory cytokines i.e. IL-1β and TNF-α at the translational and transcriptional levels. |
http://www.ncbi.nlm.nih.gov/pubmed/18957444 | Are pseudogenes enriched with housekeeping protein families? | Yes, housekeeping families tend to be enriched with a large number of pseudogenes. |
http://www.ncbi.nlm.nih.gov/pubmed/18636796,http://www.ncbi.nlm.nih.gov/pubmed/21512722,http://www.ncbi.nlm.nih.gov/pubmed/23146645,http://www.ncbi.nlm.nih.gov/pubmed/21854758 | What is the mechanism of cementogenesis in pulp regeneration? | The dental follicle (DF) consists of progenitor cells that give rise to the cementum, periodontal ligament, and alveolar bone. Dental follicle cells attach to Hertwig's epithelial root sheath (HERS), and pulp cells in the cementum promoting cementogenesis. The temporospatial regulation of Wnt/ß-catenin signaling plays critical roles in the differentiation of odontoblasts and cementoblasts.Our results indicate that persistent stabilization of ß-catenin in the dental mesenchyme leads to premature differentiation of odontoblasts and differentiation of cementoblasts, and induces excessive dentin and cementum formation in vivo. It is known that the dental follicle (DF) consists of progenitor cells that give rise to the cementum, periodontal ligament, and alveolar bone. Wnt/ß-catenin signaling plays an important role in morphogenesis and cellular differentiation during development. New vital tissues can be regenerated in permanent canine teeth after pulpectomy and enlargement of the apical foramen. Constitutive stabilization of ß-catenin in the dental mesenchyme leads to excessive dentin and cementum formation. These results suggest that temporospatial regulation of Wnt/ß-catenin signaling plays critical roles in the differentiation of odontoblasts and cementoblasts, and that inhibition of Wnt/ß-catenin signaling may be important for the formation of dentin and cementum during tooth development. HERS cells played a role in the induction and maturation of cementum-like tissues formed by DF cells. Essential roles of Wnt/ß-catenin signaling in tooth morphogenesis have been well known. |
http://www.ncbi.nlm.nih.gov/pubmed/10030434,http://www.ncbi.nlm.nih.gov/pubmed/11274308,http://www.ncbi.nlm.nih.gov/pubmed/16490100,http://www.ncbi.nlm.nih.gov/pubmed/8603631,http://www.ncbi.nlm.nih.gov/pubmed/15072101,http://www.ncbi.nlm.nih.gov/pubmed/12199723,http://www.ncbi.nlm.nih.gov/pubmed/8617181,http://www.ncbi.nlm.nih.gov/pubmed/9120226,http://www.ncbi.nlm.nih.gov/pubmed/8648543,http://www.ncbi.nlm.nih.gov/pubmed/7489697,http://www.ncbi.nlm.nih.gov/pubmed/11305405,http://www.ncbi.nlm.nih.gov/pubmed/12022084,http://www.ncbi.nlm.nih.gov/pubmed/22134010,http://www.ncbi.nlm.nih.gov/pubmed/11361047,http://www.ncbi.nlm.nih.gov/pubmed/19193587,http://www.ncbi.nlm.nih.gov/pubmed/23112238 | What are the reported adverse effects of gabapentin used in children? | Limited literature data, suggest that gabapentin may cause rash that is severe enough to necessitate discontinuation in a small percentage of children.
In a large survey of all age groups: The commonest adverse effects seen were somnolence, fainting, ataxia, nystagmus, tremor and headache, fatigue. However, their incidence was low and intensity mild. In a pediatric group only somnolence and dizziness were reported in 2 out of 33 patients.
Behavioural adverse effects are more common in children with intellectual disability and attention deficit, worse in <10yo : hyperactivity, defiance, irritability, agitation, aggression, explosive outbursts, oppositional behavior, often warranting discontinuation of the medication. |
http://www.ncbi.nlm.nih.gov/pubmed/17027025,http://www.ncbi.nlm.nih.gov/pubmed/18439620,http://www.ncbi.nlm.nih.gov/pubmed/24251065,http://www.ncbi.nlm.nih.gov/pubmed/7873471,http://www.ncbi.nlm.nih.gov/pubmed/19403851,http://www.ncbi.nlm.nih.gov/pubmed/19333133,http://www.ncbi.nlm.nih.gov/pubmed/22343711,http://www.ncbi.nlm.nih.gov/pubmed/22465693,http://www.ncbi.nlm.nih.gov/pubmed/21538388,http://www.ncbi.nlm.nih.gov/pubmed/20924097,http://www.ncbi.nlm.nih.gov/pubmed/22767404,http://www.ncbi.nlm.nih.gov/pubmed/23596505,http://www.ncbi.nlm.nih.gov/pubmed/19752362 | What is the effect of ranolazine in diastolic heart failure? | Data from in vitro and animal studies indicate that ranolazine improves diastolic function by inhibiting the late sodium current. Ranolazine is an innovative anti-ischemic and antianginal agent that reduces the Na-dependent Ca-overload, which improves diastolic tone and oxygen handling during myocardial ischemia. Furthermore, ranolazine improves cardiac diastolic dysfunction through modulation of myofilament calcium sensitivity. |
http://www.ncbi.nlm.nih.gov/pubmed/22468744,http://www.ncbi.nlm.nih.gov/pubmed/16804928,http://www.ncbi.nlm.nih.gov/pubmed/23679284,http://www.ncbi.nlm.nih.gov/pubmed/15839957,http://www.ncbi.nlm.nih.gov/pubmed/24185383,http://www.ncbi.nlm.nih.gov/pubmed/16343176,http://www.ncbi.nlm.nih.gov/pubmed/17966166,http://www.ncbi.nlm.nih.gov/pubmed/18463961,http://www.ncbi.nlm.nih.gov/pubmed/21211276,http://www.ncbi.nlm.nih.gov/pubmed/19469626,http://www.ncbi.nlm.nih.gov/pubmed/23927758,http://www.ncbi.nlm.nih.gov/pubmed/18073158,http://www.ncbi.nlm.nih.gov/pubmed/19955917,http://www.ncbi.nlm.nih.gov/pubmed/18336401,http://www.ncbi.nlm.nih.gov/pubmed/19901115,http://www.ncbi.nlm.nih.gov/pubmed/12449041,http://www.ncbi.nlm.nih.gov/pubmed/16360545,http://www.ncbi.nlm.nih.gov/pubmed/17938703,http://www.ncbi.nlm.nih.gov/pubmed/12448655,http://www.ncbi.nlm.nih.gov/pubmed/10964992 | Elaborate on the potential efficacy of gemcitabine for the treatment of recurrent, platinum-resistant epithelial ovarian cancer. | Gemcitabine is a novel agent that has shown consistent activity as a single agent in the treatment of platinum-resistant ovarian cancer and a favorable toxicity profile. Because of its clinical and preclinical synergism with platinum analogs, gemcitabine has been combined with carboplatin as a convincing approach in the treatment of platinum-sensitive recurrent ovarian cancer patients. Gemcitabine and prolonged oral etoposide have shown reproducible single-agent activity in patients with platinum/paclitaxel-resistant ovarian cancer. The combination of carboplatin and gemcitabine resulted in significantly higher response rates and improved progression-free survival when compared with carboplatin alone. A biweekly schedule of gemcitabine combined with PLD is an active and safe chemotherapy regimen with acceptable and easily manageable toxicities in women with recurrent platinum-resistant ovarian cancer. Pertuzumab may add activity to gemcitabine for the treatment of platinum-resistant ovarian cancer. The regimen of gemcitabine combined with ifosfamide and anthracycline is feasible, tolerable and effective in patients with recurrent platinum resistant/refractory epithelial ovarian cancer. Gemcitabine plus endostar significantly improved the prognosis in patients with platinum-resistant recurrent ovarian cancer, especially in those with malignant effusion. Though the endostar cohort also improved median OS by 2.1 months, there was no statistically significant difference compared with gemcitabine alone cohort in this case. |
http://www.ncbi.nlm.nih.gov/pubmed/19339686,http://www.ncbi.nlm.nih.gov/pubmed/22406422,http://www.ncbi.nlm.nih.gov/pubmed/21502411,http://www.ncbi.nlm.nih.gov/pubmed/20591647,http://www.ncbi.nlm.nih.gov/pubmed/16909212,http://www.ncbi.nlm.nih.gov/pubmed/25436603,http://www.ncbi.nlm.nih.gov/pubmed/21404180,http://www.ncbi.nlm.nih.gov/pubmed/21935353 | How does Foxa transcription factor exhibits its pioneering function? | The conceptional framework of the mechanism of action of the FoxA proteins is that these 'pioneer factors' that can engage chromatin before other transcription factors. The Fox DNA-binding domain structurally resembles linker histone and binds nucleosomes stably. FoxA induces local DNA demethylation, nucleosome destabilization and binds to mitotic chromosomes. When associated with mitotic chromatin, FoxA may "bookmark" active genes and ensure their reactivation in postmitotic cells (epigenetic memory). About one-third of the FoxA bound sites are near silent genes, including genes without detectable RNA polymerase II. The "pioneer" features of FoxA factors involve various chromatin-binding parameters seen in linker histones and distinguish the factors with respect to their regulatory and mechanistic functions.FoxA proteins are pioneer transcription factors, among the first to bind chromatin domains in development and enable gene activity. There exists a hierarchy by which transcription factors can engage their target sites in chromatin, in that a subset of factors can bind transcriptionally silent, nucleosomal DNA, whereas most factors cannot, and this hierarchy is reflected, at least in part, in the developmental function of the factors. These discoveries followed the establishment of the conceptional framework of the mechanism of action of the FoxA proteins as 'pioneer factors' that can engage chromatin before other transcription factors. Such sites are enriched in motifs for transcriptional repressors, including for Rfx1 and type II nuclear hormone receptors. |
http://www.ncbi.nlm.nih.gov/pubmed/23722259,http://www.ncbi.nlm.nih.gov/pubmed/20691899,http://www.ncbi.nlm.nih.gov/pubmed/22575762,http://www.ncbi.nlm.nih.gov/pubmed/22522929,http://www.ncbi.nlm.nih.gov/pubmed/21241459,http://www.ncbi.nlm.nih.gov/pubmed/23704920,http://www.ncbi.nlm.nih.gov/pubmed/23474887,http://www.ncbi.nlm.nih.gov/pubmed/23050819,http://www.ncbi.nlm.nih.gov/pubmed/23487791,http://www.ncbi.nlm.nih.gov/pubmed/23861494,http://www.ncbi.nlm.nih.gov/pubmed/22581928,http://www.ncbi.nlm.nih.gov/pubmed/23591016 | Which are the 3 basic transcription factors that have been used for the direct reprogramming of fibroblasts into cardiomyocytes or cardiomyocyte like-cells? | Direct reprogramming of human cardiac fibroblasts (HCFs) into cardiomyocytes may hold great potential for this purpose. We found that functional cardiomyocytes can be directly induced from fibroblasts by a combination of three cardiac transcription factors, Gata4, Mef2c and Tbx5, in vitro and in vivo.Direct reprogramming of human cardiac fibroblasts (HCFs) into cardiomyocytes may hold great potential for this purpose. We reported previously that induced cardiomyocyte-like cells (iCMs) can be directly generated from mouse cardiac fibroblasts in vitro and vivo by transduction of three transcription factors: Gata4, Mef2c, and Tbx5, collectively termed GMT. Cardiac fibroblasts, which represent 50% of the cells in the mammalian heart, can be directly reprogrammed to adult cardiomyocyte-like cells in vitro by the addition of Gata4, Mef2c and Tbx5 (GMT). Induced cardiomyocytes expressed cardiac-specific markers, had a global gene expression profile similar to cardiomyocytes, and contracted spontaneously. |
http://www.ncbi.nlm.nih.gov/pubmed/23617253,http://www.ncbi.nlm.nih.gov/pubmed/24085367,http://www.ncbi.nlm.nih.gov/pubmed/24157582,http://www.ncbi.nlm.nih.gov/pubmed/22960555,http://www.ncbi.nlm.nih.gov/pubmed/24009233,http://www.ncbi.nlm.nih.gov/pubmed/23619564,http://www.ncbi.nlm.nih.gov/pubmed/22300471,http://www.ncbi.nlm.nih.gov/pubmed/23617325,http://www.ncbi.nlm.nih.gov/pubmed/23782158,http://www.ncbi.nlm.nih.gov/pubmed/23359016,http://www.ncbi.nlm.nih.gov/pubmed/24311722,http://www.ncbi.nlm.nih.gov/pubmed/22830347,http://www.ncbi.nlm.nih.gov/pubmed/23656200 | What is the name of Bruton's tyrosine kinase inhibitor that can be used for treatment of chronic lymphocytic leukemia? | Ibrutinib is the covalent inhibitor of Bruton's tyrosine kinase that can be used for treatment of chronic lymphocytic leukemia (CLL). Ibrutinib has shown highly encouraging results in phase I/II trials in patients with treatment-naive, relapsed and refractory CLL even in the presence of high risk disease or poor prognostic markers. Ibrutinib demonstrated that Bruton's tyrosine kinase inhibition sensitizes CLL cells to apoptosis and alters their migratory behavior. Ibrutinib has excellent activity in other B cell malignancies, including in particular mantle cell lymphoma and Waldenstrom macroglobulinemia. |
http://www.ncbi.nlm.nih.gov/pubmed/19468264,http://www.ncbi.nlm.nih.gov/pubmed/2704923,http://www.ncbi.nlm.nih.gov/pubmed/18523407,http://www.ncbi.nlm.nih.gov/pubmed/16174720,http://www.ncbi.nlm.nih.gov/pubmed/17893267,http://www.ncbi.nlm.nih.gov/pubmed/16621071,http://www.ncbi.nlm.nih.gov/pubmed/16910873,http://www.ncbi.nlm.nih.gov/pubmed/21875391 | Is physical performance influenced by thyroid hormone metabolism? | Yes. |
http://www.ncbi.nlm.nih.gov/pubmed/15733327,http://www.ncbi.nlm.nih.gov/pubmed/12857799,http://www.ncbi.nlm.nih.gov/pubmed/16283384,http://www.ncbi.nlm.nih.gov/pubmed/12054347,http://www.ncbi.nlm.nih.gov/pubmed/21548945,http://www.ncbi.nlm.nih.gov/pubmed/11489175,http://www.ncbi.nlm.nih.gov/pubmed/16453856 | Do plant genomes contain CpG islands? | In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5 -terminus, share similarities with human genes having CpG islands Yes. In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. |
http://www.ncbi.nlm.nih.gov/pubmed/16339652,http://www.ncbi.nlm.nih.gov/pubmed/15920471,http://www.ncbi.nlm.nih.gov/pubmed/16888367,http://www.ncbi.nlm.nih.gov/pubmed/19196479 | Describe the isolation of transcription factor complexes by in vivo biotinylation tagging and direct binding to streptavidin beads, as applied for the case of the essential hematopoietic transcription factor GATA-1. | Owing to the very high affinity of biotin for avidin and streptavidin, biotinylation tagging offers an attractive approach for the efficient purification of protein complexes. The very high affinity of the biotin/(strept)avidin system also offers the potential for the single-step capture of lower abundance protein complexes, such as transcription factor complexes. The identification of short peptide tags that are efficiently biotinylated by the bacterial BirA biotin ligase led to an approach for the single-step purification of transcription factor complexes by specific in vivo biotinylation tagging. A short sequence tag fused N-terminally to the transcription factor of interest is very efficiently biotinylated by BirA coexpressed in the same cells, as was demonstrated by the tagging of the essential hematopoietic transcription factor GATA-1. The direct binding to streptavidin of biotinylated GATA-1 in nuclear extracts resulted in the single-step capture of the tagged factor and associated proteins, which were eluted and identified by mass spectrometry. This led to the characterization of several distinct GATA-1 complexes with other transcription factors and chromatin remodeling cofactors, which are involved in activation and repression of gene targets. Thus, BirA-mediated tagging is an efficient approach for the direct capture and characterization of transcription factor complexes. |
http://www.ncbi.nlm.nih.gov/pubmed/21563154,http://www.ncbi.nlm.nih.gov/pubmed/24225220,http://www.ncbi.nlm.nih.gov/pubmed/22518179,http://www.ncbi.nlm.nih.gov/pubmed/24106935,http://www.ncbi.nlm.nih.gov/pubmed/23782410,http://www.ncbi.nlm.nih.gov/pubmed/23143331,http://www.ncbi.nlm.nih.gov/pubmed/21276671,http://www.ncbi.nlm.nih.gov/pubmed/23955516,http://www.ncbi.nlm.nih.gov/pubmed/21682982,http://www.ncbi.nlm.nih.gov/pubmed/22958022,http://www.ncbi.nlm.nih.gov/pubmed/23947111,http://www.ncbi.nlm.nih.gov/pubmed/23903677,http://www.ncbi.nlm.nih.gov/pubmed/23260098,http://www.ncbi.nlm.nih.gov/pubmed/23114244,http://www.ncbi.nlm.nih.gov/pubmed/22173399,http://www.ncbi.nlm.nih.gov/pubmed/17989697,http://www.ncbi.nlm.nih.gov/pubmed/19762171,http://www.ncbi.nlm.nih.gov/pubmed/11331690,http://www.ncbi.nlm.nih.gov/pubmed/22964658 | Are high-flow nasal cannulae effective for treatment of preterm infants? | Yes. The use of high-flow nasal cannulae is an increasingly popular alternative to nasal continuous positive airway pressure for noninvasive respiratory support of preterm infants after extubation. However, the use of high-flow nasal cannulae in preterm infants was shown to be associated with a higher rate of reintubation, increased exposure to oxygen and longer duration of respiratory support. High-flow nasal cannulae are also effective for treatment of apnea of prematurity. |
http://www.ncbi.nlm.nih.gov/pubmed/8896563 | What are the molecular characteristics of the FAA (FANCA) cDNA? | The 5.5-kb cDNA of the FAA (FANCA) gene has an open reading frame of 4,368 nucleotides, whereas the FAA protein is predicted to have a molecular weight of approximately 163 kDa. |
http://www.ncbi.nlm.nih.gov/pubmed/21339173,http://www.ncbi.nlm.nih.gov/pubmed/17996437,http://www.ncbi.nlm.nih.gov/pubmed/17600112,http://www.ncbi.nlm.nih.gov/pubmed/22233500,http://www.ncbi.nlm.nih.gov/pubmed/21727135,http://www.ncbi.nlm.nih.gov/pubmed/26055324,http://www.ncbi.nlm.nih.gov/pubmed/24747722,http://www.ncbi.nlm.nih.gov/pubmed/19265661,http://www.ncbi.nlm.nih.gov/pubmed/25732238,http://www.ncbi.nlm.nih.gov/pubmed/26248268,http://www.ncbi.nlm.nih.gov/pubmed/12757751,http://www.ncbi.nlm.nih.gov/pubmed/24439806,http://www.ncbi.nlm.nih.gov/pubmed/26074812,http://www.ncbi.nlm.nih.gov/pubmed/26341996 | What are the skeletal muscle satellite cells? | Skeletal muscle satellite cells (SCs) are Pax7(+) myogenic stem cells that reside between the basal lamina and the plasmalemma of the myofiber. In mature muscles, SCs are typically quiescent, but can be activated in response to muscle injury. Depending on the magnitude of tissue trauma, SCs may divide minimally to repair subtle damage within individual myofibers or produce a larger progeny pool that forms new myofibers in cases of overt muscle injurySkeletal muscle satellite cells (SCs) are Pax7(+) myogenic stem cells that reside between the basal lamina and the plasmalemma of the myofiber. In mature muscles, SCs are typically quiescent, but can be activated in response to muscle injury. Depending on the magnitude of tissue trauma, SCs may divide minimally to repair subtle damage within individual myofibers or produce a larger progeny pool that forms new myofibers in cases of overt muscle injury. |
http://www.ncbi.nlm.nih.gov/pubmed/20875798,http://www.ncbi.nlm.nih.gov/pubmed/15851848,http://www.ncbi.nlm.nih.gov/pubmed/26136856,http://www.ncbi.nlm.nih.gov/pubmed/24978200 | What is the role of neurogranin in Alzheimer's disease patients? | Dendritic protein neurogranin is markedly increased in cerebrospinal fluid in Alzheimer's disease patients. Neurogranin might reflect the neurodegenerative processes within the brain, indicating a role for neurogranin as a potential novel clinical biomarker for synaptic degeneration in AD.
Neurogranin is important for synaptic plasticity and memory. |
http://www.ncbi.nlm.nih.gov/pubmed/17408701,http://www.ncbi.nlm.nih.gov/pubmed/21099301,http://www.ncbi.nlm.nih.gov/pubmed/1357067,http://www.ncbi.nlm.nih.gov/pubmed/619228,http://www.ncbi.nlm.nih.gov/pubmed/19021014,http://www.ncbi.nlm.nih.gov/pubmed/20730704,http://www.ncbi.nlm.nih.gov/pubmed/3310493,http://www.ncbi.nlm.nih.gov/pubmed/1537314,http://www.ncbi.nlm.nih.gov/pubmed/21914860,http://www.ncbi.nlm.nih.gov/pubmed/2242013 | Does triiodothyronine play a regulatory role in insulin secretion from pancreas? | YES |
http://www.ncbi.nlm.nih.gov/pubmed/11985602,http://www.ncbi.nlm.nih.gov/pubmed/21838701,http://www.ncbi.nlm.nih.gov/pubmed/22967859,http://www.ncbi.nlm.nih.gov/pubmed/21073997,http://www.ncbi.nlm.nih.gov/pubmed/22705624,http://www.ncbi.nlm.nih.gov/pubmed/24018861 | How many disulfide bridges has the protein hepcidin got? | Hepcidin contains eight cysteine residues that form four disulfide bridges. |
http://www.ncbi.nlm.nih.gov/pubmed/20601132,http://www.ncbi.nlm.nih.gov/pubmed/23567359,http://www.ncbi.nlm.nih.gov/pubmed/15316418,http://www.ncbi.nlm.nih.gov/pubmed/21438963,http://www.ncbi.nlm.nih.gov/pubmed/18853995 | What is the association between GERD and gluten ? | GERD symptoms are common in classically symptomatic untreated CD patients. The GFD is associated with a rapid and persistent improvement in reflux symptoms that resembles the healthy population.
Food intolerance is a common complaint amongst patients with functional gastrointestinal (GI) disorders (FGIDs), including those with irritable bowel syndrome (IBS), functional dyspepsia, as well as gastroesophageal reflux disease. There is a great interest in the role of a major dietary protein, gluten, in the production of symptoms...several published studies have consistently shown the efficacy of a gluten-free diet in rapidly controlling esophageal symptoms and in preventing their recurrence |
http://www.ncbi.nlm.nih.gov/pubmed/18812180 | Which are the major intramolecular phosphorylation sites of human Chk2 involved in cell cycle control? | The major phosphorylation sites of human Chk2 involved in cell cycle control are T68, S19, and S33/35. |
http://www.ncbi.nlm.nih.gov/pubmed/15191886,http://www.ncbi.nlm.nih.gov/pubmed/17030629,http://www.ncbi.nlm.nih.gov/pubmed/20807542,http://www.ncbi.nlm.nih.gov/pubmed/22952658,http://www.ncbi.nlm.nih.gov/pubmed/24125847,http://www.ncbi.nlm.nih.gov/pubmed/19403607,http://www.ncbi.nlm.nih.gov/pubmed/21742996,http://www.ncbi.nlm.nih.gov/pubmed/22040806,http://www.ncbi.nlm.nih.gov/pubmed/18617481 | Is the Histidine-Rich Calcium Binding protein (HRC) related to arrhythmias and cardiac disease? | Histidine-rich calcium binding protein (HRC) is a high capacity, low affinity Ca(2+) binding protein with a potential role in heart failure and arrhythmogenesis due to its activity as regulator of SR Ca(2+) uptake and Ca(2+) release.In addition, HRC null mice displayed a significantly exaggerated response to the induction of cardiac hypertrophy by isoproterenol compared to their wild-type littermates. A human genetic variant (Ser96Ala) in HRC has been linked to ventricular arrhythmia and sudden death in dilated cardiomyopathy. |
http://www.ncbi.nlm.nih.gov/pubmed/18582175,http://www.ncbi.nlm.nih.gov/pubmed/23093601,http://www.ncbi.nlm.nih.gov/pubmed/18237442,http://www.ncbi.nlm.nih.gov/pubmed/24822028,http://www.ncbi.nlm.nih.gov/pubmed/12218031,http://www.ncbi.nlm.nih.gov/pubmed/25309521,http://www.ncbi.nlm.nih.gov/pubmed/17188685,http://www.ncbi.nlm.nih.gov/pubmed/14643658,http://www.ncbi.nlm.nih.gov/pubmed/21364800,http://www.ncbi.nlm.nih.gov/pubmed/21945744,http://www.ncbi.nlm.nih.gov/pubmed/17584494,http://www.ncbi.nlm.nih.gov/pubmed/24808892,http://www.ncbi.nlm.nih.gov/pubmed/19332823,http://www.ncbi.nlm.nih.gov/pubmed/12732098 | Which are the methods for in silico prediction of the origin of replication (ori) among bacteria? | Several in silico methods have been applied for prediction of the origin of replication (ori). DNA base composition asymmetry, such as GC skew, is the basis of numerous in silico methods used to detect the ori in prokaryotes. The Z curve analysis is also used for ori identification. Comparative genomics, by BLAST analyses of the intergenic sequences compared to related species have been applied in ori prediction. The finding of the dnaA gene and its binding sites, DnaA boxes, as well as the finding of the binding sites of other proteins, such as CtrA and IHF, are fundamental characteristics used for in silico prediction of the ori. Also, the localization of boundary genes, such as cell division cycle (cdc6) gene, and consensus origin recognition box (ORB) sequences have been employed for ori detection. The study of the gene order around the origin sequence and the distribution of the genes encoded in the leading versus the lagging strand are also used for in silico detection of the ori. |
http://www.ncbi.nlm.nih.gov/pubmed/23398507,http://www.ncbi.nlm.nih.gov/pubmed/22668416,http://www.ncbi.nlm.nih.gov/pubmed/23148498,http://www.ncbi.nlm.nih.gov/pubmed/23900195,http://www.ncbi.nlm.nih.gov/pubmed/21513157,http://www.ncbi.nlm.nih.gov/pubmed/21543404,http://www.ncbi.nlm.nih.gov/pubmed/23546785,http://www.ncbi.nlm.nih.gov/pubmed/23744319,http://www.ncbi.nlm.nih.gov/pubmed/23665194,http://www.ncbi.nlm.nih.gov/pubmed/22355625 | What is the use of emulsion PCR in Next Generation Sequencing? | Prior to Next Generation Sequencing reactions, DNA libraries are constructed, amplified with emulsion PCR, and enriched with the use of enrichment beads. The library samples are then loaded to a sequencing chip and analyzed on an NGS platform. |
http://www.ncbi.nlm.nih.gov/pubmed/24222332,http://www.ncbi.nlm.nih.gov/pubmed/10908330,http://www.ncbi.nlm.nih.gov/pubmed/22460946,http://www.ncbi.nlm.nih.gov/pubmed/17041717,http://www.ncbi.nlm.nih.gov/pubmed/11144280,http://www.ncbi.nlm.nih.gov/pubmed/16939628,http://www.ncbi.nlm.nih.gov/pubmed/10575541,http://www.ncbi.nlm.nih.gov/pubmed/7541126,http://www.ncbi.nlm.nih.gov/pubmed/20201948,http://www.ncbi.nlm.nih.gov/pubmed/17486495,http://www.ncbi.nlm.nih.gov/pubmed/14594506,http://www.ncbi.nlm.nih.gov/pubmed/18379999,http://www.ncbi.nlm.nih.gov/pubmed/21415990,http://www.ncbi.nlm.nih.gov/pubmed/16735596,http://www.ncbi.nlm.nih.gov/pubmed/17456718,http://www.ncbi.nlm.nih.gov/pubmed/20305142,http://www.ncbi.nlm.nih.gov/pubmed/23997901,http://www.ncbi.nlm.nih.gov/pubmed/11929793 | Can adult humans be induced to produce fetal hemoglobin? | Fetal hemoglobin, or foetal haemoglobin, is the main oxygen transport protein in the human fetus during the last seven months of development in the uterus and in the newborn until roughly 6 months old. Functionally, fetal hemoglobin differs most from adult hemoglobin in that it is able to bind oxygen with greater affinity than the adult form, giving the developing fetus better access to oxygen from the mother's bloodstream.
Unusually high levels of fetal haemoglobin production can ameliorate sickle cell disease and β thalassaemia. Although efforts directed at the pharmacological stimulation of fetal haemoglobin as an approach to managing these conditions have met with limited success, there is wide variation in individual responses.
Based on results, adults humans could be induced to produce fetal hemoglobin. |
http://www.ncbi.nlm.nih.gov/pubmed/22890105,http://www.ncbi.nlm.nih.gov/pubmed/20667986,http://www.ncbi.nlm.nih.gov/pubmed/23937304,http://www.ncbi.nlm.nih.gov/pubmed/22468949,http://www.ncbi.nlm.nih.gov/pubmed/15450085,http://www.ncbi.nlm.nih.gov/pubmed/23970787,http://www.ncbi.nlm.nih.gov/pubmed/21896185,http://www.ncbi.nlm.nih.gov/pubmed/9731697,http://www.ncbi.nlm.nih.gov/pubmed/2298257,http://www.ncbi.nlm.nih.gov/pubmed/22497336,http://www.ncbi.nlm.nih.gov/pubmed/22560077,http://www.ncbi.nlm.nih.gov/pubmed/15358620,http://www.ncbi.nlm.nih.gov/pubmed/9687498,http://www.ncbi.nlm.nih.gov/pubmed/20656376,http://www.ncbi.nlm.nih.gov/pubmed/23832699,http://www.ncbi.nlm.nih.gov/pubmed/15550503,http://www.ncbi.nlm.nih.gov/pubmed/12072400,http://www.ncbi.nlm.nih.gov/pubmed/15728663,http://www.ncbi.nlm.nih.gov/pubmed/24013065,http://www.ncbi.nlm.nih.gov/pubmed/22968643,http://www.ncbi.nlm.nih.gov/pubmed/7935490 | What is the role of thyroid hormone in Stem cell differentiation? | Thyroid hormone treatment of Human-induced pluripotent stem cell-derived cardiomyocytes attenuates the fetal gene expression and induces differentiation. Liganded T3 receptor (TR) regulates cell autonomous formation of adult intestinal progenitor cells and that T3 action in the connective tissue is important for the establishment of the stem cell niche. In the intestinal epithelium, TRα1 and TRβ2 are expressed at the level of stem/progenitor cell populations where they induce cell proliferation and differentiation, respectively. Thyroid hormone is implicated in neural stem cell function and differentiation and acts as a neurogenic switch in the adult neural stem cell niche. Furthermore, thyroid hormone enhances maturation of oligodendrocyte precursor cells. Thyroid hormones also induce hemopoietic pluripotent stem cell differentiation toward erythropoiesis and c-erbA/TR appears to act as a binary switch affecting erythroid cell fate: unliganded c-erbA/TR supports growth while ligand-activated c-erbA/TR induces differentiation. Finally, thyroid hormone modulates late differentiation stages of mesenchymal stem cells chondrogenesis via BMP signaling. |
http://www.ncbi.nlm.nih.gov/pubmed/22940693,http://www.ncbi.nlm.nih.gov/pubmed/12902843,http://www.ncbi.nlm.nih.gov/pubmed/16206185,http://www.ncbi.nlm.nih.gov/pubmed/23824248,http://www.ncbi.nlm.nih.gov/pubmed/20641567,http://www.ncbi.nlm.nih.gov/pubmed/12642173,http://www.ncbi.nlm.nih.gov/pubmed/17195073,http://www.ncbi.nlm.nih.gov/pubmed/21098981,http://www.ncbi.nlm.nih.gov/pubmed/7995287,http://www.ncbi.nlm.nih.gov/pubmed/24120220,http://www.ncbi.nlm.nih.gov/pubmed/21996132,http://www.ncbi.nlm.nih.gov/pubmed/9027929,http://www.ncbi.nlm.nih.gov/pubmed/21359565,http://www.ncbi.nlm.nih.gov/pubmed/21722741,http://www.ncbi.nlm.nih.gov/pubmed/21473029,http://www.ncbi.nlm.nih.gov/pubmed/18828013,http://www.ncbi.nlm.nih.gov/pubmed/17241616,http://www.ncbi.nlm.nih.gov/pubmed/10587097,http://www.ncbi.nlm.nih.gov/pubmed/19007894,http://www.ncbi.nlm.nih.gov/pubmed/17541696,http://www.ncbi.nlm.nih.gov/pubmed/23137806,http://www.ncbi.nlm.nih.gov/pubmed/19162492,http://www.ncbi.nlm.nih.gov/pubmed/20956470,http://www.ncbi.nlm.nih.gov/pubmed/10688105,http://www.ncbi.nlm.nih.gov/pubmed/19959344,http://www.ncbi.nlm.nih.gov/pubmed/9826230,http://www.ncbi.nlm.nih.gov/pubmed/12224404,http://www.ncbi.nlm.nih.gov/pubmed/15356424,http://www.ncbi.nlm.nih.gov/pubmed/7673371,http://www.ncbi.nlm.nih.gov/pubmed/23456885,http://www.ncbi.nlm.nih.gov/pubmed/17185512,http://www.ncbi.nlm.nih.gov/pubmed/19015089,http://www.ncbi.nlm.nih.gov/pubmed/19353726,http://www.ncbi.nlm.nih.gov/pubmed/21473027,http://www.ncbi.nlm.nih.gov/pubmed/10588399,http://www.ncbi.nlm.nih.gov/pubmed/23390031,http://www.ncbi.nlm.nih.gov/pubmed/23303045,http://www.ncbi.nlm.nih.gov/pubmed/21750562,http://www.ncbi.nlm.nih.gov/pubmed/9257335,http://www.ncbi.nlm.nih.gov/pubmed/1428914,http://www.ncbi.nlm.nih.gov/pubmed/9824691 | Which receptors can be evaluated with the [18F]altanserin? | 5-HT2A (5-hydroxytryptamine type 2a) receptor can be evaluated with the [18F]altanserin. |
http://www.ncbi.nlm.nih.gov/pubmed/16277672,http://www.ncbi.nlm.nih.gov/pubmed/16391555,http://www.ncbi.nlm.nih.gov/pubmed/15790351,http://www.ncbi.nlm.nih.gov/pubmed/16464986,http://www.ncbi.nlm.nih.gov/pubmed/22237046,http://www.ncbi.nlm.nih.gov/pubmed/15719322,http://www.ncbi.nlm.nih.gov/pubmed/16320352,http://www.ncbi.nlm.nih.gov/pubmed/19248096,http://www.ncbi.nlm.nih.gov/pubmed/21752868 | Which diseases have been associated with the PTPN22 620W allele? | The functional polymorphism 620W in the intracellular tyrosine phosphatase PTPN22 gene has been shown to confer susceptibility to the development of type 1 diabetes, seropositive rheumatoid arthritis, systemic lupus erythematosus, Hashimoto thyroiditis, and Wegener's granulomatosis (granulomatosis with polyangiitis). |
http://www.ncbi.nlm.nih.gov/pubmed/22517745,http://www.ncbi.nlm.nih.gov/pubmed/22289392,http://www.ncbi.nlm.nih.gov/pubmed/22399514,http://www.ncbi.nlm.nih.gov/pubmed/21956421,http://www.ncbi.nlm.nih.gov/pubmed/22496347 | Which extra thyroid tissues have thyrotropin (TSH) receptors? | TSH receptors are expressed also in extrathyroid tissues. TSH receptors seem to be functional. Extrathyroid tissues include fibrobasts of the orbit and adipose tissue
The principal tissues with TSH receptors are:
adippose tissue
orbital fibrotic tissue |
http://www.ncbi.nlm.nih.gov/pubmed/24038352,http://www.ncbi.nlm.nih.gov/pubmed/21937433,http://www.ncbi.nlm.nih.gov/pubmed/20008934,http://www.ncbi.nlm.nih.gov/pubmed/18441229,http://www.ncbi.nlm.nih.gov/pubmed/19094206,http://www.ncbi.nlm.nih.gov/pubmed/22421546,http://www.ncbi.nlm.nih.gov/pubmed/23547170,http://www.ncbi.nlm.nih.gov/pubmed/12461564,http://www.ncbi.nlm.nih.gov/pubmed/19295514,http://www.ncbi.nlm.nih.gov/pubmed/21106759 | Which histone modifications distinguish between promoters and enhancers? | H3K27ac is a marker of active enhancers. An enhancer chromatin state signature associated with active developmental enhancers may be defined by high levels of H3K27ac marking, nucleosome displacement, hypersensitivity to sonication, and strong depletion of H3K27me3. |
http://www.ncbi.nlm.nih.gov/pubmed/19552401,http://www.ncbi.nlm.nih.gov/pubmed/11027586,http://www.ncbi.nlm.nih.gov/pubmed/17981999,http://www.ncbi.nlm.nih.gov/pubmed/17624330,http://www.ncbi.nlm.nih.gov/pubmed/10381257,http://www.ncbi.nlm.nih.gov/pubmed/9045676,http://www.ncbi.nlm.nih.gov/pubmed/9705320,http://www.ncbi.nlm.nih.gov/pubmed/17510655 | Where is the metaxin complex localized? | The metaxin complex is localized to the outer mitochondrial membrane. |
http://www.ncbi.nlm.nih.gov/pubmed/22528351,http://www.ncbi.nlm.nih.gov/pubmed/23282240,http://www.ncbi.nlm.nih.gov/pubmed/15867427,http://www.ncbi.nlm.nih.gov/pubmed/22923465,http://www.ncbi.nlm.nih.gov/pubmed/2165587,http://www.ncbi.nlm.nih.gov/pubmed/16511833,http://www.ncbi.nlm.nih.gov/pubmed/10677855,http://www.ncbi.nlm.nih.gov/pubmed/16399224,http://www.ncbi.nlm.nih.gov/pubmed/12213770,http://www.ncbi.nlm.nih.gov/pubmed/11343131,http://www.ncbi.nlm.nih.gov/pubmed/12167372,http://www.ncbi.nlm.nih.gov/pubmed/22093876,http://www.ncbi.nlm.nih.gov/pubmed/17431169 | What are the major classes of retrotransposons active in the human genome? | LINE-1 (L1), Alu, SVA |
http://www.ncbi.nlm.nih.gov/pubmed/22739174,http://www.ncbi.nlm.nih.gov/pubmed/12679976,http://www.ncbi.nlm.nih.gov/pubmed/20960466,http://www.ncbi.nlm.nih.gov/pubmed/23795277,http://www.ncbi.nlm.nih.gov/pubmed/20603584,http://www.ncbi.nlm.nih.gov/pubmed/24662257,http://www.ncbi.nlm.nih.gov/pubmed/16239073 | Which are the clinical characteristics of Diamond-Blackfan anemia? | Diamond-Blackfan anemia (DBA) is a rare congenital erythroid hypoplastic anemia that usually presents early in infancy and is characterized by red cell aplasia, congenital anomalies, and a predisposition to cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/2854007,http://www.ncbi.nlm.nih.gov/pubmed/3537733,http://www.ncbi.nlm.nih.gov/pubmed/3915784,http://www.ncbi.nlm.nih.gov/pubmed/7828814,http://www.ncbi.nlm.nih.gov/pubmed/4054606,http://www.ncbi.nlm.nih.gov/pubmed/2233735,http://www.ncbi.nlm.nih.gov/pubmed/8414992,http://www.ncbi.nlm.nih.gov/pubmed/11973302,http://www.ncbi.nlm.nih.gov/pubmed/3211135,http://www.ncbi.nlm.nih.gov/pubmed/1522546,http://www.ncbi.nlm.nih.gov/pubmed/3336362,http://www.ncbi.nlm.nih.gov/pubmed/7731807 | How can the expression of SerH3 immobilization antigen be regulated? | The expression of Tetrahymena surface proteins serotype H3 (SerH3) is under temperature regulation. SerH3 is expressed when cells are incubated between the temperatures of 20 and 35 degrees C. |
http://www.ncbi.nlm.nih.gov/pubmed/23589332,http://www.ncbi.nlm.nih.gov/pubmed/19245807,http://www.ncbi.nlm.nih.gov/pubmed/18373978,http://www.ncbi.nlm.nih.gov/pubmed/12782658,http://www.ncbi.nlm.nih.gov/pubmed/20534440,http://www.ncbi.nlm.nih.gov/pubmed/17942706,http://www.ncbi.nlm.nih.gov/pubmed/24050178,http://www.ncbi.nlm.nih.gov/pubmed/22244331,http://www.ncbi.nlm.nih.gov/pubmed/22549956,http://www.ncbi.nlm.nih.gov/pubmed/17567605,http://www.ncbi.nlm.nih.gov/pubmed/23699410,http://www.ncbi.nlm.nih.gov/pubmed/16880520,http://www.ncbi.nlm.nih.gov/pubmed/19860741,http://www.ncbi.nlm.nih.gov/pubmed/20028984,http://www.ncbi.nlm.nih.gov/pubmed/21670248,http://www.ncbi.nlm.nih.gov/pubmed/18332113,http://www.ncbi.nlm.nih.gov/pubmed/20170405 | Which factors play a role in promoter proximal pausing of RNA polymerase II? | NELF (negative elongator factor) and DSIF (DRB Sensitivity Inducing Factor) |
http://www.ncbi.nlm.nih.gov/pubmed/12525534,http://www.ncbi.nlm.nih.gov/pubmed/8058745,http://www.ncbi.nlm.nih.gov/pubmed/23444773,http://www.ncbi.nlm.nih.gov/pubmed/21956823,http://www.ncbi.nlm.nih.gov/pubmed/24773018,http://www.ncbi.nlm.nih.gov/pubmed/23585528,http://www.ncbi.nlm.nih.gov/pubmed/21131752,http://www.ncbi.nlm.nih.gov/pubmed/9389754,http://www.ncbi.nlm.nih.gov/pubmed/10915769,http://www.ncbi.nlm.nih.gov/pubmed/24604962,http://www.ncbi.nlm.nih.gov/pubmed/16675878 | Which are the main clinical features of Fanconi anemia? | Fanconi anaemia (FA) is an autosomal recessive disease characterised by congenital abnormalities, defective haemopoiesis, and increased risk of malignancies.Fanconi anemia (FA) is a genetically and phenotypically heterogeneous recessive disorder characterized by diverse congenital malformations, progressive pancytopenia and predisposition to both hematologic malignancies and solid tumors |
http://www.ncbi.nlm.nih.gov/pubmed/25707381,http://www.ncbi.nlm.nih.gov/pubmed/2477715,http://www.ncbi.nlm.nih.gov/pubmed/3043797 | Which is the receptor for the immunosuppressive drug cyclosporin A (CsA)? | Cyclophilin is the intracellular receptor protein for cyclosporin A (CsA). |
http://www.ncbi.nlm.nih.gov/pubmed/23264396,http://www.ncbi.nlm.nih.gov/pubmed/21595516,http://www.ncbi.nlm.nih.gov/pubmed/18996189,http://www.ncbi.nlm.nih.gov/pubmed/18845642,http://www.ncbi.nlm.nih.gov/pubmed/16898074,http://www.ncbi.nlm.nih.gov/pubmed/17711927,http://www.ncbi.nlm.nih.gov/pubmed/12796075,http://www.ncbi.nlm.nih.gov/pubmed/17446037,http://www.ncbi.nlm.nih.gov/pubmed/21516059,http://www.ncbi.nlm.nih.gov/pubmed/19733399,http://www.ncbi.nlm.nih.gov/pubmed/18466075,http://www.ncbi.nlm.nih.gov/pubmed/15142360,http://www.ncbi.nlm.nih.gov/pubmed/22908106,http://www.ncbi.nlm.nih.gov/pubmed/19942153,http://www.ncbi.nlm.nih.gov/pubmed/17725434,http://www.ncbi.nlm.nih.gov/pubmed/19226259,http://www.ncbi.nlm.nih.gov/pubmed/19789374,http://www.ncbi.nlm.nih.gov/pubmed/19191742,http://www.ncbi.nlm.nih.gov/pubmed/16641395,http://www.ncbi.nlm.nih.gov/pubmed/17093176,http://www.ncbi.nlm.nih.gov/pubmed/17931806,http://www.ncbi.nlm.nih.gov/pubmed/14751040,http://www.ncbi.nlm.nih.gov/pubmed/1728914,http://www.ncbi.nlm.nih.gov/pubmed/21435090,http://www.ncbi.nlm.nih.gov/pubmed/18511320,http://www.ncbi.nlm.nih.gov/pubmed/10838651,http://www.ncbi.nlm.nih.gov/pubmed/22238404,http://www.ncbi.nlm.nih.gov/pubmed/21933675,http://www.ncbi.nlm.nih.gov/pubmed/21633823,http://www.ncbi.nlm.nih.gov/pubmed/11668059,http://www.ncbi.nlm.nih.gov/pubmed/19119983,http://www.ncbi.nlm.nih.gov/pubmed/19108789,http://www.ncbi.nlm.nih.gov/pubmed/22374714,http://www.ncbi.nlm.nih.gov/pubmed/20012189,http://www.ncbi.nlm.nih.gov/pubmed/21748540,http://www.ncbi.nlm.nih.gov/pubmed/21468525,http://www.ncbi.nlm.nih.gov/pubmed/23154888,http://www.ncbi.nlm.nih.gov/pubmed/15927726,http://www.ncbi.nlm.nih.gov/pubmed/22099156,http://www.ncbi.nlm.nih.gov/pubmed/15301044 | Which drugs may interfere thyroxine absorption? | bile acid sequestrants, ferrous sulphate, sucralfate, calcium carbonate, aluminium-containing antacids, phosphate binders, raloxifene and proton-pump inhibitors, have also been shown to interfere with the absorption of levothyroxine
sevelamer hydrochloride or chromium picolinate should be advised to separate the time of ingestion of these drugs from their thyroid hormone preparation by several hours |
http://www.ncbi.nlm.nih.gov/pubmed/24310308,http://www.ncbi.nlm.nih.gov/pubmed/9505220,http://www.ncbi.nlm.nih.gov/pubmed/2165772,http://www.ncbi.nlm.nih.gov/pubmed/20657316,http://www.ncbi.nlm.nih.gov/pubmed/10921328,http://www.ncbi.nlm.nih.gov/pubmed/8127448,http://www.ncbi.nlm.nih.gov/pubmed/11339660,http://www.ncbi.nlm.nih.gov/pubmed/3032534,http://www.ncbi.nlm.nih.gov/pubmed/8025896,http://www.ncbi.nlm.nih.gov/pubmed/16000562,http://www.ncbi.nlm.nih.gov/pubmed/11907360,http://www.ncbi.nlm.nih.gov/pubmed/22676959,http://www.ncbi.nlm.nih.gov/pubmed/2540108,http://www.ncbi.nlm.nih.gov/pubmed/16144131,http://www.ncbi.nlm.nih.gov/pubmed/19822006,http://www.ncbi.nlm.nih.gov/pubmed/16960645,http://www.ncbi.nlm.nih.gov/pubmed/11975096,http://www.ncbi.nlm.nih.gov/pubmed/9343324,http://www.ncbi.nlm.nih.gov/pubmed/15701281,http://www.ncbi.nlm.nih.gov/pubmed/6307612,http://www.ncbi.nlm.nih.gov/pubmed/23119205,http://www.ncbi.nlm.nih.gov/pubmed/8387650,http://www.ncbi.nlm.nih.gov/pubmed/9695069,http://www.ncbi.nlm.nih.gov/pubmed/17138070,http://www.ncbi.nlm.nih.gov/pubmed/23320220,http://www.ncbi.nlm.nih.gov/pubmed/19156169,http://www.ncbi.nlm.nih.gov/pubmed/7515658,http://www.ncbi.nlm.nih.gov/pubmed/10223463,http://www.ncbi.nlm.nih.gov/pubmed/6274254,http://www.ncbi.nlm.nih.gov/pubmed/23729388,http://www.ncbi.nlm.nih.gov/pubmed/9508118 | Is Turcot syndrome associated with glioblastoma? | Yes, Turcot syndrome is associated with glioblastoma. Turcot syndrome is an autosomal recessive disorder clinically characterized by the occurrence of primary glial tumors of the central nervous system, including glioblastoma, and adenomatous colonic polyps during the first or second decades of life, with a spectrum of clinical features such as "café-au-lait" spots, axillary freckling, and hyperpigmented spots. |
http://www.ncbi.nlm.nih.gov/pubmed/2967444,http://www.ncbi.nlm.nih.gov/pubmed/14648242,http://www.ncbi.nlm.nih.gov/pubmed/8411703,http://www.ncbi.nlm.nih.gov/pubmed/3362213,http://www.ncbi.nlm.nih.gov/pubmed/22441121,http://www.ncbi.nlm.nih.gov/pubmed/20363167,http://www.ncbi.nlm.nih.gov/pubmed/7858168,http://www.ncbi.nlm.nih.gov/pubmed/8490625,http://www.ncbi.nlm.nih.gov/pubmed/3375249,http://www.ncbi.nlm.nih.gov/pubmed/9401008,http://www.ncbi.nlm.nih.gov/pubmed/22723944 | Which is the gene most commonly mutated in Tay-Sachs disease? | HEXA gene, encoding the alpha-subunit of the lysosomal enzyme, beta-N-acetylhexosaminidase A |
http://www.ncbi.nlm.nih.gov/pubmed/10913608,http://www.ncbi.nlm.nih.gov/pubmed/8702928,http://www.ncbi.nlm.nih.gov/pubmed/9049316,http://www.ncbi.nlm.nih.gov/pubmed/17630776,http://www.ncbi.nlm.nih.gov/pubmed/2665605,http://www.ncbi.nlm.nih.gov/pubmed/12145219,http://www.ncbi.nlm.nih.gov/pubmed/10811888,http://www.ncbi.nlm.nih.gov/pubmed/8969181,http://www.ncbi.nlm.nih.gov/pubmed/11101153,http://www.ncbi.nlm.nih.gov/pubmed/22749141,http://www.ncbi.nlm.nih.gov/pubmed/11551204,http://www.ncbi.nlm.nih.gov/pubmed/9049317,http://www.ncbi.nlm.nih.gov/pubmed/20227373 | In which types of DNA repair is the UvrAB complex involved? | UvrB and the lesion-recognition factor UvrA form the UvrAB complex, which plays a key role in bacterial nucleotide excision repair (NER). In transcription-coupled repair (TCR), the transcription repair coupling factor Mfd recruits uvrA, and the assembled UvrAB complex initiates repair. UvrAB complex also suppresses illegitimate recombination. |
http://www.ncbi.nlm.nih.gov/pubmed/17624330 | What is the localization of the protein encoded by the gene DNAJC11? | mitochondrial inner membrane |
http://www.ncbi.nlm.nih.gov/pubmed/24077098,http://www.ncbi.nlm.nih.gov/pubmed/23279377,http://www.ncbi.nlm.nih.gov/pubmed/18556468,http://www.ncbi.nlm.nih.gov/pubmed/19333131,http://www.ncbi.nlm.nih.gov/pubmed/19919992,http://www.ncbi.nlm.nih.gov/pubmed/23781262,http://www.ncbi.nlm.nih.gov/pubmed/22453965,http://www.ncbi.nlm.nih.gov/pubmed/22578240,http://www.ncbi.nlm.nih.gov/pubmed/21174213,http://www.ncbi.nlm.nih.gov/pubmed/16610345,http://www.ncbi.nlm.nih.gov/pubmed/19482609,http://www.ncbi.nlm.nih.gov/pubmed/22514276,http://www.ncbi.nlm.nih.gov/pubmed/23862619,http://www.ncbi.nlm.nih.gov/pubmed/21742790,http://www.ncbi.nlm.nih.gov/pubmed/17704163,http://www.ncbi.nlm.nih.gov/pubmed/21276796,http://www.ncbi.nlm.nih.gov/pubmed/22009705,http://www.ncbi.nlm.nih.gov/pubmed/23613689,http://www.ncbi.nlm.nih.gov/pubmed/20194790,http://www.ncbi.nlm.nih.gov/pubmed/23789646,http://www.ncbi.nlm.nih.gov/pubmed/23159442,http://www.ncbi.nlm.nih.gov/pubmed/17124532,http://www.ncbi.nlm.nih.gov/pubmed/21098440,http://www.ncbi.nlm.nih.gov/pubmed/23877259 | Is Calcium/Calmodulin dependent protein kinase II (CaMKII) involved in cardiac arrhythmias and heart failure? | Calcium/calmodulin-dependent kinase II (CaMKII) is a multifunctional serine/threonine kinase expressed abundantly in the heart. CaMKII targets numerous proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to heart failure and cardiac arrhythmias. Calcium/calmodulin-dependent kinase II (CaMKII) is a multifunctional serine/threonine kinase expressed abundantly in the heart. CaMKII targets numerous proteins involved in excitation-contraction coupling and excitability, and its activation may simultaneously contribute to heart failure and cardiac arrhythmias.Overexpression of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in transgenic mice results in heart failure and arrhythmias.The Ca-calmodulin dependent kinase II (CaMKII) seems to be involved in the development of heart failure and arrhythmias and may therefore be a promising target for the development of antiarrhythmic therapies. |
http://www.ncbi.nlm.nih.gov/pubmed/22687168,http://www.ncbi.nlm.nih.gov/pubmed/21803799,http://www.ncbi.nlm.nih.gov/pubmed/21856578,http://www.ncbi.nlm.nih.gov/pubmed/22088659,http://www.ncbi.nlm.nih.gov/pubmed/21679067,http://www.ncbi.nlm.nih.gov/pubmed/21687341,http://www.ncbi.nlm.nih.gov/pubmed/21838669,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/21755134,http://www.ncbi.nlm.nih.gov/pubmed/23523158,http://www.ncbi.nlm.nih.gov/pubmed/21839654,http://www.ncbi.nlm.nih.gov/pubmed/22648477,http://www.ncbi.nlm.nih.gov/pubmed/21136256,http://www.ncbi.nlm.nih.gov/pubmed/21808631,http://www.ncbi.nlm.nih.gov/pubmed/23034121,http://www.ncbi.nlm.nih.gov/pubmed/20373339,http://www.ncbi.nlm.nih.gov/pubmed/22951366,http://www.ncbi.nlm.nih.gov/pubmed/21107001,http://www.ncbi.nlm.nih.gov/pubmed/23380649,http://www.ncbi.nlm.nih.gov/pubmed/23354606,http://www.ncbi.nlm.nih.gov/pubmed/19958985,http://www.ncbi.nlm.nih.gov/pubmed/23402260,http://www.ncbi.nlm.nih.gov/pubmed/21876515,http://www.ncbi.nlm.nih.gov/pubmed/22155803,http://www.ncbi.nlm.nih.gov/pubmed/23301864 | What is the lay name of the treatment for CCSVI (chronic cerebro-spinal venous insufficiency) in multiple sclerosis. | The so-called "LIberation therapy" is in fact Endovascular Treatment and consists of PTA (Percutaneous Transluminal Angioplasty), which is dilatation of the internal jugular and/or azygous veins by a catheter venography. Stent placement is optional but has been strongly advised against as being dangerous. |
http://www.ncbi.nlm.nih.gov/pubmed/15279074,http://www.ncbi.nlm.nih.gov/pubmed/20298745,http://www.ncbi.nlm.nih.gov/pubmed/15355436,http://www.ncbi.nlm.nih.gov/pubmed/17697873,http://www.ncbi.nlm.nih.gov/pubmed/7492068,http://www.ncbi.nlm.nih.gov/pubmed/16263499,http://www.ncbi.nlm.nih.gov/pubmed/15807875,http://www.ncbi.nlm.nih.gov/pubmed/21511235,http://www.ncbi.nlm.nih.gov/pubmed/18692402,http://www.ncbi.nlm.nih.gov/pubmed/19205523,http://www.ncbi.nlm.nih.gov/pubmed/15863666,http://www.ncbi.nlm.nih.gov/pubmed/17322586,http://www.ncbi.nlm.nih.gov/pubmed/7852510,http://www.ncbi.nlm.nih.gov/pubmed/20822748,http://www.ncbi.nlm.nih.gov/pubmed/1159063,http://www.ncbi.nlm.nih.gov/pubmed/22116361,http://www.ncbi.nlm.nih.gov/pubmed/11375792,http://www.ncbi.nlm.nih.gov/pubmed/10571950,http://www.ncbi.nlm.nih.gov/pubmed/21745434,http://www.ncbi.nlm.nih.gov/pubmed/22109890,http://www.ncbi.nlm.nih.gov/pubmed/17365057,http://www.ncbi.nlm.nih.gov/pubmed/19196800,http://www.ncbi.nlm.nih.gov/pubmed/18538122,http://www.ncbi.nlm.nih.gov/pubmed/10637573,http://www.ncbi.nlm.nih.gov/pubmed/17120770,http://www.ncbi.nlm.nih.gov/pubmed/19692489,http://www.ncbi.nlm.nih.gov/pubmed/9618167,http://www.ncbi.nlm.nih.gov/pubmed/10650967,http://www.ncbi.nlm.nih.gov/pubmed/8706311,http://www.ncbi.nlm.nih.gov/pubmed/19318451,http://www.ncbi.nlm.nih.gov/pubmed/10700480,http://www.ncbi.nlm.nih.gov/pubmed/23235354,http://www.ncbi.nlm.nih.gov/pubmed/20834201,http://www.ncbi.nlm.nih.gov/pubmed/19189692,http://www.ncbi.nlm.nih.gov/pubmed/8630497,http://www.ncbi.nlm.nih.gov/pubmed/20583162,http://www.ncbi.nlm.nih.gov/pubmed/20501687 | Which hormone abnormalities are characteristic to Pendred syndrome? | Thyroid hormone abnormalities are characteristic to Pendred syndrome. Hypothyroidism is the most common thyroid hormone abnormality in Pendred syndrome. Pendred syndrome is an autosomal recessive disorder characterized by sensorineural deafness, goiter and a partial defect in iodide organification. |
http://www.ncbi.nlm.nih.gov/pubmed/10593671,http://www.ncbi.nlm.nih.gov/pubmed/23400408,http://www.ncbi.nlm.nih.gov/pubmed/9341873,http://www.ncbi.nlm.nih.gov/pubmed/12132284,http://www.ncbi.nlm.nih.gov/pubmed/11140949,http://www.ncbi.nlm.nih.gov/pubmed/10077519,http://www.ncbi.nlm.nih.gov/pubmed/1917338,http://www.ncbi.nlm.nih.gov/pubmed/10704188,http://www.ncbi.nlm.nih.gov/pubmed/15950200,http://www.ncbi.nlm.nih.gov/pubmed/23392653,http://www.ncbi.nlm.nih.gov/pubmed/7721491,http://www.ncbi.nlm.nih.gov/pubmed/18595190,http://www.ncbi.nlm.nih.gov/pubmed/11140992,http://www.ncbi.nlm.nih.gov/pubmed/9302275,http://www.ncbi.nlm.nih.gov/pubmed/10654932,http://www.ncbi.nlm.nih.gov/pubmed/1721555,http://www.ncbi.nlm.nih.gov/pubmed/12051962 | What is the mode of inheritance of long QT Jervell and Lange-Nielsen syndrome? | Jervell and Lange-Nielsen long QT syndrome (JLNS) is characterized by autosomal recessive mode of inheritance |
http://www.ncbi.nlm.nih.gov/pubmed/23198780,http://www.ncbi.nlm.nih.gov/pubmed/23436713,http://www.ncbi.nlm.nih.gov/pubmed/23862697,http://www.ncbi.nlm.nih.gov/pubmed/23633577,http://www.ncbi.nlm.nih.gov/pubmed/23812908,http://www.ncbi.nlm.nih.gov/pubmed/23351099,http://www.ncbi.nlm.nih.gov/pubmed/17444519,http://www.ncbi.nlm.nih.gov/pubmed/23451944,http://www.ncbi.nlm.nih.gov/pubmed/16933295,http://www.ncbi.nlm.nih.gov/pubmed/23712937,http://www.ncbi.nlm.nih.gov/pubmed/23836482,http://www.ncbi.nlm.nih.gov/pubmed/24108416,http://www.ncbi.nlm.nih.gov/pubmed/23808933,http://www.ncbi.nlm.nih.gov/pubmed/24050689,http://www.ncbi.nlm.nih.gov/pubmed/15215358,http://www.ncbi.nlm.nih.gov/pubmed/24063890,http://www.ncbi.nlm.nih.gov/pubmed/24187131,http://www.ncbi.nlm.nih.gov/pubmed/23775700,http://www.ncbi.nlm.nih.gov/pubmed/23873600,http://www.ncbi.nlm.nih.gov/pubmed/23818491,http://www.ncbi.nlm.nih.gov/pubmed/23647909,http://www.ncbi.nlm.nih.gov/pubmed/23813626,http://www.ncbi.nlm.nih.gov/pubmed/23590204,http://www.ncbi.nlm.nih.gov/pubmed/24123140,http://www.ncbi.nlm.nih.gov/pubmed/11841293,http://www.ncbi.nlm.nih.gov/pubmed/24266324,http://www.ncbi.nlm.nih.gov/pubmed/23829357 | List programs suitable for protein docking | Macromolecular docking is the computational modelling of the quaternary structure of complexes formed by two or more interacting biological macromolecules. Protein–protein complexes are the most commonly attempted targets of such modelling, followed by protein–nucleic acid complexes.
The ultimate goal of docking is the prediction of the three-dimensional structure of the macromolecular complex of interest as it would occur in a living organism. Docking itself only produces plausible candidate structures. These candidates must be ranked using methods such as scoring functions to identify structures that are most likely to occur in nature.
Nowadays there a lot of programs suitable for proteins docking such as CSBB-ConeExclusion, HADDOCK, ZDOCK, GalaxyDock, PHASE, DockRank, HotLig, SOL, AutodockVina, DockoMatic, DockoMatic, DockTrina, CAVITY, LiGenDock and DOCK. |
http://www.ncbi.nlm.nih.gov/pubmed/23861251,http://www.ncbi.nlm.nih.gov/pubmed/24325358,http://www.ncbi.nlm.nih.gov/pubmed/17209061,http://www.ncbi.nlm.nih.gov/pubmed/21765411,http://www.ncbi.nlm.nih.gov/pubmed/21765413,http://www.ncbi.nlm.nih.gov/pubmed/21765412,http://www.ncbi.nlm.nih.gov/pubmed/23100277 | Which genes have been found mutated in Gray platelet syndrome patients? | The genetic defects responsible for gray platelet syndrome are mutations in the genes NBEAL2, GATA1 and GFI1B.The genetic defect responsible for gray platelet syndrome was recently identified in biallelic mutations in the NBEAL2 gene.
A nonsense mutation in the gene encoding the transcription factor GFI1B (growth factor independent 1B) that causes autosomal dominant gray platelet syndrome.
X-linked gray platelet syndrome due to a GATA1 Arg216Gln mutation. |
http://www.ncbi.nlm.nih.gov/pubmed/19066329,http://www.ncbi.nlm.nih.gov/pubmed/18395492,http://www.ncbi.nlm.nih.gov/pubmed/17962511,http://www.ncbi.nlm.nih.gov/pubmed/19056158,http://www.ncbi.nlm.nih.gov/pubmed/18619726,http://www.ncbi.nlm.nih.gov/pubmed/19016717,http://www.ncbi.nlm.nih.gov/pubmed/18413841 | Does dasatinib promote or inhibit T-cell proliferation? | Dasatinib inhibits T-cell proliferation |
http://www.ncbi.nlm.nih.gov/pubmed/21643016,http://www.ncbi.nlm.nih.gov/pubmed/14767561,http://www.ncbi.nlm.nih.gov/pubmed/22169974,http://www.ncbi.nlm.nih.gov/pubmed/21965329,http://www.ncbi.nlm.nih.gov/pubmed/24276238,http://www.ncbi.nlm.nih.gov/pubmed/19041750,http://www.ncbi.nlm.nih.gov/pubmed/18641685,http://www.ncbi.nlm.nih.gov/pubmed/23730214,http://www.ncbi.nlm.nih.gov/pubmed/21549346 | Does SCRIB deregulation promote cancer? | Yes, deregulation of scribble promotes cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/22375189,http://www.ncbi.nlm.nih.gov/pubmed/21567995,http://www.ncbi.nlm.nih.gov/pubmed/22375228,http://www.ncbi.nlm.nih.gov/pubmed/22653640,http://www.ncbi.nlm.nih.gov/pubmed/19734502,http://www.ncbi.nlm.nih.gov/pubmed/20599016,http://www.ncbi.nlm.nih.gov/pubmed/16831826,http://www.ncbi.nlm.nih.gov/pubmed/20048491,http://www.ncbi.nlm.nih.gov/pubmed/10663764,http://www.ncbi.nlm.nih.gov/pubmed/19055989,http://www.ncbi.nlm.nih.gov/pubmed/24029371,http://www.ncbi.nlm.nih.gov/pubmed/21118665,http://www.ncbi.nlm.nih.gov/pubmed/20705486,http://www.ncbi.nlm.nih.gov/pubmed/15689345,http://www.ncbi.nlm.nih.gov/pubmed/21791458,http://www.ncbi.nlm.nih.gov/pubmed/22983606,http://www.ncbi.nlm.nih.gov/pubmed/22853772,http://www.ncbi.nlm.nih.gov/pubmed/16004915,http://www.ncbi.nlm.nih.gov/pubmed/15166900,http://www.ncbi.nlm.nih.gov/pubmed/12446071,http://www.ncbi.nlm.nih.gov/pubmed/18325444,http://www.ncbi.nlm.nih.gov/pubmed/23897528,http://www.ncbi.nlm.nih.gov/pubmed/21278396,http://www.ncbi.nlm.nih.gov/pubmed/20833588,http://www.ncbi.nlm.nih.gov/pubmed/16914373,http://www.ncbi.nlm.nih.gov/pubmed/18208827,http://www.ncbi.nlm.nih.gov/pubmed/21782775,http://www.ncbi.nlm.nih.gov/pubmed/23097483,http://www.ncbi.nlm.nih.gov/pubmed/21486912,http://www.ncbi.nlm.nih.gov/pubmed/22457200 | Is cardiac magnetic resonance imaging indicated in the pre-participation screening of athletes? | Currently cardiac magnetic resonance imaging is not indicated in the pre-participation screening of athletes. However the potential of this imaging technique to provide new information on cardiac function morphology and myocardial composition, in particular with regard to myocardial fibrosis, gets it potentially suitable to be applied in the pre-participation screening of athletes |
http://www.ncbi.nlm.nih.gov/pubmed/20676553,http://www.ncbi.nlm.nih.gov/pubmed/19110398,http://www.ncbi.nlm.nih.gov/pubmed/22593820,http://www.ncbi.nlm.nih.gov/pubmed/16403813,http://www.ncbi.nlm.nih.gov/pubmed/22460758,http://www.ncbi.nlm.nih.gov/pubmed/16566359,http://www.ncbi.nlm.nih.gov/pubmed/21938530,http://www.ncbi.nlm.nih.gov/pubmed/17554495,http://www.ncbi.nlm.nih.gov/pubmed/22035758,http://www.ncbi.nlm.nih.gov/pubmed/22831984,http://www.ncbi.nlm.nih.gov/pubmed/22487918,http://www.ncbi.nlm.nih.gov/pubmed/15966213,http://www.ncbi.nlm.nih.gov/pubmed/20442314,http://www.ncbi.nlm.nih.gov/pubmed/21073206,http://www.ncbi.nlm.nih.gov/pubmed/22484890,http://www.ncbi.nlm.nih.gov/pubmed/20726677,http://www.ncbi.nlm.nih.gov/pubmed/20407930,http://www.ncbi.nlm.nih.gov/pubmed/21607924,http://www.ncbi.nlm.nih.gov/pubmed/23394826,http://www.ncbi.nlm.nih.gov/pubmed/18506179,http://www.ncbi.nlm.nih.gov/pubmed/22110503,http://www.ncbi.nlm.nih.gov/pubmed/21087500,http://www.ncbi.nlm.nih.gov/pubmed/22678007,http://www.ncbi.nlm.nih.gov/pubmed/19628568,http://www.ncbi.nlm.nih.gov/pubmed/22135725 | Is imatinib an antidepressant drug? | No. Imatinib is a tyrosine-kinase inhibitor used in the treatment of multiple cancers, most notably Chronic myelogenous leukemia (CML) and Gastrointestinal stromal tumor (GIST). |
http://www.ncbi.nlm.nih.gov/pubmed/17071637,http://www.ncbi.nlm.nih.gov/pubmed/17207658,http://www.ncbi.nlm.nih.gov/pubmed/23468525,http://www.ncbi.nlm.nih.gov/pubmed/16621731,http://www.ncbi.nlm.nih.gov/pubmed/21787772,http://www.ncbi.nlm.nih.gov/pubmed/22556419,http://www.ncbi.nlm.nih.gov/pubmed/24277933,http://www.ncbi.nlm.nih.gov/pubmed/22790201,http://www.ncbi.nlm.nih.gov/pubmed/20144704,http://www.ncbi.nlm.nih.gov/pubmed/16716086,http://www.ncbi.nlm.nih.gov/pubmed/21195604,http://www.ncbi.nlm.nih.gov/pubmed/23295485,http://www.ncbi.nlm.nih.gov/pubmed/22757673,http://www.ncbi.nlm.nih.gov/pubmed/20542142,http://www.ncbi.nlm.nih.gov/pubmed/17425590,http://www.ncbi.nlm.nih.gov/pubmed/16607562,http://www.ncbi.nlm.nih.gov/pubmed/21389046,http://www.ncbi.nlm.nih.gov/pubmed/17917452 | What is the function of the MTH1 enzyme in cancer cells? | The MTH1 protein catalyzes hydrolysis of oxidatively damaged purine nucleotides including 8-hydroxy-dGTP to the monophosphates. The MTH1 protein seems to act as an important defense system against mutagenesis, carcinogenesis, and cell death induced by oxidized purine nucleotides. |
http://www.ncbi.nlm.nih.gov/pubmed/16998490,http://www.ncbi.nlm.nih.gov/pubmed/18957701,http://www.ncbi.nlm.nih.gov/pubmed/18174240,http://www.ncbi.nlm.nih.gov/pubmed/25340765,http://www.ncbi.nlm.nih.gov/pubmed/21092253 | Are ultraconserved elements depleted among copy number variants (CNVs)? | Yes. Interestingly, human ultraconserved elements (UCEs) have been reported to be strongly depleted among segmental duplications and benign copy number variants (CNVs). These elements may be interpreted as hallmarks for dose-sensitive genes, particularly for those genes whose gain or loss may be directly implied in neurodevelopmental disorders. Therefore, their presence in genomic imbalances of unknown effect might be suggestive of a clinically relevant condition |
http://www.ncbi.nlm.nih.gov/pubmed/19458943,http://www.ncbi.nlm.nih.gov/pubmed/21813326,http://www.ncbi.nlm.nih.gov/pubmed/22315408,http://www.ncbi.nlm.nih.gov/pubmed/21945804,http://www.ncbi.nlm.nih.gov/pubmed/23001356,http://www.ncbi.nlm.nih.gov/pubmed/19557767,http://www.ncbi.nlm.nih.gov/pubmed/21807765,http://www.ncbi.nlm.nih.gov/pubmed/21035445,http://www.ncbi.nlm.nih.gov/pubmed/20010955,http://www.ncbi.nlm.nih.gov/pubmed/23144617,http://www.ncbi.nlm.nih.gov/pubmed/21136867,http://www.ncbi.nlm.nih.gov/pubmed/17314675 | Is the microRNA 132 (miR-132) involved in brain pathologies? | Yes. MicroRNA 132 (miR-132), is involved in brain pathologies. |
http://www.ncbi.nlm.nih.gov/pubmed/22955980,http://www.ncbi.nlm.nih.gov/pubmed/22829947,http://www.ncbi.nlm.nih.gov/pubmed/15229244,http://www.ncbi.nlm.nih.gov/pubmed/15670593,http://www.ncbi.nlm.nih.gov/pubmed/8034708,http://www.ncbi.nlm.nih.gov/pubmed/11854173,http://www.ncbi.nlm.nih.gov/pubmed/23707059,http://www.ncbi.nlm.nih.gov/pubmed/11076856,http://www.ncbi.nlm.nih.gov/pubmed/22709888 | What is an approximate number of CTCF binding sites in the human genome? | The number of CTCF binding sites in the human genome lies between 31,000 and 50,000. |
http://www.ncbi.nlm.nih.gov/pubmed/21264099,http://www.ncbi.nlm.nih.gov/pubmed/937227,http://www.ncbi.nlm.nih.gov/pubmed/2620957,http://www.ncbi.nlm.nih.gov/pubmed/19854256,http://www.ncbi.nlm.nih.gov/pubmed/11451723,http://www.ncbi.nlm.nih.gov/pubmed/17650589,http://www.ncbi.nlm.nih.gov/pubmed/20614191,http://www.ncbi.nlm.nih.gov/pubmed/22419465,http://www.ncbi.nlm.nih.gov/pubmed/22416705,http://www.ncbi.nlm.nih.gov/pubmed/8569244,http://www.ncbi.nlm.nih.gov/pubmed/19276533,http://www.ncbi.nlm.nih.gov/pubmed/22897583,http://www.ncbi.nlm.nih.gov/pubmed/16179750 | Does cucumber lower blood sugar in diabetics? | Yes. Based on several scientific reports, ethanolic extract of cucumber and some other Cucurbitaceae plants are associated with a significant reduction of elevated blood glucose level, suggesting that cucumber could have antidiabetic activity. |
http://www.ncbi.nlm.nih.gov/pubmed/23498838,http://www.ncbi.nlm.nih.gov/pubmed/21659649,http://www.ncbi.nlm.nih.gov/pubmed/12919952,http://www.ncbi.nlm.nih.gov/pubmed/15890976,http://www.ncbi.nlm.nih.gov/pubmed/23152493,http://www.ncbi.nlm.nih.gov/pubmed/18483626,http://www.ncbi.nlm.nih.gov/pubmed/22828895,http://www.ncbi.nlm.nih.gov/pubmed/14571276,http://www.ncbi.nlm.nih.gov/pubmed/20676041,http://www.ncbi.nlm.nih.gov/pubmed/23746327 | Which mutations in the cardiac isoform of the ryanodine receptor (RyR2) have been found to be related to CPVT? | Recently, a novel CPVT RyR2 mutation, G230C, was found to increase the cytosolic, but not the luminal, Ca2+ sensitivity of single RyR2 channels in lipid bilayers. The novel RYR2-S4153R mutation has been implicated as a cause of CPVT and atrial fibrillation. A novel RyR2-V2475F mutation is associated with CPVT in humans. 3 CPVT mouse models are: RyR2-R2474S+/-, RyR2-N2386I+/-, and RyR2-L433P+/-. The E189D RyR2 mutation is causative for CPVT. A knock-in mouse model carrier of the R4496C mutation is the mouse equivalent to the R4497C mutations identified in CPVT families. Scanning of 12 Finnish CPVT probands identified three novel RYR2 mutations (V2306I, P4902L, R4959Q), which were absent in unaffected and control individuals. Three CPVT-linked human RyR2 (hRyR2) mutations are: S2246L, N4104K, and R4497C. |
http://www.ncbi.nlm.nih.gov/pubmed/16415921,http://www.ncbi.nlm.nih.gov/pubmed/21424386,http://www.ncbi.nlm.nih.gov/pubmed/15057820,http://www.ncbi.nlm.nih.gov/pubmed/19915237,http://www.ncbi.nlm.nih.gov/pubmed/19694795,http://www.ncbi.nlm.nih.gov/pubmed/21306565,http://www.ncbi.nlm.nih.gov/pubmed/20345939,http://www.ncbi.nlm.nih.gov/pubmed/18637831,http://www.ncbi.nlm.nih.gov/pubmed/21169036,http://www.ncbi.nlm.nih.gov/pubmed/18855540,http://www.ncbi.nlm.nih.gov/pubmed/22211527 | Which population has a high frequency of the HLA-B*1502 allele? | HLA-B*1502 has a high frequency in Han Chinese and other Asian populations, except Japanese. (There is a strong association between human leucocyte antigen (HLA)-B*1502 and carbamazepine-induced Stevens-Johnson syndrome (SJS)). |
http://www.ncbi.nlm.nih.gov/pubmed/23571757,http://www.ncbi.nlm.nih.gov/pubmed/15319283,http://www.ncbi.nlm.nih.gov/pubmed/11591364,http://www.ncbi.nlm.nih.gov/pubmed/11854176,http://www.ncbi.nlm.nih.gov/pubmed/19129235 | What are the observations regarding telomere integrity and function in Fanconi anemia? | In Fanconi anemia patients, a higher rate of breakage at TTAGGG sequences in vivo is causing telomere erosion in differentiated cells. Moreover, it has been demonstrated that αIISp is important for telomere maintenance after DNA damage due to interstrand cross-links (ICL), localizing to telomeres in S phase after ICL damage where it has enhanced association with TRF1 and TRF2 and is required for recruitment of the ICL repair protein, XPF, to damage-induced foci at telomeres. In telomerase-positive normal cells depleted of αIISp by siRNA or in Fanconi anemia, complementation group A (FANCA) cells, where αIISp levels are 35-40% of normal, ICL damage results in failure of XPF to localize to telomeres, with markedly increased telomere dysfunction-induced foci, and catastrophic loss of telomeres.A higher frequency of extra-chromosomic TTAGGG signals and of chromosome ends with undetectable TTAGGG repeats was observed in FA cells by fluorescence in situ hybridization (FISH), suggesting intensive breakage at telomeric sequences. This was proven by measuring the frequency of excess of telomeric signals per cell, which was 2.8-fold higher in FAWe now demonstrate that αIISp is also important for telomere maintenance after ICL damage. It localizes to telomeres in S phase after ICL damage where it has enhanced association with TRF1 and TRF2 and is required for recruitment of the ICL repair protein, XPF, to damage-induced foci at telomeres. In telomerase-positive normal cells depleted of αIISp by siRNA or in Fanconi anemia, complementation group A (FA-A) cells, where αIISp levels are 35-40% of normal, ICL damage results in failure of XPF to localize to telomeres, markedly increased telomere dysfunction-induced foci, followed by catastrophic loss of telomeres |
http://www.ncbi.nlm.nih.gov/pubmed/21302811,http://www.ncbi.nlm.nih.gov/pubmed/24301524,http://www.ncbi.nlm.nih.gov/pubmed/24252593,http://www.ncbi.nlm.nih.gov/pubmed/18056171,http://www.ncbi.nlm.nih.gov/pubmed/23033986,http://www.ncbi.nlm.nih.gov/pubmed/23730497,http://www.ncbi.nlm.nih.gov/pubmed/24401270,http://www.ncbi.nlm.nih.gov/pubmed/24140475,http://www.ncbi.nlm.nih.gov/pubmed/21463127,http://www.ncbi.nlm.nih.gov/pubmed/20008221,http://www.ncbi.nlm.nih.gov/pubmed/17575125,http://www.ncbi.nlm.nih.gov/pubmed/20015880,http://www.ncbi.nlm.nih.gov/pubmed/16707600,http://www.ncbi.nlm.nih.gov/pubmed/24068942,http://www.ncbi.nlm.nih.gov/pubmed/25493453,http://www.ncbi.nlm.nih.gov/pubmed/18184405,http://www.ncbi.nlm.nih.gov/pubmed/20967796,http://www.ncbi.nlm.nih.gov/pubmed/21263446,http://www.ncbi.nlm.nih.gov/pubmed/23022380 | Are Notch mutations related to T-cell Acute Lymphoblastic Leukemia (T-ALL)? | Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL). Activating mutations in NOTCH1, an essential regulator of T cell development, are frequently found in human T cell acute lymphoblastic leukemia (T-ALL). Yes, Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL).T-cell acute lymphoblastic leukemia/lymphoma (T-ALL) is characterized by aberrant activation of NOTCH1 in over 60% of T-ALL cases. |
http://www.ncbi.nlm.nih.gov/pubmed/17333538,http://www.ncbi.nlm.nih.gov/pubmed/16648248,http://www.ncbi.nlm.nih.gov/pubmed/19013827,http://www.ncbi.nlm.nih.gov/pubmed/21826206,http://www.ncbi.nlm.nih.gov/pubmed/12023758 | What is the role of the Tsix gene during X chromosome inactivation? | One of the two X chromosomes in female mammalian cells is subject to inactivation (XCI) initiated by the Xist gene. Xist works as a functional RNA molecule that recruits repressive chromatin factors towards one of the female Xs for inactivation. The Tsix gene, antisense of Xist, through transcription negatively regulates Xist and protects one X-chromosome in cis from inactivation by Xist. Although, the precise molecular mechanism is still unclear it has been shown that Tsix transcription regulates the chromatin structure by altering histone tail modifications and DNA methylation at the Xist promoter. In addition, Xist and Tsix RNAs form duplexes in vivo and are processed to small RNAs, which have a potential regulatory function. |
http://www.ncbi.nlm.nih.gov/pubmed/24058594,http://www.ncbi.nlm.nih.gov/pubmed/23970932,http://www.ncbi.nlm.nih.gov/pubmed/24157923,http://www.ncbi.nlm.nih.gov/pubmed/24311785,http://www.ncbi.nlm.nih.gov/pubmed/24217647,http://www.ncbi.nlm.nih.gov/pubmed/24121272,http://www.ncbi.nlm.nih.gov/pubmed/23817042,http://www.ncbi.nlm.nih.gov/pubmed/24006257,http://www.ncbi.nlm.nih.gov/pubmed/24091658,http://www.ncbi.nlm.nih.gov/pubmed/24164869,http://www.ncbi.nlm.nih.gov/pubmed/24115647,http://www.ncbi.nlm.nih.gov/pubmed/23990393,http://www.ncbi.nlm.nih.gov/pubmed/23906871 | Is the protein FAK (Focal Adhesion Kinase) phosphorylated? | yes, the protein FAK (Focal Adhesion Kinase) is phosphorylated. |
http://www.ncbi.nlm.nih.gov/pubmed/20953165,http://www.ncbi.nlm.nih.gov/pubmed/17084365,http://www.ncbi.nlm.nih.gov/pubmed/19918057,http://www.ncbi.nlm.nih.gov/pubmed/23973165,http://www.ncbi.nlm.nih.gov/pubmed/21514157,http://www.ncbi.nlm.nih.gov/pubmed/21447816,http://www.ncbi.nlm.nih.gov/pubmed/20705815,http://www.ncbi.nlm.nih.gov/pubmed/20705812,http://www.ncbi.nlm.nih.gov/pubmed/15846065,http://www.ncbi.nlm.nih.gov/pubmed/21749502,http://www.ncbi.nlm.nih.gov/pubmed/15681610,http://www.ncbi.nlm.nih.gov/pubmed/24184212,http://www.ncbi.nlm.nih.gov/pubmed/21527018,http://www.ncbi.nlm.nih.gov/pubmed/22335895,http://www.ncbi.nlm.nih.gov/pubmed/21804608,http://www.ncbi.nlm.nih.gov/pubmed/21401527,http://www.ncbi.nlm.nih.gov/pubmed/19997740,http://www.ncbi.nlm.nih.gov/pubmed/18978305,http://www.ncbi.nlm.nih.gov/pubmed/23746640,http://www.ncbi.nlm.nih.gov/pubmed/21658950,http://www.ncbi.nlm.nih.gov/pubmed/22732840,http://www.ncbi.nlm.nih.gov/pubmed/23071152,http://www.ncbi.nlm.nih.gov/pubmed/23071153,http://www.ncbi.nlm.nih.gov/pubmed/20929775 | Which is the substrate of the haspin kinase during mitosis? | Haspin phosphorylates histone H3 at Thr3 (H3T3ph) during mitosis |
http://www.ncbi.nlm.nih.gov/pubmed/20458240,http://www.ncbi.nlm.nih.gov/pubmed/3069176,http://www.ncbi.nlm.nih.gov/pubmed/30666,http://www.ncbi.nlm.nih.gov/pubmed/21254868,http://www.ncbi.nlm.nih.gov/pubmed/18989561,http://www.ncbi.nlm.nih.gov/pubmed/9005529,http://www.ncbi.nlm.nih.gov/pubmed/11205659,http://www.ncbi.nlm.nih.gov/pubmed/10981226,http://www.ncbi.nlm.nih.gov/pubmed/12603508,http://www.ncbi.nlm.nih.gov/pubmed/19420815,http://www.ncbi.nlm.nih.gov/pubmed/17667053,http://www.ncbi.nlm.nih.gov/pubmed/6139796,http://www.ncbi.nlm.nih.gov/pubmed/9399771,http://www.ncbi.nlm.nih.gov/pubmed/18469440,http://www.ncbi.nlm.nih.gov/pubmed/21453886,http://www.ncbi.nlm.nih.gov/pubmed/18788068,http://www.ncbi.nlm.nih.gov/pubmed/20919963,http://www.ncbi.nlm.nih.gov/pubmed/21317611,http://www.ncbi.nlm.nih.gov/pubmed/17628557,http://www.ncbi.nlm.nih.gov/pubmed/9097825,http://www.ncbi.nlm.nih.gov/pubmed/7084615 | Which are the most widely reported side-effects in the treatment of Crohn's disease? | Leukopenia, paresthesia, psoriasis, alopecia and hemolysis are the most commonly reported side effects depending on the treatment. Severe adverse effects include myelosuppression, liver toxicity and hyperplasia, pancreatitis and pericarditis. The most severe but rare side-effects reported are progressive multifocal leukoencephalopathy (PML), serious infections, and lymphoma. |
http://www.ncbi.nlm.nih.gov/pubmed/22072984,http://www.ncbi.nlm.nih.gov/pubmed/23799614,http://www.ncbi.nlm.nih.gov/pubmed/15946860,http://www.ncbi.nlm.nih.gov/pubmed/23819581,http://www.ncbi.nlm.nih.gov/pubmed/19633228,http://www.ncbi.nlm.nih.gov/pubmed/23015295,http://www.ncbi.nlm.nih.gov/pubmed/23450047,http://www.ncbi.nlm.nih.gov/pubmed/24147068,http://www.ncbi.nlm.nih.gov/pubmed/23935863,http://www.ncbi.nlm.nih.gov/pubmed/23704925,http://www.ncbi.nlm.nih.gov/pubmed/23694700,http://www.ncbi.nlm.nih.gov/pubmed/22649506,http://www.ncbi.nlm.nih.gov/pubmed/22893128 | Are most driver gene mutations synonymous or non-synonymous? | A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency. A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency. |
http://www.ncbi.nlm.nih.gov/pubmed/21455477,http://www.ncbi.nlm.nih.gov/pubmed/16641100,http://www.ncbi.nlm.nih.gov/pubmed/18785766,http://www.ncbi.nlm.nih.gov/pubmed/21526838,http://www.ncbi.nlm.nih.gov/pubmed/15665377,http://www.ncbi.nlm.nih.gov/pubmed/19241031,http://www.ncbi.nlm.nih.gov/pubmed/22844594,http://www.ncbi.nlm.nih.gov/pubmed/19056867,http://www.ncbi.nlm.nih.gov/pubmed/19504542,http://www.ncbi.nlm.nih.gov/pubmed/23918812,http://www.ncbi.nlm.nih.gov/pubmed/21033674 | What is the advantage of neutral loss detection in phosphoproteomics? | The localization of phosphorylation sites in peptide sequences is a challenging problem in large-scale phosphoproteomics analysis. The intense neutral loss peaks and the coexistence of multiple serine/threonine and/or tyrosine residues are limiting factors for objectively scoring site patterns across thousands of peptides.
CID of phosphopeptides typically results in spectra dominated by a neutral loss of the phosphate group allowing detection and sequencing of phosphopeptides. |
http://www.ncbi.nlm.nih.gov/pubmed/19352052,http://www.ncbi.nlm.nih.gov/pubmed/23576609,http://www.ncbi.nlm.nih.gov/pubmed/22167137,http://www.ncbi.nlm.nih.gov/pubmed/24961317,http://www.ncbi.nlm.nih.gov/pubmed/24768795,http://www.ncbi.nlm.nih.gov/pubmed/20720512,http://www.ncbi.nlm.nih.gov/pubmed/22190447,http://www.ncbi.nlm.nih.gov/pubmed/15613277 | Does ghrelin play a role in ischemic stroke? | Yes. It has been shown that serum ghrelin levels are reduced after ischemic stroke and ghrelin is associated with stroke type. Ghrelin can be a useful marker for the prediction of stoke after cardiopulmonary bypass. Ghrelin may be neuroprotective after injury in animal models of cerebral ischemia by inhibiting apoptotic processes, inflammation, nNOS activity and modulating gastrointestinal motility. |
http://www.ncbi.nlm.nih.gov/pubmed/16712728,http://www.ncbi.nlm.nih.gov/pubmed/8233439,http://www.ncbi.nlm.nih.gov/pubmed/15221438,http://www.ncbi.nlm.nih.gov/pubmed/23878564,http://www.ncbi.nlm.nih.gov/pubmed/16006738,http://www.ncbi.nlm.nih.gov/pubmed/12466121,http://www.ncbi.nlm.nih.gov/pubmed/11453236 | What is the mechanism of drug-induced gingival overgrowth? | Drug-induced gingival overgrowth (GO) is a frequent and adverse side-effect associated principally with the administration of the immunosuppressive drug cyclosporin A (CsA) and also certain anti-epileptic and anti-hypertensive drugs. It is characterized by a marked increase in the thickness of the epithelial layer and the accumulation of excessive amounts of connective tissue. Keratinocyte growth factor (KGF), which is a potent epithelial cell mitogen that has been implicated in other hyperplastic conditions could be involved in the molecular pathology of GO. Also, since cathepsin-L deficiency was reported to be associated with thickening of the skin, impaired cathepsin-L activity may play a key role in the establishment of skin and gingival abnormalities seen in I-cell disease. In addition, reduced cathepsin-L activity may play an important role in inducing drug-induced gingival overgrowth. Furthermore, the enhanced proliferation of gingival fibroblasts observed in this disease could be caused at least partly by the effects of the drugs on the cell cycle and cyclin expression in these cells. The increase in cell growth that occurs in drug-induced gingival overgrowth may be mediated by over-expression of cyclin B1. |
http://www.ncbi.nlm.nih.gov/pubmed/25957290,http://www.ncbi.nlm.nih.gov/pubmed/18406367,http://www.ncbi.nlm.nih.gov/pubmed/26029695,http://www.ncbi.nlm.nih.gov/pubmed/25259707 | Is LPS a microbial product? | Yes, the lipopolysaccharide (LPS) is a component of the bacterial cell wall. |
http://www.ncbi.nlm.nih.gov/pubmed/19390085,http://www.ncbi.nlm.nih.gov/pubmed/17989730,http://www.ncbi.nlm.nih.gov/pubmed/18275833,http://www.ncbi.nlm.nih.gov/pubmed/17102614,http://www.ncbi.nlm.nih.gov/pubmed/17651940,http://www.ncbi.nlm.nih.gov/pubmed/21496667,http://www.ncbi.nlm.nih.gov/pubmed/19321450,http://www.ncbi.nlm.nih.gov/pubmed/9923679,http://www.ncbi.nlm.nih.gov/pubmed/11355949,http://www.ncbi.nlm.nih.gov/pubmed/15892997,http://www.ncbi.nlm.nih.gov/pubmed/20551323,http://www.ncbi.nlm.nih.gov/pubmed/18371338,http://www.ncbi.nlm.nih.gov/pubmed/20661663,http://www.ncbi.nlm.nih.gov/pubmed/21928107,http://www.ncbi.nlm.nih.gov/pubmed/16869752,http://www.ncbi.nlm.nih.gov/pubmed/18346113,http://www.ncbi.nlm.nih.gov/pubmed/16778197,http://www.ncbi.nlm.nih.gov/pubmed/17597110,http://www.ncbi.nlm.nih.gov/pubmed/14982841,http://www.ncbi.nlm.nih.gov/pubmed/15964994,http://www.ncbi.nlm.nih.gov/pubmed/20591222,http://www.ncbi.nlm.nih.gov/pubmed/21164364,http://www.ncbi.nlm.nih.gov/pubmed/17233832,http://www.ncbi.nlm.nih.gov/pubmed/19389366,http://www.ncbi.nlm.nih.gov/pubmed/14536079,http://www.ncbi.nlm.nih.gov/pubmed/14574365,http://www.ncbi.nlm.nih.gov/pubmed/14732230,http://www.ncbi.nlm.nih.gov/pubmed/16537449,http://www.ncbi.nlm.nih.gov/pubmed/17145810,http://www.ncbi.nlm.nih.gov/pubmed/16155021,http://www.ncbi.nlm.nih.gov/pubmed/12482990,http://www.ncbi.nlm.nih.gov/pubmed/12714971,http://www.ncbi.nlm.nih.gov/pubmed/19907431,http://www.ncbi.nlm.nih.gov/pubmed/16157028,http://www.ncbi.nlm.nih.gov/pubmed/18371328 | Which cyclin- dependent kinase inhibitor is regulated by Bmi-1? | p16INK4 (also known as CDKN2A) |
http://www.ncbi.nlm.nih.gov/pubmed/19440340,http://www.ncbi.nlm.nih.gov/pubmed/21690193,http://www.ncbi.nlm.nih.gov/pubmed/23242657,http://www.ncbi.nlm.nih.gov/pubmed/23047984,http://www.ncbi.nlm.nih.gov/pubmed/21311168,http://www.ncbi.nlm.nih.gov/pubmed/20724368 | Which microRNAs are involved in exercise adaptation? | miR-1, miR-133, miR-208a, miR-206, miR-494, miR-146a, miR-222, miR-21, miR-221, miR-20a, miR-133a, miR-133b, miR-23, miR-107 and miR-181 are involved in exercise adaptation |
http://www.ncbi.nlm.nih.gov/pubmed/21724593,http://www.ncbi.nlm.nih.gov/pubmed/17555593,http://www.ncbi.nlm.nih.gov/pubmed/18048180,http://www.ncbi.nlm.nih.gov/pubmed/17946720,http://www.ncbi.nlm.nih.gov/pubmed/22151470,http://www.ncbi.nlm.nih.gov/pubmed/18798993,http://www.ncbi.nlm.nih.gov/pubmed/16342039,http://www.ncbi.nlm.nih.gov/pubmed/15919726,http://www.ncbi.nlm.nih.gov/pubmed/18412963,http://www.ncbi.nlm.nih.gov/pubmed/19273034,http://www.ncbi.nlm.nih.gov/pubmed/19208138,http://www.ncbi.nlm.nih.gov/pubmed/19492068,http://www.ncbi.nlm.nih.gov/pubmed/8481828 | Has field-programmable gate array (FPGA) technology been used to solve sequence alignment problems? | Yes. Field-Programmable Gate Arrays (FPGAs) are reconfigurable computing platforms that have found several applications in diverse domains, including digital signal processing, medical imaging and bioinformatics. Specific applications of FPGAs for biological sequence alignment have been reported for dynamic programming-based pairwise (local or global) sequence alignment, progressive multiple sequence alignment, profile alignment, Burrows-Wheeler transform (BWT) based alignment, heuristic pairwise alignment. |
http://www.ncbi.nlm.nih.gov/pubmed/24968303,http://www.ncbi.nlm.nih.gov/pubmed/20960209,http://www.ncbi.nlm.nih.gov/pubmed/25063991,http://www.ncbi.nlm.nih.gov/pubmed/12952973,http://www.ncbi.nlm.nih.gov/pubmed/20966765,http://www.ncbi.nlm.nih.gov/pubmed/20668412,http://www.ncbi.nlm.nih.gov/pubmed/21542787,http://www.ncbi.nlm.nih.gov/pubmed/25502879,http://www.ncbi.nlm.nih.gov/pubmed/24615518,http://www.ncbi.nlm.nih.gov/pubmed/21294074,http://www.ncbi.nlm.nih.gov/pubmed/20937730,http://www.ncbi.nlm.nih.gov/pubmed/24675465,http://www.ncbi.nlm.nih.gov/pubmed/24627421,http://www.ncbi.nlm.nih.gov/pubmed/15961375,http://www.ncbi.nlm.nih.gov/pubmed/24998301,http://www.ncbi.nlm.nih.gov/pubmed/22732280,http://www.ncbi.nlm.nih.gov/pubmed/22198507,http://www.ncbi.nlm.nih.gov/pubmed/24273204,http://www.ncbi.nlm.nih.gov/pubmed/23536162,http://www.ncbi.nlm.nih.gov/pubmed/25767484,http://www.ncbi.nlm.nih.gov/pubmed/24349464,http://www.ncbi.nlm.nih.gov/pubmed/24951958,http://www.ncbi.nlm.nih.gov/pubmed/22745676,http://www.ncbi.nlm.nih.gov/pubmed/25351957,http://www.ncbi.nlm.nih.gov/pubmed/14627909,http://www.ncbi.nlm.nih.gov/pubmed/21669242,http://www.ncbi.nlm.nih.gov/pubmed/25793558,http://www.ncbi.nlm.nih.gov/pubmed/24657357,http://www.ncbi.nlm.nih.gov/pubmed/21297983,http://www.ncbi.nlm.nih.gov/pubmed/25319443,http://www.ncbi.nlm.nih.gov/pubmed/16516918,http://www.ncbi.nlm.nih.gov/pubmed/21372381,http://www.ncbi.nlm.nih.gov/pubmed/19819119,http://www.ncbi.nlm.nih.gov/pubmed/24885907,http://www.ncbi.nlm.nih.gov/pubmed/22197697,http://www.ncbi.nlm.nih.gov/pubmed/24801220,http://www.ncbi.nlm.nih.gov/pubmed/24297180,http://www.ncbi.nlm.nih.gov/pubmed/24434143,http://www.ncbi.nlm.nih.gov/pubmed/23423267,http://www.ncbi.nlm.nih.gov/pubmed/18660440,http://www.ncbi.nlm.nih.gov/pubmed/10413027 | List inhibtors targeting the mitochondrial permeability transition pore. | Cyclosporine A
Atractyloside
N-metyl-4-isoleucine-cyclosporine
Sanglifehrin A
TRO-19622The opening of the mitochondrial permeability transition pore appears to be inhibited by KB-R 7943, diacylglycerol analog 1-oleoyl-2-acetyl-sn-glycerol, cyclosporin A (CsA) and BRL37344. |
http://www.ncbi.nlm.nih.gov/pubmed/24675041,http://www.ncbi.nlm.nih.gov/pubmed/24891360,http://www.ncbi.nlm.nih.gov/pubmed/25228534,http://www.ncbi.nlm.nih.gov/pubmed/25733882,http://www.ncbi.nlm.nih.gov/pubmed/25458559,http://www.ncbi.nlm.nih.gov/pubmed/25101329,http://www.ncbi.nlm.nih.gov/pubmed/25258279,http://www.ncbi.nlm.nih.gov/pubmed/25170107,http://www.ncbi.nlm.nih.gov/pubmed/24980964,http://www.ncbi.nlm.nih.gov/pubmed/24670165,http://www.ncbi.nlm.nih.gov/pubmed/25381900,http://www.ncbi.nlm.nih.gov/pubmed/26018086,http://www.ncbi.nlm.nih.gov/pubmed/25258420 | What is ceritinib? | Ceritinib is a second generation tyrosine kinase inhibitor, that serves as an effective and approved oral therapy for patients with ALK-rearranged non-small cell lung cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/12393810,http://www.ncbi.nlm.nih.gov/pubmed/24242291,http://www.ncbi.nlm.nih.gov/pubmed/20819074,http://www.ncbi.nlm.nih.gov/pubmed/18206656,http://www.ncbi.nlm.nih.gov/pubmed/12174969,http://www.ncbi.nlm.nih.gov/pubmed/23247094,http://www.ncbi.nlm.nih.gov/pubmed/11823441,http://www.ncbi.nlm.nih.gov/pubmed/25430730,http://www.ncbi.nlm.nih.gov/pubmed/16510442,http://www.ncbi.nlm.nih.gov/pubmed/18463734,http://www.ncbi.nlm.nih.gov/pubmed/12194387,http://www.ncbi.nlm.nih.gov/pubmed/25929520,http://www.ncbi.nlm.nih.gov/pubmed/18537827,http://www.ncbi.nlm.nih.gov/pubmed/12140189,http://www.ncbi.nlm.nih.gov/pubmed/25597503,http://www.ncbi.nlm.nih.gov/pubmed/9700204,http://www.ncbi.nlm.nih.gov/pubmed/16787388,http://www.ncbi.nlm.nih.gov/pubmed/20674094 | Which protein is found to be mutated in Friedreich's ataxia? | It is generally accepted that Friedreich's ataxia (FRDA) is caused by a deficiency in frataxin expression, a mitochondrial protein involved in iron homeostasis, which mainly affects the brain, dorsal root ganglia of the spinal cord, heart and in certain cases the pancreasIt is generally accepted that Friedreich's ataxia (FRDA) is caused by a deficiency in frataxin expression, a mitochondrial protein involved in iron homeostasis, which mainly affects the brain, dorsal root ganglia of the spinal cord, heart and in certain cases the pancreas. |
http://www.ncbi.nlm.nih.gov/pubmed/19492354,http://www.ncbi.nlm.nih.gov/pubmed/18282512,http://www.ncbi.nlm.nih.gov/pubmed/21629789,http://www.ncbi.nlm.nih.gov/pubmed/21731768,http://www.ncbi.nlm.nih.gov/pubmed/17096848,http://www.ncbi.nlm.nih.gov/pubmed/21478460,http://www.ncbi.nlm.nih.gov/pubmed/21175683,http://www.ncbi.nlm.nih.gov/pubmed/18279518,http://www.ncbi.nlm.nih.gov/pubmed/16533910,http://www.ncbi.nlm.nih.gov/pubmed/16630819,http://www.ncbi.nlm.nih.gov/pubmed/18056681,http://www.ncbi.nlm.nih.gov/pubmed/17442748,http://www.ncbi.nlm.nih.gov/pubmed/23042552,http://www.ncbi.nlm.nih.gov/pubmed/19698106,http://www.ncbi.nlm.nih.gov/pubmed/19704032,http://www.ncbi.nlm.nih.gov/pubmed/18334644,http://www.ncbi.nlm.nih.gov/pubmed/19073165 | Which is the process that Conserved noncoding elements mostly regulate? | Conserved noncoding elements play a fundamental role in regulating animal development |
http://www.ncbi.nlm.nih.gov/pubmed/10809724,http://www.ncbi.nlm.nih.gov/pubmed/17768080,http://www.ncbi.nlm.nih.gov/pubmed/9537653,http://www.ncbi.nlm.nih.gov/pubmed/8207801,http://www.ncbi.nlm.nih.gov/pubmed/1331501,http://www.ncbi.nlm.nih.gov/pubmed/9223480,http://www.ncbi.nlm.nih.gov/pubmed/20088881,http://www.ncbi.nlm.nih.gov/pubmed/16249186,http://www.ncbi.nlm.nih.gov/pubmed/8397367,http://www.ncbi.nlm.nih.gov/pubmed/21643539,http://www.ncbi.nlm.nih.gov/pubmed/10698500,http://www.ncbi.nlm.nih.gov/pubmed/17332339,http://www.ncbi.nlm.nih.gov/pubmed/9817205,http://www.ncbi.nlm.nih.gov/pubmed/21980285 | What is the main mechanism by which human papillomavirus proteins E6 and E7 contribute to cell transformation? | Although they may have other targets, human papillomavirus proteins E6 and E7 interact with and block the function of p53 and pRb, respectively, therefore deregulating cell cycle and leading to cellular transformation. |
http://www.ncbi.nlm.nih.gov/pubmed/10640948,http://www.ncbi.nlm.nih.gov/pubmed/10861348,http://www.ncbi.nlm.nih.gov/pubmed/24941044 | List bacterial species identified in the iceman tissues. | Spirochete Treponema denticola
Clostridium perfringens
Clostridium ghonii
Clostridium sordellii
Eubacterium tenue
Bacteroides sp
Vibrio
Sphingomonas
Afipia
Curtobacterium
Microbacterium
Agromyces |
http://www.ncbi.nlm.nih.gov/pubmed/26121403,http://www.ncbi.nlm.nih.gov/pubmed/25412662,http://www.ncbi.nlm.nih.gov/pubmed/19180239,http://www.ncbi.nlm.nih.gov/pubmed/25475057,http://www.ncbi.nlm.nih.gov/pubmed/3029112,http://www.ncbi.nlm.nih.gov/pubmed/9409616,http://www.ncbi.nlm.nih.gov/pubmed/6592581,http://www.ncbi.nlm.nih.gov/pubmed/6318439,http://www.ncbi.nlm.nih.gov/pubmed/22575960,http://www.ncbi.nlm.nih.gov/pubmed/25452335,http://www.ncbi.nlm.nih.gov/pubmed/25569111,http://www.ncbi.nlm.nih.gov/pubmed/24981863,http://www.ncbi.nlm.nih.gov/pubmed/25430002 | Which properties of the mRNA does N6-methyladenosine (m6A) affect? | N(6)-methyladenosine (m6A) is the most abundant modified base in eukaryotic mRNA and has been linked to diverse effects on mRNA fate. m6A predominantly and directly reduces mRNA stability. |
http://www.ncbi.nlm.nih.gov/pubmed/23179372,http://www.ncbi.nlm.nih.gov/pubmed/23184418,http://www.ncbi.nlm.nih.gov/pubmed/19270706 | What is the implication of histone lysine methylation in medulloblastoma? | Aberrant patterns of H3K4, H3K9, and H3K27 histone lysine methylation were shown to result in histone code alterations, which induce changes in gene expression, and affect the proliferation rate of cells in medulloblastoma. |
http://www.ncbi.nlm.nih.gov/pubmed/22269900,http://www.ncbi.nlm.nih.gov/pubmed/23292750,http://www.ncbi.nlm.nih.gov/pubmed/23894621,http://www.ncbi.nlm.nih.gov/pubmed/22272331,http://www.ncbi.nlm.nih.gov/pubmed/21555561,http://www.ncbi.nlm.nih.gov/pubmed/23352695,http://www.ncbi.nlm.nih.gov/pubmed/22174894,http://www.ncbi.nlm.nih.gov/pubmed/23719379 | What is the Orco protein in mosquitos? | Odorant co-receptor. |
http://www.ncbi.nlm.nih.gov/pubmed/12212772,http://www.ncbi.nlm.nih.gov/pubmed/16806196,http://www.ncbi.nlm.nih.gov/pubmed/20471717,http://www.ncbi.nlm.nih.gov/pubmed/16687499,http://www.ncbi.nlm.nih.gov/pubmed/18755209 | List some ways to reverse Tau hyperphosphorylation in Tauopathies? | Different ways have been used to try to reverse Tau hyperphosphorylation through administration of inhibitors such as: 7-nitroindazole, memantine, glycogen synthase kinase-3 inhibitors.
Other approaches are transplantation of Human umbilical cord blood-derived mesenchymal stem cells and administration of M1 muscarinic agonists. |
http://www.ncbi.nlm.nih.gov/pubmed/24838624,http://www.ncbi.nlm.nih.gov/pubmed/21514197,http://www.ncbi.nlm.nih.gov/pubmed/22722204,http://www.ncbi.nlm.nih.gov/pubmed/23403924,http://www.ncbi.nlm.nih.gov/pubmed/21873190,http://www.ncbi.nlm.nih.gov/pubmed/25263596,http://www.ncbi.nlm.nih.gov/pubmed/22234893,http://www.ncbi.nlm.nih.gov/pubmed/22730288,http://www.ncbi.nlm.nih.gov/pubmed/24735881,http://www.ncbi.nlm.nih.gov/pubmed/25179373,http://www.ncbi.nlm.nih.gov/pubmed/25071199,http://www.ncbi.nlm.nih.gov/pubmed/26275994,http://www.ncbi.nlm.nih.gov/pubmed/21460836 | What is the role of 5hmC (5 hydroxy-methyl-Cytocine) in differentiation? | The balance between 5hmC and 5mC in the genome is linked with cell-differentiation processes such as pluripotency and lineage commitment. Tet1-mediated antagonism of CpG methylation imparts differential maintenance of DNA methylation status at Tet1 targets, ultimately contributing to mESC differentiation and the onset of embryonic development. By mapping DNA methylation and hydroxymethylation at base resolution, we find that deletion of Tet2 causes extensive loss of 5hmC at enhancers, accompanied by enhancer hypermethylation, reduction of enhancer activity, and delayed gene induction in the early steps of differentiation.Dynamic hydroxymethylation of deoxyribonucleic acid marks differentiation-associated enhancers |
http://www.ncbi.nlm.nih.gov/pubmed/18562676,http://www.ncbi.nlm.nih.gov/pubmed/16651450,http://www.ncbi.nlm.nih.gov/pubmed/19855399,http://www.ncbi.nlm.nih.gov/pubmed/17942719,http://www.ncbi.nlm.nih.gov/pubmed/15960975,http://www.ncbi.nlm.nih.gov/pubmed/21875999,http://www.ncbi.nlm.nih.gov/pubmed/22666422,http://www.ncbi.nlm.nih.gov/pubmed/21124902,http://www.ncbi.nlm.nih.gov/pubmed/19187761,http://www.ncbi.nlm.nih.gov/pubmed/18838538,http://www.ncbi.nlm.nih.gov/pubmed/15941828,http://www.ncbi.nlm.nih.gov/pubmed/17168535,http://www.ncbi.nlm.nih.gov/pubmed/21113167,http://www.ncbi.nlm.nih.gov/pubmed/22488473,http://www.ncbi.nlm.nih.gov/pubmed/19818711,http://www.ncbi.nlm.nih.gov/pubmed/19219072,http://www.ncbi.nlm.nih.gov/pubmed/23399917,http://www.ncbi.nlm.nih.gov/pubmed/20861184,http://www.ncbi.nlm.nih.gov/pubmed/22046413,http://www.ncbi.nlm.nih.gov/pubmed/19481096,http://www.ncbi.nlm.nih.gov/pubmed/23038103 | Which is the histone residue methylated by MLL1? | Histone H3 at lysine 4 (H3K4) |
http://www.ncbi.nlm.nih.gov/pubmed/26098216,http://www.ncbi.nlm.nih.gov/pubmed/25409531,http://www.ncbi.nlm.nih.gov/pubmed/24136345,http://www.ncbi.nlm.nih.gov/pubmed/25566532,http://www.ncbi.nlm.nih.gov/pubmed/23452860,http://www.ncbi.nlm.nih.gov/pubmed/23849981,http://www.ncbi.nlm.nih.gov/pubmed/26047700,http://www.ncbi.nlm.nih.gov/pubmed/26080438 | What is CRISPRi? | Clustered regularly interspaced palindromic repeats interference (CRISPRi). This discovery tool is is used for genetic screening based on loss-of-function phenotypes.The Clustered Regularly Interspaced Short Palindromic Repeats interference (CRISPRi) system is used for targeted silencing of transcription in different types of cells. The CRISPRi system is derived from the Streptococcus pyogenes CRISPR pathway, requiring only the coexpression of a catalytically inactive Cas9 protein and a customizable single guide RNA (sgRNA). The Cas9-sgRNA complex binds to DNA elements complementary to the sgRNA and causes a steric block that halts transcript elongation by RNA polymerase, resulting in the repression of the target gene. CRISPRi provides a simplified approach for rapid gene repression within 1-2 weeks. The method can also be adapted for high-throughput interrogation of genome-wide gene functions and genetic interactions, thus providing a complementary approach to RNA interference, which can be used in a wider variety of organisms. |
http://www.ncbi.nlm.nih.gov/pubmed/23197818,http://www.ncbi.nlm.nih.gov/pubmed/24269728,http://www.ncbi.nlm.nih.gov/pubmed/20846186,http://www.ncbi.nlm.nih.gov/pubmed/22900096,http://www.ncbi.nlm.nih.gov/pubmed/24971881,http://www.ncbi.nlm.nih.gov/pubmed/22797053,http://www.ncbi.nlm.nih.gov/pubmed/25384799,http://www.ncbi.nlm.nih.gov/pubmed/23114367 | Which type of cells is affected in Amyotrophic Lateral Sclerosis? | Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder in which motor neurons are affected. |
http://www.ncbi.nlm.nih.gov/pubmed/3143244,http://www.ncbi.nlm.nih.gov/pubmed/22628261,http://www.ncbi.nlm.nih.gov/pubmed/9733026,http://www.ncbi.nlm.nih.gov/pubmed/8456822,http://www.ncbi.nlm.nih.gov/pubmed/22183904,http://www.ncbi.nlm.nih.gov/pubmed/3240244,http://www.ncbi.nlm.nih.gov/pubmed/8267016,http://www.ncbi.nlm.nih.gov/pubmed/18328977 | Is Achondroplasia associated with hearing loss? | Yes, there is hearing deficit in achondroplasia |
http://www.ncbi.nlm.nih.gov/pubmed/18671679,http://www.ncbi.nlm.nih.gov/pubmed/21338344,http://www.ncbi.nlm.nih.gov/pubmed/20207439,http://www.ncbi.nlm.nih.gov/pubmed/21354444,http://www.ncbi.nlm.nih.gov/pubmed/18382767,http://www.ncbi.nlm.nih.gov/pubmed/16797887,http://www.ncbi.nlm.nih.gov/pubmed/11709497,http://www.ncbi.nlm.nih.gov/pubmed/15970430,http://www.ncbi.nlm.nih.gov/pubmed/12668975,http://www.ncbi.nlm.nih.gov/pubmed/23035542,http://www.ncbi.nlm.nih.gov/pubmed/17762881,http://www.ncbi.nlm.nih.gov/pubmed/20578144,http://www.ncbi.nlm.nih.gov/pubmed/16242670 | Is the JNK pathway activated during liver regeneration? | Yes, the Jun-N-terminal kinase (JNK) pathway is strongly activated after partial hepatectomy. |
http://www.ncbi.nlm.nih.gov/pubmed/24931163,http://www.ncbi.nlm.nih.gov/pubmed/22055460,http://www.ncbi.nlm.nih.gov/pubmed/26026060,http://www.ncbi.nlm.nih.gov/pubmed/24302004,http://www.ncbi.nlm.nih.gov/pubmed/23641065 | Is STAT3 transcription factor regulated by mTORC1? | mTORC1 was found to regulate STAT3 activity in, at least, three ways: 1) after induction by IL6, 2) by direct phosphorylation during hypoxia, to promote HIF-1α mRNA transcription, and 3) after activation by excess amino acids, which then positively regulate Notch1 expression through STAT3 activation. |
http://www.ncbi.nlm.nih.gov/pubmed/21177857 | How is mTORC1 involved in the regulation of heat stress? | mTORC1 attenuates stress response by inhibiting cap-independent Hsp70 translation. |
http://www.ncbi.nlm.nih.gov/pubmed/14759369,http://www.ncbi.nlm.nih.gov/pubmed/12050112,http://www.ncbi.nlm.nih.gov/pubmed/15175162,http://www.ncbi.nlm.nih.gov/pubmed/9989412,http://www.ncbi.nlm.nih.gov/pubmed/12509459,http://www.ncbi.nlm.nih.gov/pubmed/24820420,http://www.ncbi.nlm.nih.gov/pubmed/15195149,http://www.ncbi.nlm.nih.gov/pubmed/10377381,http://www.ncbi.nlm.nih.gov/pubmed/19571180,http://www.ncbi.nlm.nih.gov/pubmed/11834832 | List components of the CRSP/Med complex. | Mediator of RNA polymerase II transcription subunit 7
Mediator of RNA polymerase II transcription subunit 14
Mediator of RNA polymerase II transcription subunit 17
Mediator of RNA polymerase II transcription subunit 23
Mediator of RNA polymerase II transcription subunit 24
Mediator of RNA polymerase II transcription subunit 26
Mediator of RNA polymerase II transcription subunit 27 |
http://www.ncbi.nlm.nih.gov/pubmed/23104007 | Patients of which disease could be treated by utilizing knowledge obtained from experiments suppressing TDP-43 toxicity in yeast? | Amyotrophic lateral sclerosis (ALS).The strongest suppressor of TDP-43 toxicity was deletion of DBR1, which encodes an RNA lariat debranching enzyme. We show that, in the absence of Dbr1 enzymatic activity, intronic lariats accumulate in the cytoplasm and likely act as decoys to sequester TDP-43, preventing it from interfering with essential cellular RNAs and RNA-binding proteins. Knockdown of Dbr1 in a human neuronal cell line or in primary rat neurons is also sufficient to rescue TDP-43 toxicity. Our findings provide insight into TDP-43-mediated cytotoxicity and suggest that decreasing Dbr1 activity could be a potential therapeutic approach for ALS |
http://www.ncbi.nlm.nih.gov/pubmed/22402252,http://www.ncbi.nlm.nih.gov/pubmed/3850773,http://www.ncbi.nlm.nih.gov/pubmed/8864644,http://www.ncbi.nlm.nih.gov/pubmed/10359740,http://www.ncbi.nlm.nih.gov/pubmed/3384188,http://www.ncbi.nlm.nih.gov/pubmed/8761317 | Is calcium overload involved in the development of diabetic cardiomyopathy? | Yes. |
http://www.ncbi.nlm.nih.gov/pubmed/9356244,http://www.ncbi.nlm.nih.gov/pubmed/18370255,http://www.ncbi.nlm.nih.gov/pubmed/15448723,http://www.ncbi.nlm.nih.gov/pubmed/25287502,http://www.ncbi.nlm.nih.gov/pubmed/1717335,http://www.ncbi.nlm.nih.gov/pubmed/21994552,http://www.ncbi.nlm.nih.gov/pubmed/3860809,http://www.ncbi.nlm.nih.gov/pubmed/9601006,http://www.ncbi.nlm.nih.gov/pubmed/6760914,http://www.ncbi.nlm.nih.gov/pubmed/11907231,http://www.ncbi.nlm.nih.gov/pubmed/7231549,http://www.ncbi.nlm.nih.gov/pubmed/18190946,http://www.ncbi.nlm.nih.gov/pubmed/17438124,http://www.ncbi.nlm.nih.gov/pubmed/7747427 | What is the mechanism of viroid replication? | The replication of many viral and subviral pathogens as well as the amplification of certain cellular genes proceeds via a rolling circle mechanism. Viroid replication occurs via a rolling circle mechanism using either a symmetric or asymmetric pathway in three steps, RNA transcription, processing and ligation. Replication of these minimal genomes, composed exclusively by a circular RNA of 246-401 nt, occurs in the nucleus (family Pospiviroidae) or in the chloroplast (family Avsunviroidae) by an RNA-based rolling-circle mechanism with three steps: (1) synthesis of longer-than-unit strands catalyzed by host DNA-dependent RNA polymerases recruited and redirected to transcribe RNA templates, (2) cleavage to unit-length, which in family Avsunviroidae is mediated by hammerhead ribozymes, and (3) circularization through an RNA ligase or autocatalytically. |
http://www.ncbi.nlm.nih.gov/pubmed/1331777,http://www.ncbi.nlm.nih.gov/pubmed/12225634,http://www.ncbi.nlm.nih.gov/pubmed/7763274 | Which mitochondrial genes are regulated by thyroid hormone? | subunit 6 of ATP synthase, ATPase-6, mitochondrial II and III subunits of cytochrome-c oxidase, NADH dehydrogenase subunit 3 |
http://www.ncbi.nlm.nih.gov/pubmed/11099667,http://www.ncbi.nlm.nih.gov/pubmed/11761473,http://www.ncbi.nlm.nih.gov/pubmed/19909712,http://www.ncbi.nlm.nih.gov/pubmed/11562915,http://www.ncbi.nlm.nih.gov/pubmed/1734714,http://www.ncbi.nlm.nih.gov/pubmed/24098554,http://www.ncbi.nlm.nih.gov/pubmed/23943810,http://www.ncbi.nlm.nih.gov/pubmed/17300882,http://www.ncbi.nlm.nih.gov/pubmed/21145924,http://www.ncbi.nlm.nih.gov/pubmed/10846875,http://www.ncbi.nlm.nih.gov/pubmed/12899725,http://www.ncbi.nlm.nih.gov/pubmed/8004674,http://www.ncbi.nlm.nih.gov/pubmed/17277857,http://www.ncbi.nlm.nih.gov/pubmed/17469188,http://www.ncbi.nlm.nih.gov/pubmed/12243006,http://www.ncbi.nlm.nih.gov/pubmed/10651848,http://www.ncbi.nlm.nih.gov/pubmed/3334897,http://www.ncbi.nlm.nih.gov/pubmed/18167163,http://www.ncbi.nlm.nih.gov/pubmed/16344536,http://www.ncbi.nlm.nih.gov/pubmed/17870653,http://www.ncbi.nlm.nih.gov/pubmed/10930599,http://www.ncbi.nlm.nih.gov/pubmed/8634708,http://www.ncbi.nlm.nih.gov/pubmed/10426139,http://www.ncbi.nlm.nih.gov/pubmed/19040496,http://www.ncbi.nlm.nih.gov/pubmed/22383943,http://www.ncbi.nlm.nih.gov/pubmed/12823753,http://www.ncbi.nlm.nih.gov/pubmed/11746618,http://www.ncbi.nlm.nih.gov/pubmed/11703337,http://www.ncbi.nlm.nih.gov/pubmed/24179763,http://www.ncbi.nlm.nih.gov/pubmed/16314760,http://www.ncbi.nlm.nih.gov/pubmed/10882128,http://www.ncbi.nlm.nih.gov/pubmed/8619554,http://www.ncbi.nlm.nih.gov/pubmed/11261514,http://www.ncbi.nlm.nih.gov/pubmed/17302777 | Mutation of which gene is associated with McLeod syndrome? | Mutation of XK gene is associated with McLeod syndrome. The XK gene is an X-chromosomal gene. The McLeod phenotype is derived from various forms of XK gene defects that result in the absence of XK protein, and is defined hematologically by the absence of Kx antigen, weakening of Kell system antigens, and red cell acanthocytosis. |
http://www.ncbi.nlm.nih.gov/pubmed/22421439,http://www.ncbi.nlm.nih.gov/pubmed/23612963,http://www.ncbi.nlm.nih.gov/pubmed/24059293,http://www.ncbi.nlm.nih.gov/pubmed/23898178,http://www.ncbi.nlm.nih.gov/pubmed/23162759,http://www.ncbi.nlm.nih.gov/pubmed/22016814,http://www.ncbi.nlm.nih.gov/pubmed/22817896,http://www.ncbi.nlm.nih.gov/pubmed/22033613,http://www.ncbi.nlm.nih.gov/pubmed/21749897,http://www.ncbi.nlm.nih.gov/pubmed/22666585,http://www.ncbi.nlm.nih.gov/pubmed/24098568,http://www.ncbi.nlm.nih.gov/pubmed/22576661,http://www.ncbi.nlm.nih.gov/pubmed/21890409 | Is RIP1 (RIP-1) part of the necrosome? | Yes, RIP1 is part of the necrosome. |