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http://www.ncbi.nlm.nih.gov/pubmed/10777687,http://www.ncbi.nlm.nih.gov/pubmed/8063775,http://www.ncbi.nlm.nih.gov/pubmed/8702907,http://www.ncbi.nlm.nih.gov/pubmed/9261349,http://www.ncbi.nlm.nih.gov/pubmed/12684058,http://www.ncbi.nlm.nih.gov/pubmed/22021377 | Which is the binding site motif of Sp1? | Sp1 binds to a GC-rich sequence element containing the decanucleotide consensus sequence 5′-(G/T)GGGCGG(G/A)(G/A)(C/T)-3′ (GC box element) in double stranded DNA (dsDNA). Gel shift competition studies and DNase I footprinting analyses revealed that Sp1 specifically interacts with the CACCC motif. |
http://www.ncbi.nlm.nih.gov/pubmed/25566057,http://www.ncbi.nlm.nih.gov/pubmed/12691864,http://www.ncbi.nlm.nih.gov/pubmed/8816973,http://www.ncbi.nlm.nih.gov/pubmed/25870548,http://www.ncbi.nlm.nih.gov/pubmed/9451598,http://www.ncbi.nlm.nih.gov/pubmed/14679108 | List autoimmune disorders associated with GAD65 autoantibodies. | Autoantibodies to the smaller isoform of glutamate decarboxylase (GAD) can be found in patients with type 1 diabetes and a number of neurological disorders, including stiff-person syndrome, cerebellar ataxia and limbic encephalitis. |
http://www.ncbi.nlm.nih.gov/pubmed/20225016,http://www.ncbi.nlm.nih.gov/pubmed/24148153,http://www.ncbi.nlm.nih.gov/pubmed/23913485,http://www.ncbi.nlm.nih.gov/pubmed/22068481 | Elaborate on the TREAT-NMD initiative for DMD patients | TREAT-NMD is a worldwide network for neuromuscular diseases that provides an infrastructure to support the delivery of promising new therapies for patients in Europe. TREAT-NMD has worked on the generation of brief standards of care for DMD. Guidelines are presented for diagnostics, neurological follow up, gastrointestinal and nutritional issues, respiratory and cardiac care as well as orthopaedics, rehabilitation, psychosocial interventions and oral care. |
http://www.ncbi.nlm.nih.gov/pubmed/17999592,http://www.ncbi.nlm.nih.gov/pubmed/25102299 | Is muscle regeneration possible in mdx mice with the use of induced mesenchymal stem cells? | Purified induced mesenchymal stem cells (iMSCs) display fibroblast-like morphology, form three-dimensional spheroid structures, express characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105, and are capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplantation of iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowers oxidative damage, and restores the expression levels of normal dystrophin, leading to skeletal muscle regeneration.Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored |
http://www.ncbi.nlm.nih.gov/pubmed/17985985,http://www.ncbi.nlm.nih.gov/pubmed/20969692,http://www.ncbi.nlm.nih.gov/pubmed/21169742,http://www.ncbi.nlm.nih.gov/pubmed/21553140,http://www.ncbi.nlm.nih.gov/pubmed/8608779,http://www.ncbi.nlm.nih.gov/pubmed/21272686,http://www.ncbi.nlm.nih.gov/pubmed/24163390 | List the different subtypes of thyroid cancer. | The different histologic subtypes of thyroid cancer include papillary, follicular, anaplastic, medullary, and Hürthle cell carcinomas. |
http://www.ncbi.nlm.nih.gov/pubmed/24630051,http://www.ncbi.nlm.nih.gov/pubmed/18342287,http://www.ncbi.nlm.nih.gov/pubmed/24035762,http://www.ncbi.nlm.nih.gov/pubmed/25044251,http://www.ncbi.nlm.nih.gov/pubmed/25273398,http://www.ncbi.nlm.nih.gov/pubmed/20949524,http://www.ncbi.nlm.nih.gov/pubmed/24839169,http://www.ncbi.nlm.nih.gov/pubmed/24285247,http://www.ncbi.nlm.nih.gov/pubmed/24779060,http://www.ncbi.nlm.nih.gov/pubmed/21932316,http://www.ncbi.nlm.nih.gov/pubmed/22541666 | What are the characteristics of Christianson syndrome? | Christianson syndrome (CS) is caused by mutations in the X-linked Na(+) /H(+) exchanger 6 (NHE6). Patients present with prominent neurological, medical, and behavioral symptoms. All CS participants were nonverbal and had intellectual disability, epilepsy, and ataxia. Other neurologic symptoms included eye movement abnormalities (79%), postnatal microcephaly (92%), and magnetic resonance imaging evidence of cerebellar atrophy (33%). Regression was noted in 50%, with recurrent presentations involving loss of words and/or the ability to walk. Medical symptoms, particularly gastrointestinal symptoms, are common. Height and body mass index measures were below normal ranges in most participants. Behavioral symptoms included hyperkinetic behavior (100%), and a majority exhibited high pain threshold. |
http://www.ncbi.nlm.nih.gov/pubmed/21752896,http://www.ncbi.nlm.nih.gov/pubmed/23036115,http://www.ncbi.nlm.nih.gov/pubmed/19732718,http://www.ncbi.nlm.nih.gov/pubmed/23061808 | Is the SDHAF2 gene encoding a protein necessary for flavination of SDHA? | Yes, SDHAF2 or hSDH5, is the gene encoding the enzyme responsible for the flavination of SDHA.Yes, SDHAF2 is required for flavination of SDHA. |
http://www.ncbi.nlm.nih.gov/pubmed/20020146 | What is the physiological role of LKB1 involved in Peutz-Jeghers syndrome? | LKB1 plays a physiological role in controlling the Wnt-signaling. |
http://www.ncbi.nlm.nih.gov/pubmed/19687305,http://www.ncbi.nlm.nih.gov/pubmed/20724379,http://www.ncbi.nlm.nih.gov/pubmed/19822637,http://www.ncbi.nlm.nih.gov/pubmed/17366138,http://www.ncbi.nlm.nih.gov/pubmed/12880207,http://www.ncbi.nlm.nih.gov/pubmed/19482090,http://www.ncbi.nlm.nih.gov/pubmed/16209710,http://www.ncbi.nlm.nih.gov/pubmed/16014870,http://www.ncbi.nlm.nih.gov/pubmed/18852097,http://www.ncbi.nlm.nih.gov/pubmed/17974035,http://www.ncbi.nlm.nih.gov/pubmed/16151191,http://www.ncbi.nlm.nih.gov/pubmed/18319244,http://www.ncbi.nlm.nih.gov/pubmed/21186190,http://www.ncbi.nlm.nih.gov/pubmed/20045073,http://www.ncbi.nlm.nih.gov/pubmed/11752184,http://www.ncbi.nlm.nih.gov/pubmed/16672284,http://www.ncbi.nlm.nih.gov/pubmed/17288568,http://www.ncbi.nlm.nih.gov/pubmed/21235782,http://www.ncbi.nlm.nih.gov/pubmed/15746012 | What heterotachy states about molecular evolutionary processes? | Functional constraints may account for heterogeneity in the evolutionary rates among different sites of amino acid or DNA sequences. Apart from variations of substitution rates among different sites (spatial variation), heterotachy states that there are variations of substitution rates of a given site throughout time. Heterotachy is the within-site evolutionary rate variations across different lineages over time. Heterotachy (temporal rate variation) occurs with varying severity because the intensity of purifying selection and adaptive forces acting at a given position of a homologous amino acid or DNA sequence are not the same in different species. Heterotachy may mislead phylogenetic inferences. |
http://www.ncbi.nlm.nih.gov/pubmed/12605978,http://www.ncbi.nlm.nih.gov/pubmed/23104453,http://www.ncbi.nlm.nih.gov/pubmed/18481737,http://www.ncbi.nlm.nih.gov/pubmed/21994513,http://www.ncbi.nlm.nih.gov/pubmed/19159080,http://www.ncbi.nlm.nih.gov/pubmed/23438646,http://www.ncbi.nlm.nih.gov/pubmed/18061752,http://www.ncbi.nlm.nih.gov/pubmed/24152975,http://www.ncbi.nlm.nih.gov/pubmed/23615145,http://www.ncbi.nlm.nih.gov/pubmed/23187335,http://www.ncbi.nlm.nih.gov/pubmed/23989499,http://www.ncbi.nlm.nih.gov/pubmed/23633116,http://www.ncbi.nlm.nih.gov/pubmed/16532486,http://www.ncbi.nlm.nih.gov/pubmed/23384776,http://www.ncbi.nlm.nih.gov/pubmed/22585179,http://www.ncbi.nlm.nih.gov/pubmed/22307475,http://www.ncbi.nlm.nih.gov/pubmed/18329220,http://www.ncbi.nlm.nih.gov/pubmed/21968946,http://www.ncbi.nlm.nih.gov/pubmed/17760798 | What is known about depression in caregivers of brain tumor patients? | Depression is common affecting up to 40% of caregivers of brain tumor patients. Depression is associated with poor quality of life of caregivers of brain tumor patients. Greater anxiety, patients’ emotional distress, economic hardship, lower caregivers’ age, lower income, less social support and lower patient functioning were associated with more caregivers’ depressive symptoms. Reports of caregiver depressive symptoms were lower when paired with higher reports of spirituality. It is important to monitor and treat caregiver's depression. |
http://www.ncbi.nlm.nih.gov/pubmed/16237557,http://www.ncbi.nlm.nih.gov/pubmed/12939697,http://www.ncbi.nlm.nih.gov/pubmed/11324313,http://www.ncbi.nlm.nih.gov/pubmed/11891690,http://www.ncbi.nlm.nih.gov/pubmed/9885824,http://www.ncbi.nlm.nih.gov/pubmed/8852660 | What are the effects of homozygosity of EDNRB mutations in addition to Hirschsprung disease? | Three susceptibility genes have been recently identified in HSCR, namely the RET proto-oncogene, the endothelin B receptor (EDNRB) gene, and the endothelin 3 (EDN3) gene. RET gene mutations were found in significant proportions of familial (50%) and sporadic (15-20%) HSCR, while homozygosity for EDNRB or EDN3 mutations accounted for the rare HSCR-Waardenburg syndrome (WS) association. More recently, heterozygous EDNRB an EDN3 missense mutations have been reported in isolated HSCR patients EDNRB homozygous mutations have been found to account for the rare Waardenburg-Hirschsprung syndrome (WS), whereas heterozygous EDNRB missense mutations have been reported in isolated Hirschsprung disease patients. |
http://www.ncbi.nlm.nih.gov/pubmed/12475369,http://www.ncbi.nlm.nih.gov/pubmed/14500064,http://www.ncbi.nlm.nih.gov/pubmed/15868525,http://www.ncbi.nlm.nih.gov/pubmed/21959513,http://www.ncbi.nlm.nih.gov/pubmed/21097430,http://www.ncbi.nlm.nih.gov/pubmed/19303793,http://www.ncbi.nlm.nih.gov/pubmed/1929631,http://www.ncbi.nlm.nih.gov/pubmed/16677263,http://www.ncbi.nlm.nih.gov/pubmed/19463607 | What is the prognostic role of alterred thyroid profile after cardiosurgery? | Altered thyroid profile after cardiosurgery is associated with high incidence of atrial fibrillation e delay in recovery (prolonged hospitalisation) in adults and higher score on The Pediatric Risk of Mortality (PRISM; P < 0.042) and a longer duration of ventilation in children.Impportantly in transplanted patients altered thyroid metabolism,low T3 syndrome, is characterized by highest mortality, highest incidence of acute rejection or reoperations and infections |
http://www.ncbi.nlm.nih.gov/pubmed/24594084,http://www.ncbi.nlm.nih.gov/pubmed/17283405,http://www.ncbi.nlm.nih.gov/pubmed/22461877,http://www.ncbi.nlm.nih.gov/pubmed/26393185,http://www.ncbi.nlm.nih.gov/pubmed/11432800,http://www.ncbi.nlm.nih.gov/pubmed/23758042 | List Pentalogy of Fallot. | Pentalogy of Fallot consists of a pulmonic stenosis, a ventricular septal defect, an overriding aorta, a right ventricular hypertrophy and a patent foramen ovale. |
http://www.ncbi.nlm.nih.gov/pubmed/21111234,http://www.ncbi.nlm.nih.gov/pubmed/25173175,http://www.ncbi.nlm.nih.gov/pubmed/25266476,http://www.ncbi.nlm.nih.gov/pubmed/23901111,http://www.ncbi.nlm.nih.gov/pubmed/22101327,http://www.ncbi.nlm.nih.gov/pubmed/25220052,http://www.ncbi.nlm.nih.gov/pubmed/25257310,http://www.ncbi.nlm.nih.gov/pubmed/24141881,http://www.ncbi.nlm.nih.gov/pubmed/25092792,http://www.ncbi.nlm.nih.gov/pubmed/25092791,http://www.ncbi.nlm.nih.gov/pubmed/21115494,http://www.ncbi.nlm.nih.gov/pubmed/25257309,http://www.ncbi.nlm.nih.gov/pubmed/22580470 | Which is the major function of sororin? | Sororin is a positive regulator of sister chromatid cohesion that interacts with the cohesin complex. |
http://www.ncbi.nlm.nih.gov/pubmed/12730117,http://www.ncbi.nlm.nih.gov/pubmed/11919388,http://www.ncbi.nlm.nih.gov/pubmed/17987804,http://www.ncbi.nlm.nih.gov/pubmed/16616117,http://www.ncbi.nlm.nih.gov/pubmed/2820585,http://www.ncbi.nlm.nih.gov/pubmed/21279819,http://www.ncbi.nlm.nih.gov/pubmed/8697423,http://www.ncbi.nlm.nih.gov/pubmed/9916508,http://www.ncbi.nlm.nih.gov/pubmed/8656667,http://www.ncbi.nlm.nih.gov/pubmed/21332651,http://www.ncbi.nlm.nih.gov/pubmed/18722880,http://www.ncbi.nlm.nih.gov/pubmed/3670297,http://www.ncbi.nlm.nih.gov/pubmed/2157692,http://www.ncbi.nlm.nih.gov/pubmed/22058195,http://www.ncbi.nlm.nih.gov/pubmed/17001000,http://www.ncbi.nlm.nih.gov/pubmed/1423227,http://www.ncbi.nlm.nih.gov/pubmed/1434792,http://www.ncbi.nlm.nih.gov/pubmed/11535505,http://www.ncbi.nlm.nih.gov/pubmed/11984797,http://www.ncbi.nlm.nih.gov/pubmed/8490164,http://www.ncbi.nlm.nih.gov/pubmed/22783385 | Which gene fusion is the result of the "philadelphia translocation" or the "philadelphia chromosome" mutation? | Chronic myeloid leukemia (CML) is genetically characterized by the presence of the reciprocal translocation t(9;22)(q34;q11), resulting in a BCR/ABL gene fusion on the derivative chromosome 22 called the Philadelphia (Ph) chromosome. The Philadelphia chromosome and its corresponding fusion gene, BCR-ABL, is one of the best-known genetic abnormalities in hematological malignancies. Major BCR-ABL translocation is much more common in chronic myelogenous leukemia (CML) and minor BCR-ABL in acute lymphoblastic leukemia. Chronic myeloid leukemia (CML) is genetically characterized by the presence of the reciprocal translocation t(9;22)(q34;q11), resulting in a BCR/ABL gene fusion on the derivative chromosome 22 called the Philadelphia (Ph) chromosome. The Philadelphia chromosome is recognized as the cytogenetic result of a rearrangement of the ABL gene on chromosome 9 and the BCL gene on chromosome 22, which leads to the creation of a BCR/ABL fusion gene on chromosome 22. |
http://www.ncbi.nlm.nih.gov/pubmed/8098760,http://www.ncbi.nlm.nih.gov/pubmed/1403792,http://www.ncbi.nlm.nih.gov/pubmed/11154097,http://www.ncbi.nlm.nih.gov/pubmed/9433391,http://www.ncbi.nlm.nih.gov/pubmed/2871178 | Is zolpidem an antibiotic? | No, zolpidem is a short-acting imidazopyridine hypnotic drug |
http://www.ncbi.nlm.nih.gov/pubmed/23587982,http://www.ncbi.nlm.nih.gov/pubmed/21067460,http://www.ncbi.nlm.nih.gov/pubmed/23881185,http://www.ncbi.nlm.nih.gov/pubmed/20107296,http://www.ncbi.nlm.nih.gov/pubmed/18507895,http://www.ncbi.nlm.nih.gov/pubmed/23517291,http://www.ncbi.nlm.nih.gov/pubmed/22173281,http://www.ncbi.nlm.nih.gov/pubmed/19407711,http://www.ncbi.nlm.nih.gov/pubmed/23473348,http://www.ncbi.nlm.nih.gov/pubmed/19407730 | Can desvenlafaxine be used at a dose of 50mg/day? | Yes, desvenlafaxine can be at 50mg/day to treat patients with major depressive disorder. Studies suggest that 50 mg is the minimum effective dose of desvenlafaxine for the treatment of major depressive disorder. The recommended dose of DVS ranges from 50 to 100 mg. |
http://www.ncbi.nlm.nih.gov/pubmed/22982575,http://www.ncbi.nlm.nih.gov/pubmed/22232210 | Which syndrome is associated with OATP1B1 and OATP1B3 deficiency? | Complete and simultaneous deficiency of the organic anion transporting polypeptides OATP1B1 and OATP1B3 due to mutations in their corresponding genes, has been linked to Rotor syndrome. |
http://www.ncbi.nlm.nih.gov/pubmed/21554040,http://www.ncbi.nlm.nih.gov/pubmed/22452896,http://www.ncbi.nlm.nih.gov/pubmed/24086949,http://www.ncbi.nlm.nih.gov/pubmed/18408761,http://www.ncbi.nlm.nih.gov/pubmed/23664448,http://www.ncbi.nlm.nih.gov/pubmed/18520300,http://www.ncbi.nlm.nih.gov/pubmed/22071596,http://www.ncbi.nlm.nih.gov/pubmed/23683257 | Which type of lung cancer is afatinib used for? | Afatinib is a small molecule covalently binding and inhibiting the EGFR, HER2 and HER4 receptor tyrosine kinases. Trials showed promising efficacy in patients with EGFR-mutant NSCLC or enriched for clinical benefit from EGFR tyrosine kinase inhibitors gefitinib or erlotinib.Afatinib is a novel irreversible inhibitor of the ErbB family members EGFR, tyrosine kinase-type cell surface receptors HER2 and HER4. It shows preclinical efficacy in NSCLC with common EGFR-activating mutations and the T790M mutation typically associated with EGFR TKI resistanceBIBW2992 is an irreversible EGFR TKI that also inhibits HER2 and vascular epidermal growth factor receptors |
http://www.ncbi.nlm.nih.gov/pubmed/21340038,http://www.ncbi.nlm.nih.gov/pubmed/19787830,http://www.ncbi.nlm.nih.gov/pubmed/20648930,http://www.ncbi.nlm.nih.gov/pubmed/23078888,http://www.ncbi.nlm.nih.gov/pubmed/23889159,http://www.ncbi.nlm.nih.gov/pubmed/24114623,http://www.ncbi.nlm.nih.gov/pubmed/21479141,http://www.ncbi.nlm.nih.gov/pubmed/22023204,http://www.ncbi.nlm.nih.gov/pubmed/18371137,http://www.ncbi.nlm.nih.gov/pubmed/21699794,http://www.ncbi.nlm.nih.gov/pubmed/23644823,http://www.ncbi.nlm.nih.gov/pubmed/24081613,http://www.ncbi.nlm.nih.gov/pubmed/22179489 | Can ferric carboxymaltose be used to treat anemia in inflammatory bowel disease patients? | Ferric carboxymaltose can be used to treat anemia in patients with inflammatory bowel disease, and prevents recurrence of anemia in these patients, compared with placebo. Treatment with ferric carboxymaltose is efficious, safe and well tolerated in iron-deficient IBD patients. |
http://www.ncbi.nlm.nih.gov/pubmed/25256118,http://www.ncbi.nlm.nih.gov/pubmed/25688781,http://www.ncbi.nlm.nih.gov/pubmed/24835462,http://www.ncbi.nlm.nih.gov/pubmed/20864621,http://www.ncbi.nlm.nih.gov/pubmed/25819691,http://www.ncbi.nlm.nih.gov/pubmed/20439622,http://www.ncbi.nlm.nih.gov/pubmed/24816856,http://www.ncbi.nlm.nih.gov/pubmed/22058426,http://www.ncbi.nlm.nih.gov/pubmed/20713962 | Which disease is treated with Eliglustat? | Eliglustat was developed for treatment of Gaucher's disease type 1. |
http://www.ncbi.nlm.nih.gov/pubmed/16872538,http://www.ncbi.nlm.nih.gov/pubmed/24299017,http://www.ncbi.nlm.nih.gov/pubmed/22174556,http://www.ncbi.nlm.nih.gov/pubmed/21682895,http://www.ncbi.nlm.nih.gov/pubmed/19534736,http://www.ncbi.nlm.nih.gov/pubmed/23419374,http://www.ncbi.nlm.nih.gov/pubmed/22894160,http://www.ncbi.nlm.nih.gov/pubmed/21047377,http://www.ncbi.nlm.nih.gov/pubmed/22685080,http://www.ncbi.nlm.nih.gov/pubmed/19435747,http://www.ncbi.nlm.nih.gov/pubmed/23210476,http://www.ncbi.nlm.nih.gov/pubmed/18574858,http://www.ncbi.nlm.nih.gov/pubmed/22990765,http://www.ncbi.nlm.nih.gov/pubmed/23046740,http://www.ncbi.nlm.nih.gov/pubmed/22165822,http://www.ncbi.nlm.nih.gov/pubmed/22711784,http://www.ncbi.nlm.nih.gov/pubmed/24214996,http://www.ncbi.nlm.nih.gov/pubmed/23688127,http://www.ncbi.nlm.nih.gov/pubmed/24144986,http://www.ncbi.nlm.nih.gov/pubmed/17094256,http://www.ncbi.nlm.nih.gov/pubmed/21721046,http://www.ncbi.nlm.nih.gov/pubmed/22488467,http://www.ncbi.nlm.nih.gov/pubmed/22185599,http://www.ncbi.nlm.nih.gov/pubmed/24565338,http://www.ncbi.nlm.nih.gov/pubmed/17688314 | List algorithms suitable for predicting protein complexes | Protein-Protein interactions (PPI) play a key role in determining the outcome of most cellular processes. The correct identification and characterization of protein interactions and the networks, which they comprise, is critical for understanding the molecular mechanisms within the cell. Large-scale techniques such as pull down assays and tandem affinity purification are used in order to detect protein interactions in an organism. Today, relatively new high-throughput methods like yeast two hybrid, mass spectrometry, microarrays, and phage display are also used to reveal protein interaction networks. Some suitable algorithms for predicting protein complexes are Naive Bayes Classifier, Negatome, Support Vector Machine, PEWCC, iPTMClust, NDComplex, PROCOMOSS, PPI network, metaPIS, EPOF, EAGLE, NFC, MCODE, DPClus, IPCA, CPM, MCL, CMC, SPICi, Core-Attachment, ProRank, ClusterONE, CFinder, Spectral, RNSC, Affinity Propagation, HKC, NWE, CP-DR, Struct2net and PIPE. |
http://www.ncbi.nlm.nih.gov/pubmed/21948799,http://www.ncbi.nlm.nih.gov/pubmed/23358416,http://www.ncbi.nlm.nih.gov/pubmed/22155246,http://www.ncbi.nlm.nih.gov/pubmed/21447194,http://www.ncbi.nlm.nih.gov/pubmed/23149543,http://www.ncbi.nlm.nih.gov/pubmed/23476064,http://www.ncbi.nlm.nih.gov/pubmed/20080581,http://www.ncbi.nlm.nih.gov/pubmed/17164785,http://www.ncbi.nlm.nih.gov/pubmed/21247877,http://www.ncbi.nlm.nih.gov/pubmed/21822869,http://www.ncbi.nlm.nih.gov/pubmed/21516337,http://www.ncbi.nlm.nih.gov/pubmed/16096065,http://www.ncbi.nlm.nih.gov/pubmed/21205896,http://www.ncbi.nlm.nih.gov/pubmed/18354502,http://www.ncbi.nlm.nih.gov/pubmed/20947725,http://www.ncbi.nlm.nih.gov/pubmed/19471016,http://www.ncbi.nlm.nih.gov/pubmed/19391106,http://www.ncbi.nlm.nih.gov/pubmed/20104210,http://www.ncbi.nlm.nih.gov/pubmed/19809403,http://www.ncbi.nlm.nih.gov/pubmed/24164672 | What are piggyBAC transposons? | The piggyBAC transposons are a nonviral gene delivery approach, that have been developed as tools for insertional mutagenesis. It can mobilize 100-kb DNA fragments in mouse embryonic stem (ES) cells, making it the only known transposon with such a large cargo capacity. The integrity of the cargo is maintained during transposition, the copy number can be controlled and the inserted giant transposons express the genomic cargo. Furthermore, these 100-kb transposons can also be excised from the genome without leaving a footprint. The development of piggyBac as a large cargo vector will facilitate a wider range of genetic and genomic applications. |
http://www.ncbi.nlm.nih.gov/pubmed/22614287,http://www.ncbi.nlm.nih.gov/pubmed/24373612,http://www.ncbi.nlm.nih.gov/pubmed/25136889,http://www.ncbi.nlm.nih.gov/pubmed/25414627,http://www.ncbi.nlm.nih.gov/pubmed/24618187,http://www.ncbi.nlm.nih.gov/pubmed/24461634,http://www.ncbi.nlm.nih.gov/pubmed/21926972,http://www.ncbi.nlm.nih.gov/pubmed/21926974 | Is there any association of the chromosomal region harboring the gene ITIH3 with schizophrenia? | Yes, genome-wide significant associations in schizophrenia has been linked to the locus harboring the ITIH3/4 genes. |
http://www.ncbi.nlm.nih.gov/pubmed/21715505,http://www.ncbi.nlm.nih.gov/pubmed/18667511,http://www.ncbi.nlm.nih.gov/pubmed/23388464,http://www.ncbi.nlm.nih.gov/pubmed/22446380,http://www.ncbi.nlm.nih.gov/pubmed/16648136,http://www.ncbi.nlm.nih.gov/pubmed/23389445 | Is APOBEC3B protein predominantly cytoplasmic or nuclear? | Contrary to other APOBEC family members, APOBEC3B was found to predominantly concentrate to the cell nucleus. |
http://www.ncbi.nlm.nih.gov/pubmed/10400606,http://www.ncbi.nlm.nih.gov/pubmed/15184558,http://www.ncbi.nlm.nih.gov/pubmed/12067333,http://www.ncbi.nlm.nih.gov/pubmed/9537396 | Is the regulation of Vsr endonuclease independent of the growth phase of bacteria? | The regulation of Vsr endonuclease levels is growth phase dependent. |
http://www.ncbi.nlm.nih.gov/pubmed/23549118 | Are there interactomes available for POU5F1 and SOX2? | Yes. Long-range chromosomal interactions on putative enhancers of POU5F1 and SOX2 genes in human embryonic stem cells (hESCs) have been assayed using 4C-Seq technique. Their frequent interacting regions mainly overlap with early DNA replication domains. The interactomes are associated with active histone marks and enriched with 5-hydroxymethylcytosine sites. |
http://www.ncbi.nlm.nih.gov/pubmed/25653163 | Which tool is used for promoterome mining using CAGE data? | Despite their high resolution and functional significance, published CAGE data are still underused in promoter analysis due to the absence of tools that enable its efficient manipulation and integration with other genome data types. CAGEr is an R implementation of novel methods for the analysis of differential TSS usage and promoter dynamics, integrated with CAGE data processing and promoterome mining into a first comprehensive CAGE toolbox on a common analysis platform. |
http://www.ncbi.nlm.nih.gov/pubmed/12682624,http://www.ncbi.nlm.nih.gov/pubmed/19642078,http://www.ncbi.nlm.nih.gov/pubmed/17296665,http://www.ncbi.nlm.nih.gov/pubmed/10555889,http://www.ncbi.nlm.nih.gov/pubmed/12652413,http://www.ncbi.nlm.nih.gov/pubmed/15909088,http://www.ncbi.nlm.nih.gov/pubmed/23171360 | Is Rheumatoid Arthritis related to myopathy? | Vacuolar myopathy and statin-induced myopathy have been reported in rheumatoid arthritis patients, but this association may be due to the anti-malarial treatment received. An increased prevalence of neurogenic but not myogenic changes in patients with RA compared with controls has been reported. |
http://www.ncbi.nlm.nih.gov/pubmed/22748493,http://www.ncbi.nlm.nih.gov/pubmed/19591228,http://www.ncbi.nlm.nih.gov/pubmed/21344679,http://www.ncbi.nlm.nih.gov/pubmed/20870802,http://www.ncbi.nlm.nih.gov/pubmed/22898045,http://www.ncbi.nlm.nih.gov/pubmed/20200331,http://www.ncbi.nlm.nih.gov/pubmed/16304579,http://www.ncbi.nlm.nih.gov/pubmed/18290252,http://www.ncbi.nlm.nih.gov/pubmed/15883211,http://www.ncbi.nlm.nih.gov/pubmed/20971132 | what is the role of GATA-4 in regeneration of the heart after myocardial infarction? | GATA-4 is implicated in cardiogenic differentiation of cardiac c-kit+AT2+ cells that represent approximately 0.19% of total cardiac cells in infarcted heart. GATA-4 overexpression in mesenchymal stem cells increases both survival and angiogenic potential in ischemic myocardium and may therefore represent a novel and efficient therapeutic approach for postinfarct regenaration. In addition, interventions, such as hypergravity and 5-Aza treatment, induce expression of early muscle and cardiac markers like GATA-4 in BMSCs. A subpopulation of primitive cells from rat heart, expressing c-kit and myogenic transcriptional factors, GATA-4 and MEF 2C, exhibit a high in vitro proliferative potential. Progeny of these implanted cells have been shown to migrate along the infarcted scar, reconstitute regenerated cardiomyocytes with incorporation into host myocardium, and inhibit cardiac remodeling with decreased scar formation. In another study, TGF-beta has been shown to conduct the myogenic differentiation of stem cells by upregulating GATA-4 and NKx-2.5 expression and the intramyocardial implantation of TGF-beta-preprogrammed stem cells effectively assisted the myocardial regeneration. Furthermore, G-CSF treatment in postinfarcted murine hearts appears to be an effective approach for treating heart failure and also leads to induction of GATA-4 resulting in expression of various sarcomeric proteins. |
http://www.ncbi.nlm.nih.gov/pubmed/17849604,http://www.ncbi.nlm.nih.gov/pubmed/8450727,http://www.ncbi.nlm.nih.gov/pubmed/17436206,http://www.ncbi.nlm.nih.gov/pubmed/19574095,http://www.ncbi.nlm.nih.gov/pubmed/16389882,http://www.ncbi.nlm.nih.gov/pubmed/9177584,http://www.ncbi.nlm.nih.gov/pubmed/20061269,http://www.ncbi.nlm.nih.gov/pubmed/21435018,http://www.ncbi.nlm.nih.gov/pubmed/23450998,http://www.ncbi.nlm.nih.gov/pubmed/8164540,http://www.ncbi.nlm.nih.gov/pubmed/21618162,http://www.ncbi.nlm.nih.gov/pubmed/22625998,http://www.ncbi.nlm.nih.gov/pubmed/11761838,http://www.ncbi.nlm.nih.gov/pubmed/17214401,http://www.ncbi.nlm.nih.gov/pubmed/22811911,http://www.ncbi.nlm.nih.gov/pubmed/2253729,http://www.ncbi.nlm.nih.gov/pubmed/18369530,http://www.ncbi.nlm.nih.gov/pubmed/23241269,http://www.ncbi.nlm.nih.gov/pubmed/20424397,http://www.ncbi.nlm.nih.gov/pubmed/18634917 | What is the life expectancy of professional athletes in respect to the general population? | Elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes show higher longevity than the general population, but results about power (anaerobic) athletes are inconsistent.It remains unclear if high-intensity sports activities further increase life expectancy.
Competitive exercise does not induce cardiac damage in individuals with healthy hearts, but does induce physiological functional and structural cardiac adaptations which have positive effects on life expectancy
It appears that elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes survive longer than the general population, as indicated by lower mortality and higher longevity. |
http://www.ncbi.nlm.nih.gov/pubmed/21941025,http://www.ncbi.nlm.nih.gov/pubmed/24375374,http://www.ncbi.nlm.nih.gov/pubmed/23739676,http://www.ncbi.nlm.nih.gov/pubmed/17134822,http://www.ncbi.nlm.nih.gov/pubmed/16330673,http://www.ncbi.nlm.nih.gov/pubmed/22505648,http://www.ncbi.nlm.nih.gov/pubmed/16015586,http://www.ncbi.nlm.nih.gov/pubmed/16575874,http://www.ncbi.nlm.nih.gov/pubmed/17914578,http://www.ncbi.nlm.nih.gov/pubmed/17252556,http://www.ncbi.nlm.nih.gov/pubmed/23636686,http://www.ncbi.nlm.nih.gov/pubmed/12734317,http://www.ncbi.nlm.nih.gov/pubmed/18095286,http://www.ncbi.nlm.nih.gov/pubmed/25017995,http://www.ncbi.nlm.nih.gov/pubmed/12374981,http://www.ncbi.nlm.nih.gov/pubmed/18637271,http://www.ncbi.nlm.nih.gov/pubmed/21241820,http://www.ncbi.nlm.nih.gov/pubmed/23286483,http://www.ncbi.nlm.nih.gov/pubmed/15264237,http://www.ncbi.nlm.nih.gov/pubmed/18159594,http://www.ncbi.nlm.nih.gov/pubmed/22272343,http://www.ncbi.nlm.nih.gov/pubmed/25115397,http://www.ncbi.nlm.nih.gov/pubmed/22805308 | Is EZH2 associated with prostate cancer? | EZH2 is an epigenetic driver of prostate cancer. EZH2 dependent H3K27me3 is involved in epigenetic silencing of ID4 in prostate cancer. EZH2 plays an active role in this process by repressing the expression of TIMP2 and TIMP3 in prostate cancer cells. EZH2 knockdown markedly reduces the proteolytic activity of MMP-9, thereby decreasing the invasive activity of prostate cancer cells. Composite index of c-Myc, EZH2, and p27 can be valued as powerful prognosis parameter for intermediate-risk prostate cancer patients after the surgery, and postoperative adjuvant therapy can be adopted accordingly. |
http://www.ncbi.nlm.nih.gov/pubmed/18622044 | How does adrenergic signaling affect thyroid hormone receptors? | alpha1- adrenergic signalling increases TRalpha1 expression in nucleus and decreases TRalpha1 expression in cytosol. |
http://www.ncbi.nlm.nih.gov/pubmed/15647112,http://www.ncbi.nlm.nih.gov/pubmed/16844989,http://www.ncbi.nlm.nih.gov/pubmed/16844988,http://www.ncbi.nlm.nih.gov/pubmed/15980447,http://www.ncbi.nlm.nih.gov/pubmed/18434251,http://www.ncbi.nlm.nih.gov/pubmed/17597890,http://www.ncbi.nlm.nih.gov/pubmed/21328706,http://www.ncbi.nlm.nih.gov/pubmed/20952406,http://www.ncbi.nlm.nih.gov/pubmed/23297037,http://www.ncbi.nlm.nih.gov/pubmed/22540951,http://www.ncbi.nlm.nih.gov/pubmed/18989393,http://www.ncbi.nlm.nih.gov/pubmed/18006547,http://www.ncbi.nlm.nih.gov/pubmed/21426944,http://www.ncbi.nlm.nih.gov/pubmed/12169530,http://www.ncbi.nlm.nih.gov/pubmed/18783592,http://www.ncbi.nlm.nih.gov/pubmed/15141026,http://www.ncbi.nlm.nih.gov/pubmed/15980452,http://www.ncbi.nlm.nih.gov/pubmed/18467177,http://www.ncbi.nlm.nih.gov/pubmed/19421989,http://www.ncbi.nlm.nih.gov/pubmed/22987359,http://www.ncbi.nlm.nih.gov/pubmed/15070403,http://www.ncbi.nlm.nih.gov/pubmed/17597895,http://www.ncbi.nlm.nih.gov/pubmed/15769290,http://www.ncbi.nlm.nih.gov/pubmed/16351738,http://www.ncbi.nlm.nih.gov/pubmed/15215418,http://www.ncbi.nlm.nih.gov/pubmed/15215419,http://www.ncbi.nlm.nih.gov/pubmed/16225682,http://www.ncbi.nlm.nih.gov/pubmed/15261149,http://www.ncbi.nlm.nih.gov/pubmed/23555228,http://www.ncbi.nlm.nih.gov/pubmed/16542876,http://www.ncbi.nlm.nih.gov/pubmed/16597327,http://www.ncbi.nlm.nih.gov/pubmed/17557332,http://www.ncbi.nlm.nih.gov/pubmed/22247276,http://www.ncbi.nlm.nih.gov/pubmed/17958348 | What are the computational tools for the prediction of beta-barrel transmembrane proteins? | The computational tools for the prediction of beta-barrel transmembrane proteins (TMBs) are based mainly on the following methodologies: Hidden Markov Models (HMMs), hydrophobicity, structural data, k-nearest neighbor algorithm, Neural Networks and Support Vector Machines. The state-of-the-art computational tools for the prediction of TMBs are: BETAWARE, BOCTOPUS, BOMP, BTMX, HMM-B2TMR, OMPdb,PRED-TMBB, PROB, ProfTMB, PV, TMBETA-NET, TMB finding pipeline, TMBETADISC-RBF, TMBETAPRED-RBF, TMBHMM, TMB-Hunt, TMB-Hunt2, TMBKNN, TMBpro, transFold. |
http://www.ncbi.nlm.nih.gov/pubmed/25840010 | Which kinase is regulating stress granule biogenesis? | 5'-AMP-activated protein kinase alpha regulates stress granule biogenesisMultiple lines of evidence define the master metabolic regulator 5'-AMP-activated protein kinase alpha (AMPK-alpha) as a novel component of stress granules (SGs) that also controls their biogenesis. |
http://www.ncbi.nlm.nih.gov/pubmed/24348390,http://www.ncbi.nlm.nih.gov/pubmed/24064953,http://www.ncbi.nlm.nih.gov/pubmed/19261451,http://www.ncbi.nlm.nih.gov/pubmed/20215713,http://www.ncbi.nlm.nih.gov/pubmed/16804530,http://www.ncbi.nlm.nih.gov/pubmed/18941554,http://www.ncbi.nlm.nih.gov/pubmed/16570042,http://www.ncbi.nlm.nih.gov/pubmed/23261330,http://www.ncbi.nlm.nih.gov/pubmed/22882019,http://www.ncbi.nlm.nih.gov/pubmed/10375602,http://www.ncbi.nlm.nih.gov/pubmed/19494549,http://www.ncbi.nlm.nih.gov/pubmed/19126439,http://www.ncbi.nlm.nih.gov/pubmed/17902192,http://www.ncbi.nlm.nih.gov/pubmed/14648713,http://www.ncbi.nlm.nih.gov/pubmed/12527940,http://www.ncbi.nlm.nih.gov/pubmed/17851009,http://www.ncbi.nlm.nih.gov/pubmed/23095687 | What is the association between cell phone use and glioblastoma? | The association between cell phone use and incident glioblastoma remains unclear. Some studies have reported that cell phone use was associated with incident glioblastoma, and with reduced survival of patients diagnosed with glioblastoma. However, other studies have repeatedly replicated to find an association between cell phone use and glioblastoma. |
http://www.ncbi.nlm.nih.gov/pubmed/22337886,http://www.ncbi.nlm.nih.gov/pubmed/19158508,http://www.ncbi.nlm.nih.gov/pubmed/19850932,http://www.ncbi.nlm.nih.gov/pubmed/19887570,http://www.ncbi.nlm.nih.gov/pubmed/20888802,http://www.ncbi.nlm.nih.gov/pubmed/15537647,http://www.ncbi.nlm.nih.gov/pubmed/23776620,http://www.ncbi.nlm.nih.gov/pubmed/23646150,http://www.ncbi.nlm.nih.gov/pubmed/17896924,http://www.ncbi.nlm.nih.gov/pubmed/16940750,http://www.ncbi.nlm.nih.gov/pubmed/18687666,http://www.ncbi.nlm.nih.gov/pubmed/11782444,http://www.ncbi.nlm.nih.gov/pubmed/23657601,http://www.ncbi.nlm.nih.gov/pubmed/20028853,http://www.ncbi.nlm.nih.gov/pubmed/15655376 | Is there any cross-talk between the Wnt and the Akt pathways? | The Wnt/β-catenin and PI3K/Akt signaling pathways cross-talk mainly through the activity of GSK-3β, a common component of both pathways, but also through the activity of other signaling transducers, such as Cby or WISP-1. |
http://www.ncbi.nlm.nih.gov/pubmed/23480392,http://www.ncbi.nlm.nih.gov/pubmed/21708138,http://www.ncbi.nlm.nih.gov/pubmed/22497513,http://www.ncbi.nlm.nih.gov/pubmed/24312079,http://www.ncbi.nlm.nih.gov/pubmed/20378924,http://www.ncbi.nlm.nih.gov/pubmed/21248708,http://www.ncbi.nlm.nih.gov/pubmed/24297703,http://www.ncbi.nlm.nih.gov/pubmed/19087237,http://www.ncbi.nlm.nih.gov/pubmed/20085825,http://www.ncbi.nlm.nih.gov/pubmed/22700411,http://www.ncbi.nlm.nih.gov/pubmed/22173943,http://www.ncbi.nlm.nih.gov/pubmed/22551423,http://www.ncbi.nlm.nih.gov/pubmed/22493255,http://www.ncbi.nlm.nih.gov/pubmed/19688097,http://www.ncbi.nlm.nih.gov/pubmed/20226563,http://www.ncbi.nlm.nih.gov/pubmed/21316751,http://www.ncbi.nlm.nih.gov/pubmed/21490567,http://www.ncbi.nlm.nih.gov/pubmed/19549299,http://www.ncbi.nlm.nih.gov/pubmed/21406720 | Has the protein GFP been used in transgenesis for live protein imaging? | Yes, the stable transgenesis of genes encoding functional or spatially localized proteins, fused to fluorescent proteins such as green fluorescent protein (GFP) or red fluorescent protein (RFP), is an extremely important research tool in cell and developmental biology. |
http://www.ncbi.nlm.nih.gov/pubmed/24311433,http://www.ncbi.nlm.nih.gov/pubmed/18320030,http://www.ncbi.nlm.nih.gov/pubmed/22694955,http://www.ncbi.nlm.nih.gov/pubmed/21977908,http://www.ncbi.nlm.nih.gov/pubmed/22237428,http://www.ncbi.nlm.nih.gov/pubmed/22495932,http://www.ncbi.nlm.nih.gov/pubmed/20588305,http://www.ncbi.nlm.nih.gov/pubmed/20803659,http://www.ncbi.nlm.nih.gov/pubmed/22664655,http://www.ncbi.nlm.nih.gov/pubmed/23686718,http://www.ncbi.nlm.nih.gov/pubmed/23918391,http://www.ncbi.nlm.nih.gov/pubmed/21952424,http://www.ncbi.nlm.nih.gov/pubmed/23700380 | Is the Snord116 cluster associated with the Prader-Willi syndrome? | Yes, SNORD116 has a major role in Prader-Willi syndrome etiology. |
http://www.ncbi.nlm.nih.gov/pubmed/22244809,http://www.ncbi.nlm.nih.gov/pubmed/19515415,http://www.ncbi.nlm.nih.gov/pubmed/22113345,http://www.ncbi.nlm.nih.gov/pubmed/21114416,http://www.ncbi.nlm.nih.gov/pubmed/21251281,http://www.ncbi.nlm.nih.gov/pubmed/20837369,http://www.ncbi.nlm.nih.gov/pubmed/20336066,http://www.ncbi.nlm.nih.gov/pubmed/24157957,http://www.ncbi.nlm.nih.gov/pubmed/24016490,http://www.ncbi.nlm.nih.gov/pubmed/25407798,http://www.ncbi.nlm.nih.gov/pubmed/24682069,http://www.ncbi.nlm.nih.gov/pubmed/22514701,http://www.ncbi.nlm.nih.gov/pubmed/26093872 | Aleglitazar is agonist of which receptor? | Aleglitazar is a balanced peroxisome proliferator-activated receptor-α/γ agonist. |
http://www.ncbi.nlm.nih.gov/pubmed/22119737,http://www.ncbi.nlm.nih.gov/pubmed/25092222,http://www.ncbi.nlm.nih.gov/pubmed/20517833,http://www.ncbi.nlm.nih.gov/pubmed/22987135,http://www.ncbi.nlm.nih.gov/pubmed/25440180,http://www.ncbi.nlm.nih.gov/pubmed/19216760,http://www.ncbi.nlm.nih.gov/pubmed/24025405,http://www.ncbi.nlm.nih.gov/pubmed/25112803,http://www.ncbi.nlm.nih.gov/pubmed/23908839 | What are the main characteristics of Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)? | Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic cardiac disorder characterized by life-threatening arrhythmias induced by physical or emotional stress, in the absence structural heart abnormalities. The phenotype of CPVT is characterized by polymorphic ventricular arrhythmias under stress and it potentially leads to syncope and/or sudden cardiac death (SCD). Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a lethal, rare hereditary disease with an estimated prevalence of 1:10 000 and is caused by mutations in proteins controlling Ca(2+) homeostasis. To date, about 189 variants in 5 genes (RYR2, CASQ2, CALM1, TRND, and KCNJ2) have been associated with CPVT pathogenesis.Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic cardiac disorder characterized by life-threatening arrhythmias induced by physical or emotional stress, in the absence structural heart abnormalities. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a lethal, rare hereditary disease with an estimated prevalence of 1:10 000. The genetic variants that cause CPVT are usually highly penetrant. To date, about 189 variants in 5 genes (RYR2, CASQ2, CALM1, TRND, and KCNJ2) have been associated with CPVT pathogenesis. Catecholaminergic polymorphic ventricular tachycardia is a malignant disease, due to mutations in proteins controlling Ca(2+) homeostasis |
http://www.ncbi.nlm.nih.gov/pubmed/1828533,http://www.ncbi.nlm.nih.gov/pubmed/9790974,http://www.ncbi.nlm.nih.gov/pubmed/18396434,http://www.ncbi.nlm.nih.gov/pubmed/17158748,http://www.ncbi.nlm.nih.gov/pubmed/17286852,http://www.ncbi.nlm.nih.gov/pubmed/18851700 | Is poly (ADP- ribosylation) involved in transcriptional control? | Yes, poly (ADP- ribosylation) plays a role in the maintenance of transcriptional fidelity. |
http://www.ncbi.nlm.nih.gov/pubmed/18847340,http://www.ncbi.nlm.nih.gov/pubmed/17029347,http://www.ncbi.nlm.nih.gov/pubmed/17705883,http://www.ncbi.nlm.nih.gov/pubmed/22543491,http://www.ncbi.nlm.nih.gov/pubmed/17479073,http://www.ncbi.nlm.nih.gov/pubmed/3521193,http://www.ncbi.nlm.nih.gov/pubmed/15846536,http://www.ncbi.nlm.nih.gov/pubmed/19066110,http://www.ncbi.nlm.nih.gov/pubmed/9706722,http://www.ncbi.nlm.nih.gov/pubmed/19108757,http://www.ncbi.nlm.nih.gov/pubmed/16998274,http://www.ncbi.nlm.nih.gov/pubmed/21608279,http://www.ncbi.nlm.nih.gov/pubmed/22152574,http://www.ncbi.nlm.nih.gov/pubmed/7785750,http://www.ncbi.nlm.nih.gov/pubmed/22027241,http://www.ncbi.nlm.nih.gov/pubmed/18842226,http://www.ncbi.nlm.nih.gov/pubmed/9164696 | Is nimodipine recommended for prevention of vasospasm in aneurysmal subarachnoid hemorrhage patients? | Yes, nimodipine is recommended and FDA approved for prevention of vasospasm after aneurysmal subarachnoid hemorrhage. Multiple studies have demonstrated that nimodipine (administered orally or intravenously) is safe and effective for prevention of vasospasm, and reduce frequency of ischemic complications, lowered mortality and improved overall outcomes. Other preventive medication can be also effective for vasomotor prevention in aneurysmal subarachnoid hemorrhage patients. |
http://www.ncbi.nlm.nih.gov/pubmed/8782069,http://www.ncbi.nlm.nih.gov/pubmed/20451268,http://www.ncbi.nlm.nih.gov/pubmed/21219910 | what is the role of prostaglandins in cardiac regenaration after myocardial infarction? | Prostaglandins are involved in tissue regeneration after myocardial infarction and inhibitors of prostanoid production, such as aspirin and COX-2 inhibitors, have negative impact in this process. Furthermore, pharmacological interference with prostaglandin synthesis following myocardial infarction is associated with reduced fibrillar collagen formation. |
http://www.ncbi.nlm.nih.gov/pubmed/23382701,http://www.ncbi.nlm.nih.gov/pubmed/18003948,http://www.ncbi.nlm.nih.gov/pubmed/21724828,http://www.ncbi.nlm.nih.gov/pubmed/25464900,http://www.ncbi.nlm.nih.gov/pubmed/25079683,http://www.ncbi.nlm.nih.gov/pubmed/24105599,http://www.ncbi.nlm.nih.gov/pubmed/21474073,http://www.ncbi.nlm.nih.gov/pubmed/23428873,http://www.ncbi.nlm.nih.gov/pubmed/18977325,http://www.ncbi.nlm.nih.gov/pubmed/24797370,http://www.ncbi.nlm.nih.gov/pubmed/18511943,http://www.ncbi.nlm.nih.gov/pubmed/22190683,http://www.ncbi.nlm.nih.gov/pubmed/18285465,http://www.ncbi.nlm.nih.gov/pubmed/21741597,http://www.ncbi.nlm.nih.gov/pubmed/24795146,http://www.ncbi.nlm.nih.gov/pubmed/25417107,http://www.ncbi.nlm.nih.gov/pubmed/17675446,http://www.ncbi.nlm.nih.gov/pubmed/25359765 | What is the general function of H3K79 methylation? | ChIP-chip tiling arrays revealed that levels of all degrees of genic H3K79 methylation correlate with mRNA abundance and dynamically respond to changes in gene activity. ChIP-chip tiling arrays revealed that levels of all degrees of genic H3K79 methylation correlate with mRNA abundance and dynamically respond to changes in gene activity. Conversion of H3K79 monomethylation into di- and trimethylation correlated with the transition from low- to high-level gene transcription. Findings highlight several similarities between the patterning of H3K4 methylation and that of H3K79 methylation in mammalian chromatin.
Methylation of H3K79 is associated with chromatin at expressed genes, though it is unclear if this histone modification is required for transcription of all genes.H3K79 methylation is a histone modification that correlates with histone H4 hyperacetylation prior to histone-to-protamine transition, and is accompanied by chromatin reorganization, playing an important role in the regulation of cell proliferation. |
http://www.ncbi.nlm.nih.gov/pubmed/22918641,http://www.ncbi.nlm.nih.gov/pubmed/23425695,http://www.ncbi.nlm.nih.gov/pubmed/16982797,http://www.ncbi.nlm.nih.gov/pubmed/22956620,http://www.ncbi.nlm.nih.gov/pubmed/19770725,http://www.ncbi.nlm.nih.gov/pubmed/19714880,http://www.ncbi.nlm.nih.gov/pubmed/17850790,http://www.ncbi.nlm.nih.gov/pubmed/11419941,http://www.ncbi.nlm.nih.gov/pubmed/16865190,http://www.ncbi.nlm.nih.gov/pubmed/22871838,http://www.ncbi.nlm.nih.gov/pubmed/16488965,http://www.ncbi.nlm.nih.gov/pubmed/14574570,http://www.ncbi.nlm.nih.gov/pubmed/18334948,http://www.ncbi.nlm.nih.gov/pubmed/23422824,http://www.ncbi.nlm.nih.gov/pubmed/21087963,http://www.ncbi.nlm.nih.gov/pubmed/16923831,http://www.ncbi.nlm.nih.gov/pubmed/20375347,http://www.ncbi.nlm.nih.gov/pubmed/15952718,http://www.ncbi.nlm.nih.gov/pubmed/23482462,http://www.ncbi.nlm.nih.gov/pubmed/22300579 | Where can we find the protein lacritin? | The protein lacritin can be found in lacrimal and salivary glands as well as in tear fluid and in the thyroid. |
http://www.ncbi.nlm.nih.gov/pubmed/23626547,http://www.ncbi.nlm.nih.gov/pubmed/25055737,http://www.ncbi.nlm.nih.gov/pubmed/25271322,http://www.ncbi.nlm.nih.gov/pubmed/22448321,http://www.ncbi.nlm.nih.gov/pubmed/24916439,http://www.ncbi.nlm.nih.gov/pubmed/24969620,http://www.ncbi.nlm.nih.gov/pubmed/24652391,http://www.ncbi.nlm.nih.gov/pubmed/25347115,http://www.ncbi.nlm.nih.gov/pubmed/22588119,http://www.ncbi.nlm.nih.gov/pubmed/22262861,http://www.ncbi.nlm.nih.gov/pubmed/24828484,http://www.ncbi.nlm.nih.gov/pubmed/25330301,http://www.ncbi.nlm.nih.gov/pubmed/24562771,http://www.ncbi.nlm.nih.gov/pubmed/23426625,http://www.ncbi.nlm.nih.gov/pubmed/24991806,http://www.ncbi.nlm.nih.gov/pubmed/25485461,http://www.ncbi.nlm.nih.gov/pubmed/22455996 | Where can we find the protein dermcidin? | Dermcidin is a secretes protein found mainly in sweat but it is also found in serum.In previous work we reported the expression of Y-P30 \/ dermcidin in maternal peripheral blood mononuclear cells and the transport of the protein to the fetal brain. In this study we analyzed hormonal regulation of Y-P30 in human immune cells and expression of Y-P30 in the placenta. This article provides an overview on the identification, activity, 3D structure, and mechanism of action of human AMPs selected from the antimicrobial peptide database. the discovery of dermcidin-derived antimicrobial peptides in eccrine sweat demonstrated that sweat actively participates in the constitutive innate immune defense of human skin against infection. Several reports also state that peptides processed from the dermcidin precursor protein exhibit a range of other biological functions in neuronal and cancer cells. Using an immunoaffinity approach followed by multipoint validation, we identified the target of seriniquinone as the small protein, dermcidin. Hypertension and diabetes mellitus are considered to be two major atherosclerotic risk factors for coronary artery disease. ``Pustulosis palmaris et plantaris'', or palmoplantar pustulosis, is a chronic pustular dermatitis characterized by intraepidermal palmoplantar pustules. Semi-quantitative dot-blot analysis revealed higher concentrations of hCAP-18 \/ LL-37 in PPP-VF compared to healthy sweat. In conclusion, the expression of various AMPs is altered in acne vulgaris. |
http://www.ncbi.nlm.nih.gov/pubmed/7522195,http://www.ncbi.nlm.nih.gov/pubmed/9333577,http://www.ncbi.nlm.nih.gov/pubmed/11925409,http://www.ncbi.nlm.nih.gov/pubmed/20120938,http://www.ncbi.nlm.nih.gov/pubmed/18817910,http://www.ncbi.nlm.nih.gov/pubmed/7688977,http://www.ncbi.nlm.nih.gov/pubmed/18839465,http://www.ncbi.nlm.nih.gov/pubmed/11920888 | What is the triple screening test performed during pregnancy measuring? | Alpha-fetoprotein (AFP), human chorionic gonadotropin (hCG) and unconjugated estriol (uE3) |
http://www.ncbi.nlm.nih.gov/pubmed/21054594,http://www.ncbi.nlm.nih.gov/pubmed/22386826,http://www.ncbi.nlm.nih.gov/pubmed/22925379,http://www.ncbi.nlm.nih.gov/pubmed/21591526,http://www.ncbi.nlm.nih.gov/pubmed/20338870,http://www.ncbi.nlm.nih.gov/pubmed/14662775,http://www.ncbi.nlm.nih.gov/pubmed/21324833 | What are the generic versions of Viagra? | Generic versions of sildenafil are Elonza, Caverta, Zenegra-100, Vega Asia, Suhagra-100, Vega, Revatio. |
http://www.ncbi.nlm.nih.gov/pubmed/25561175,http://www.ncbi.nlm.nih.gov/pubmed/25567906,http://www.ncbi.nlm.nih.gov/pubmed/25963655 | Which protein interacts with the Ragulator-RAG GTPases to control mTOR activity? | Extensive functional proteomic analysis established SLC38A9 as an integral part of the Ragulator-RAG GTPases machinery that controls the activation of mTOR.SLC38A9 localizes with Rag-Ragulator complex components on lysosomes and associates with Rag GTPases in an amino acid-sensitive and nucleotide binding state-dependent manner. Depletion of SLC38A9 inhibits mTORC1 activity in the presence of amino acids and in response to amino acid replenishment following starvation. Thus SLC38A9 is a physical and functional component of the amino acid sensing machinery that controls the activation of mTOR. The serine/threonine kinase mTORC1 regulates cellular homeostasis in response to many cues, such as nutrient status and energy level. |
http://www.ncbi.nlm.nih.gov/pubmed/23527566,http://www.ncbi.nlm.nih.gov/pubmed/22261504,http://www.ncbi.nlm.nih.gov/pubmed/16107075,http://www.ncbi.nlm.nih.gov/pubmed/23514126,http://www.ncbi.nlm.nih.gov/pubmed/17291333,http://www.ncbi.nlm.nih.gov/pubmed/16848907,http://www.ncbi.nlm.nih.gov/pubmed/22521592,http://www.ncbi.nlm.nih.gov/pubmed/20127115,http://www.ncbi.nlm.nih.gov/pubmed/21993656,http://www.ncbi.nlm.nih.gov/pubmed/20671958,http://www.ncbi.nlm.nih.gov/pubmed/22434357,http://www.ncbi.nlm.nih.gov/pubmed/23533646,http://www.ncbi.nlm.nih.gov/pubmed/12531326,http://www.ncbi.nlm.nih.gov/pubmed/11257410,http://www.ncbi.nlm.nih.gov/pubmed/19179021 | Against which organisms has reverse vaccinology been used? | Reverse Vaccinology (RV) was first applied to serogroup B Neisseria meningitidis. This work induced further research of other pathogens in the same way: Porphyromonas gingivalis, Streptococcus pneumoniae, Chlamydia pneumoniae, Bacillus anthracis, group B streptococci, Helicobacter pylori and Mycobacterium tuberculosis. Concerning animal-affecting organisms, RV has been applied for vaccine design against Theileria parva, Brachyspira hyodysenteriae, Echinococcus granulosus, Ehrlichia ruminantium, Leishmania spp, Rhipicephalus microplus and Brucella melitensis. |
http://www.ncbi.nlm.nih.gov/pubmed/16096939,http://www.ncbi.nlm.nih.gov/pubmed/14676729,http://www.ncbi.nlm.nih.gov/pubmed/10663819,http://www.ncbi.nlm.nih.gov/pubmed/12922037,http://www.ncbi.nlm.nih.gov/pubmed/18704305,http://www.ncbi.nlm.nih.gov/pubmed/23696293,http://www.ncbi.nlm.nih.gov/pubmed/12218836 | Galassi classification is used for which disorder? | Galassi classification system is used to classify arachnoid cysts. |
http://www.ncbi.nlm.nih.gov/pubmed/25383198,http://www.ncbi.nlm.nih.gov/pubmed/21689988,http://www.ncbi.nlm.nih.gov/pubmed/23154636,http://www.ncbi.nlm.nih.gov/pubmed/12509211,http://www.ncbi.nlm.nih.gov/pubmed/23304207,http://www.ncbi.nlm.nih.gov/pubmed/11437309,http://www.ncbi.nlm.nih.gov/pubmed/23724071,http://www.ncbi.nlm.nih.gov/pubmed/21292560,http://www.ncbi.nlm.nih.gov/pubmed/10407891,http://www.ncbi.nlm.nih.gov/pubmed/25060169,http://www.ncbi.nlm.nih.gov/pubmed/23540417 | Describe Mozart effect. | The Mozart effect implies the enhancement of reasoning skills solving spatial problems in normal subjects after listening to Mozart's piano sonata K 448. |
http://www.ncbi.nlm.nih.gov/pubmed/24212518,http://www.ncbi.nlm.nih.gov/pubmed/17593839,http://www.ncbi.nlm.nih.gov/pubmed/23328875,http://www.ncbi.nlm.nih.gov/pubmed/21223698,http://www.ncbi.nlm.nih.gov/pubmed/21772622,http://www.ncbi.nlm.nih.gov/pubmed/21796024,http://www.ncbi.nlm.nih.gov/pubmed/22973387,http://www.ncbi.nlm.nih.gov/pubmed/25085251,http://www.ncbi.nlm.nih.gov/pubmed/25035829,http://www.ncbi.nlm.nih.gov/pubmed/17094910 | What is the purpose of the Tokuhashi scoring system? | Tokuhashi scoring system was developed to predict life expectancy of patients with spinal metastases. The revised Tokuhashi score has been widely used to evaluate indications for surgery and predict survival in patients with metastatic spinal disease. |
http://www.ncbi.nlm.nih.gov/pubmed/18954857,http://www.ncbi.nlm.nih.gov/pubmed/12010632,http://www.ncbi.nlm.nih.gov/pubmed/6327972,http://www.ncbi.nlm.nih.gov/pubmed/19074582,http://www.ncbi.nlm.nih.gov/pubmed/17164749,http://www.ncbi.nlm.nih.gov/pubmed/3359982,http://www.ncbi.nlm.nih.gov/pubmed/16384862,http://www.ncbi.nlm.nih.gov/pubmed/19903697,http://www.ncbi.nlm.nih.gov/pubmed/21239431,http://www.ncbi.nlm.nih.gov/pubmed/15148346,http://www.ncbi.nlm.nih.gov/pubmed/10329215,http://www.ncbi.nlm.nih.gov/pubmed/20937391,http://www.ncbi.nlm.nih.gov/pubmed/3756504,http://www.ncbi.nlm.nih.gov/pubmed/3707599,http://www.ncbi.nlm.nih.gov/pubmed/8301561,http://www.ncbi.nlm.nih.gov/pubmed/15572044,http://www.ncbi.nlm.nih.gov/pubmed/21670063 | Which compounds exist that are thyroid hormone analogs? | Compoounds such as 3,5-diiodo-L-thyronine, T2, GC-24, CO23, DITPA, 3,5-diiodothyropropionic acid, GC-1, Tetrac, 3,3',5,5'-tetraiodo-thyroacetic acid, KB- 2115, KB - 141, thyronamines, T4-agarose, CGS 23425, D-T3, 3,3',5-triiodo-D-thyronine, 3,5-T2, 3,5-diiodo-L-thyronine, DIT, 3,5-diiodo-L-tyrosine, MIT, 3-monoiodo-L-tyrosine, triac, 3, 3',5-triiodo-thyroacetic acid, 3,5-Diiodo-4-hydroxyphenylpropionic acid, DIHPA, 3,5-Dimethyl-3'-isopropyl-L-thyronine, DIMIT, 3,5-diiodo-3'-isopropylthyroacetic acid and IpTA2 are compounds that are thyroid hormone analogs. |
http://www.ncbi.nlm.nih.gov/pubmed/25974026,http://www.ncbi.nlm.nih.gov/pubmed/26105190,http://www.ncbi.nlm.nih.gov/pubmed/26316818,http://www.ncbi.nlm.nih.gov/pubmed/25553081,http://www.ncbi.nlm.nih.gov/pubmed/25671254,http://www.ncbi.nlm.nih.gov/pubmed/25913680 | Is lenvatinib effective for thyroid cancer? | Yes, lenvatinib is effective for thyroid cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/24327800,http://www.ncbi.nlm.nih.gov/pubmed/21123097,http://www.ncbi.nlm.nih.gov/pubmed/22695536,http://www.ncbi.nlm.nih.gov/pubmed/23678008,http://www.ncbi.nlm.nih.gov/pubmed/23358415,http://www.ncbi.nlm.nih.gov/pubmed/24272208,http://www.ncbi.nlm.nih.gov/pubmed/24289229,http://www.ncbi.nlm.nih.gov/pubmed/24183724,http://www.ncbi.nlm.nih.gov/pubmed/24302665,http://www.ncbi.nlm.nih.gov/pubmed/23318652,http://www.ncbi.nlm.nih.gov/pubmed/24319537,http://www.ncbi.nlm.nih.gov/pubmed/18485221,http://www.ncbi.nlm.nih.gov/pubmed/24298072,http://www.ncbi.nlm.nih.gov/pubmed/17132159,http://www.ncbi.nlm.nih.gov/pubmed/24026986,http://www.ncbi.nlm.nih.gov/pubmed/24324792,http://www.ncbi.nlm.nih.gov/pubmed/24296317 | What genes are related to breast cancer? | Breast cancer is a disease in which certain cells in the breast become abnormal and multiply without control or order to form a tumor. The most common form of breast cancer begins in cells lining the ducts that carry milk to the nipple (ductal cancer). Other forms of breast cancer begin in the glands that produce milk (lobular cancer) or in other parts of the breast.
Early breast cancer usually does not cause pain and may exhibit no noticeable symptoms. As the cancer progresses, signs and symptoms can include a lump or thickening in or near the breast; a change in the size or shape of the breast; nipple discharge, tenderness, or retraction (turning inward); and skin irritation, dimpling, or scaliness. These changes can occur as part of many different conditions, however. Having one or more of these symptoms does not mean that a person definitely has breast cancer.
In some cases, cancerous tumors can invade surrounding tissue and spread to other parts of the body. If breast cancer spreads, cancerous cells most often appear in the bones, liver, lungs, or brain. Tumors that begin at one site and then spread to other areas of the body are called metastatic cancers.
A small percentage of all breast cancers cluster in families. Hereditary cancers are those associated with inherited gene mutations. Hereditary breast cancers tend to occur earlier in life than noninherited (sporadic) cases and are more likely to involve both breasts.
Variations of the BRCA1, BRCA2, BRCT, and P53 genes increase the risk of developing breast cancer.
The and NFR2, HER2 and TOP2A genes are associated with breast cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/23616122,http://www.ncbi.nlm.nih.gov/pubmed/23241893,http://www.ncbi.nlm.nih.gov/pubmed/19098925,http://www.ncbi.nlm.nih.gov/pubmed/22338309,http://www.ncbi.nlm.nih.gov/pubmed/22322981,http://www.ncbi.nlm.nih.gov/pubmed/22815185,http://www.ncbi.nlm.nih.gov/pubmed/21243489,http://www.ncbi.nlm.nih.gov/pubmed/16527005,http://www.ncbi.nlm.nih.gov/pubmed/18632461,http://www.ncbi.nlm.nih.gov/pubmed/16188502,http://www.ncbi.nlm.nih.gov/pubmed/22401778,http://www.ncbi.nlm.nih.gov/pubmed/22815651,http://www.ncbi.nlm.nih.gov/pubmed/23139212,http://www.ncbi.nlm.nih.gov/pubmed/20671739,http://www.ncbi.nlm.nih.gov/pubmed/21623686,http://www.ncbi.nlm.nih.gov/pubmed/20703154,http://www.ncbi.nlm.nih.gov/pubmed/21677475 | To the ligand of which receptors does Denosumab (Prolia) bind? | Denosumab is a monoclonal antibody against the RANKL |
http://www.ncbi.nlm.nih.gov/pubmed/23741385,http://www.ncbi.nlm.nih.gov/pubmed/18501461,http://www.ncbi.nlm.nih.gov/pubmed/14579736,http://www.ncbi.nlm.nih.gov/pubmed/15258449,http://www.ncbi.nlm.nih.gov/pubmed/16468989,http://www.ncbi.nlm.nih.gov/pubmed/18556507,http://www.ncbi.nlm.nih.gov/pubmed/17407539,http://www.ncbi.nlm.nih.gov/pubmed/18473954,http://www.ncbi.nlm.nih.gov/pubmed/23822504,http://www.ncbi.nlm.nih.gov/pubmed/20532610,http://www.ncbi.nlm.nih.gov/pubmed/20471991,http://www.ncbi.nlm.nih.gov/pubmed/12771211,http://www.ncbi.nlm.nih.gov/pubmed/17646710,http://www.ncbi.nlm.nih.gov/pubmed/20601526,http://www.ncbi.nlm.nih.gov/pubmed/23347004,http://www.ncbi.nlm.nih.gov/pubmed/24128932,http://www.ncbi.nlm.nih.gov/pubmed/18592415,http://www.ncbi.nlm.nih.gov/pubmed/18566430,http://www.ncbi.nlm.nih.gov/pubmed/20429918,http://www.ncbi.nlm.nih.gov/pubmed/17553146 | List fluorescent reporter proteins. | Fluorescent and luminescent reporter genes have become popular tools for the real-time monitoring of gene expression in living cells:
green fluorescent protein
Timer
red fluorescent protein
yellow fluorescent protein
beta-phycoerythrin
coral fluorescent reporter protein
enhanced green fluorescent reporter protein
mCherry |
http://www.ncbi.nlm.nih.gov/pubmed/23354752,http://www.ncbi.nlm.nih.gov/pubmed/15850400,http://www.ncbi.nlm.nih.gov/pubmed/22556419,http://www.ncbi.nlm.nih.gov/pubmed/9328176,http://www.ncbi.nlm.nih.gov/pubmed/23463507,http://www.ncbi.nlm.nih.gov/pubmed/25294823,http://www.ncbi.nlm.nih.gov/pubmed/11856756,http://www.ncbi.nlm.nih.gov/pubmed/20345942,http://www.ncbi.nlm.nih.gov/pubmed/1309939,http://www.ncbi.nlm.nih.gov/pubmed/10608900,http://www.ncbi.nlm.nih.gov/pubmed/9603880,http://www.ncbi.nlm.nih.gov/pubmed/9756871,http://www.ncbi.nlm.nih.gov/pubmed/23481913,http://www.ncbi.nlm.nih.gov/pubmed/12717778,http://www.ncbi.nlm.nih.gov/pubmed/12717453,http://www.ncbi.nlm.nih.gov/pubmed/21178309,http://www.ncbi.nlm.nih.gov/pubmed/15475388,http://www.ncbi.nlm.nih.gov/pubmed/17545288,http://www.ncbi.nlm.nih.gov/pubmed/7739614,http://www.ncbi.nlm.nih.gov/pubmed/22092761,http://www.ncbi.nlm.nih.gov/pubmed/12767940,http://www.ncbi.nlm.nih.gov/pubmed/9140059,http://www.ncbi.nlm.nih.gov/pubmed/21111690,http://www.ncbi.nlm.nih.gov/pubmed/21147134,http://www.ncbi.nlm.nih.gov/pubmed/23043439,http://www.ncbi.nlm.nih.gov/pubmed/20880409,http://www.ncbi.nlm.nih.gov/pubmed/23376345,http://www.ncbi.nlm.nih.gov/pubmed/23006569,http://www.ncbi.nlm.nih.gov/pubmed/11892789,http://www.ncbi.nlm.nih.gov/pubmed/17616589,http://www.ncbi.nlm.nih.gov/pubmed/10954591,http://www.ncbi.nlm.nih.gov/pubmed/12531387 | By which mechanism MutT proteins act against DNA lesions in bacteria? | MutT proteins belong to a class of Nudix hydrolases. The common substrate structure for the proteins of the functionally diverse Nudix superfamily is nucleotide-diphosphate-X, where X is a large variety of leaving groups. The activities of Nudix hydrolases usually result in the release of an inorganic phosphate ion or of a product bearing a terminal phosphate moiety. MutT proteins hydrolyze 8-oxo-G nucleoside triphosphates/diphosphates to the corresponding nucleoside monophosphates and sanitize the nucleotide pool. MutT proteins cleave 8-oxo-dGTP (8-oxo-7,8-dihydro-2'-deoxyguanosine 5'-triphosphate) at the α-β position; they also cleave 8-oxo-dGTP at the β-γ phosphate bond at a rate of 3% of that recorded for hydrolysis at the α-β position. 8-oxo-dGTP induces A to C transversions when misincorporated in DNA opposite to template A. By hydrolyzing 8-oxo-dGTP before their incorporation into DNA, MutT proteins play a critical role in allowing bacteria to avoid A-to-C mutations, which are a hallmark of MutT deficiency. Thus, MutT proteins prevent oxidative DNA lesions, as part of the GO system. Oxidized nucleotides can occur when bacteria are exposed to reactive oxygen species. Also, reactive oxygen species are produced as side products of oxygen utilization, leading to the oxidation of nucleic acids and their precursor nucleotides. Distinct from the Escherichia coli MutT, which hydrolyzes 8-oxo-dGTP and 8-oxo-GTP, the mycobacterial proteins hydrolyze not only 8-oxo-dGTP and 8-oxo-GTP but also dCTP and 5-methyl-dCTP. Moreover, the hydrolysis of 8-oxo-dGTP and 8-oxo-GTP in mycobacteria seems to be catalysed in a two-stage mechanism, since MutT converts these oxidized nucleoside triphosphates to their corresponding nucleoside diphosphates, and not to monophosphates. |
http://www.ncbi.nlm.nih.gov/pubmed/9773800,http://www.ncbi.nlm.nih.gov/pubmed/16710748,http://www.ncbi.nlm.nih.gov/pubmed/10715294,http://www.ncbi.nlm.nih.gov/pubmed/9815790,http://www.ncbi.nlm.nih.gov/pubmed/12712458,http://www.ncbi.nlm.nih.gov/pubmed/15022287,http://www.ncbi.nlm.nih.gov/pubmed/12680157,http://www.ncbi.nlm.nih.gov/pubmed/8837815,http://www.ncbi.nlm.nih.gov/pubmed/19810975,http://www.ncbi.nlm.nih.gov/pubmed/20238235,http://www.ncbi.nlm.nih.gov/pubmed/10797257,http://www.ncbi.nlm.nih.gov/pubmed/9266439,http://www.ncbi.nlm.nih.gov/pubmed/9524096,http://www.ncbi.nlm.nih.gov/pubmed/21353747 | Was tamoxifen tested for treatment of glioma patients? | Yes, tamoxifen was tested for glioma treatment. However, clinical efficacy of tamoxifen in glioma patients remains unclear and should be tested in further studies. |
http://www.ncbi.nlm.nih.gov/pubmed/21839145,http://www.ncbi.nlm.nih.gov/pubmed/23149977,http://www.ncbi.nlm.nih.gov/pubmed/23704989,http://www.ncbi.nlm.nih.gov/pubmed/23272148,http://www.ncbi.nlm.nih.gov/pubmed/24706886,http://www.ncbi.nlm.nih.gov/pubmed/23658991,http://www.ncbi.nlm.nih.gov/pubmed/23939864,http://www.ncbi.nlm.nih.gov/pubmed/23266889,http://www.ncbi.nlm.nih.gov/pubmed/23104133,http://www.ncbi.nlm.nih.gov/pubmed/23166588 | Which transcription factors are known as the four (4) "Yamanaka factors" that have been used to create induced pluripotent stem cells (iPSCs)? | Fibroblasts can be reprogrammed into induced pluripotent stem cells (iPSCs) by the application of Yamanaka factors (OSKM). In particular, the mechanisms how the Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc) directly drive reprogramming and which additional components are involved are still not yet understood.Through the ectopic expression of four transcription factors, Oct4, Klf4, Sox2 and cMyc, human somatic cells can be converted to a pluripotent state, generating so-called induced pluripotent stem cells (iPSCs)(1-4). Delivery of the transcription factors Oct4, Klf4, Sox2 and c-Myc via integrating viral vectors has been widely employed to generate induced pluripotent stem cell (iPSC) lines from both normal and disease-specific somatic tissues, providing an invaluable resource for medical research and drug development. Through the ectopic expression of four transcription factors, Oct4, Klf4, Sox2 and cMyc, human somatic cells can be converted to a pluripotent state, generating so-called induced pluripotent stem cells (iPSCs)(1-4).Fibroblasts can be reprogrammed into induced pluripotent stem cells (iPSCs) by the application of Yamanaka factors (OSKM), but the mechanisms underlying this reprogramming remain poorly understood. |
http://www.ncbi.nlm.nih.gov/pubmed/20439829,http://www.ncbi.nlm.nih.gov/pubmed/19430927,http://www.ncbi.nlm.nih.gov/pubmed/18069998,http://www.ncbi.nlm.nih.gov/pubmed/20105694,http://www.ncbi.nlm.nih.gov/pubmed/19932820,http://www.ncbi.nlm.nih.gov/pubmed/21082266,http://www.ncbi.nlm.nih.gov/pubmed/22923700,http://www.ncbi.nlm.nih.gov/pubmed/22345679,http://www.ncbi.nlm.nih.gov/pubmed/21491341 | What is the role of anhedonia in coronary disease patients? | Anhedonia is associated with poor prognosis in patients with coronary disease. Namely, in patients with coronary disease, anhedonia was associated with increased mortality, greater risk for major cardiac event, impaired physical health status, more cardiac symptoms, more feelings of disability. These associations were independent from clinical and demographic factors. |
http://www.ncbi.nlm.nih.gov/pubmed/152622,http://www.ncbi.nlm.nih.gov/pubmed/11254789,http://www.ncbi.nlm.nih.gov/pubmed/22426027,http://www.ncbi.nlm.nih.gov/pubmed/7969211,http://www.ncbi.nlm.nih.gov/pubmed/23634190,http://www.ncbi.nlm.nih.gov/pubmed/25037206 | What is the clinical value of naltrexone in Parkinson's disease patients? | Naltrexone does not improve clinical features, including motor function, in Parkinson's disease patients. Naltrexone was shown to be effective for treatment of pathological gambling in Parkinson's disease patients. |
http://www.ncbi.nlm.nih.gov/pubmed/15879624,http://www.ncbi.nlm.nih.gov/pubmed/16702162,http://www.ncbi.nlm.nih.gov/pubmed/9704726,http://www.ncbi.nlm.nih.gov/pubmed/10408744,http://www.ncbi.nlm.nih.gov/pubmed/18094427 | What is the efficacy of oxaliplatin monotherapy in the management of colorectal cancer? | Oxaliplatin is a promising treatment option for patients with metastatic colorectal cancer. It appears to be particularly advantageous (in terms of response rate and duration of progression-free survival) when used in combination with fluorouracil/calcium folinate as both a first- and second-line option, although preliminary studies have failed to show any survival advantage over fluorouracil/calcium folinate alone. Promising results have been found in studies of the drug as monotherapy, and oxaliplatin may also prove useful in the neoadjuvant setting in patients with unresectable liver metastases; however, data are limited at present |
http://www.ncbi.nlm.nih.gov/pubmed/24044630,http://www.ncbi.nlm.nih.gov/pubmed/22325094,http://www.ncbi.nlm.nih.gov/pubmed/19875890,http://www.ncbi.nlm.nih.gov/pubmed/20864542,http://www.ncbi.nlm.nih.gov/pubmed/22404083,http://www.ncbi.nlm.nih.gov/pubmed/12297829,http://www.ncbi.nlm.nih.gov/pubmed/22198570,http://www.ncbi.nlm.nih.gov/pubmed/16940355,http://www.ncbi.nlm.nih.gov/pubmed/19458211,http://www.ncbi.nlm.nih.gov/pubmed/22048958,http://www.ncbi.nlm.nih.gov/pubmed/20581737,http://www.ncbi.nlm.nih.gov/pubmed/23843985,http://www.ncbi.nlm.nih.gov/pubmed/21176403,http://www.ncbi.nlm.nih.gov/pubmed/21995947,http://www.ncbi.nlm.nih.gov/pubmed/20607864,http://www.ncbi.nlm.nih.gov/pubmed/17216601 | Are there any animal models for Niemann-Pick C1 disease? | Yes, murine models of Niemann-Pick type C disease (NPC) exist. They are either homozygous or heterozygous NPC1-deficient [NPC1 (-/-)]/ [NPC1 (+/-)] mouse models. |
http://www.ncbi.nlm.nih.gov/pubmed/15371550,http://www.ncbi.nlm.nih.gov/pubmed/16034473,http://www.ncbi.nlm.nih.gov/pubmed/21841785 | Which type of genes are modulated by SATB1? | Lack of effector T cell (T(eff) cell) function and gain of suppressive activity by T(reg) cells are dependent on the transcriptional program induced by Foxp3. Here we report that repression of SATB1, a genome organizer that regulates chromatin structure and gene expression, was crucial for the phenotype and function of T(reg) cells. Release of SATB1 from the control of Foxp3 in T(reg) cells caused loss of suppressive function, establishment of transcriptional T(eff) cell programs and induction of T(eff) cell cytokines. At an Associative t-test threshold of PRepression of the genome organizer SATB1 in regulatory T cells is required for suppressive function and inhibition of effector differentiationRelease of SATB1 from the control of Foxp3 in T(reg) cells caused loss of suppressive function, establishment of transcriptional T(eff) cell programs and induction of T(eff) cell cytokines. |
http://www.ncbi.nlm.nih.gov/pubmed/22711713,http://www.ncbi.nlm.nih.gov/pubmed/20392785,http://www.ncbi.nlm.nih.gov/pubmed/23082154,http://www.ncbi.nlm.nih.gov/pubmed/19606230,http://www.ncbi.nlm.nih.gov/pubmed/12503030,http://www.ncbi.nlm.nih.gov/pubmed/21709140,http://www.ncbi.nlm.nih.gov/pubmed/18534031,http://www.ncbi.nlm.nih.gov/pubmed/19920112,http://www.ncbi.nlm.nih.gov/pubmed/19435924,http://www.ncbi.nlm.nih.gov/pubmed/22580986,http://www.ncbi.nlm.nih.gov/pubmed/11148461,http://www.ncbi.nlm.nih.gov/pubmed/19624808,http://www.ncbi.nlm.nih.gov/pubmed/22658319 | Does HER2 under-expression lead to favorable response to trastuzumab? | No, trastuzumab is effective only in cancers where Her2 is over-expessed. |
http://www.ncbi.nlm.nih.gov/pubmed/9886562,http://www.ncbi.nlm.nih.gov/pubmed/22840402,http://www.ncbi.nlm.nih.gov/pubmed/22718948,http://www.ncbi.nlm.nih.gov/pubmed/17270048,http://www.ncbi.nlm.nih.gov/pubmed/12490325,http://www.ncbi.nlm.nih.gov/pubmed/22840393,http://www.ncbi.nlm.nih.gov/pubmed/22916204,http://www.ncbi.nlm.nih.gov/pubmed/23129630,http://www.ncbi.nlm.nih.gov/pubmed/8785513,http://www.ncbi.nlm.nih.gov/pubmed/23243023,http://www.ncbi.nlm.nih.gov/pubmed/20459797,http://www.ncbi.nlm.nih.gov/pubmed/24035497,http://www.ncbi.nlm.nih.gov/pubmed/22858678,http://www.ncbi.nlm.nih.gov/pubmed/22684254,http://www.ncbi.nlm.nih.gov/pubmed/23073843 | Which are the most abundant human lincRNA? | MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) locus is misregulated in many human cancers and produces an abundant long nuclear-retained noncoding RNA. MALAT/NEAT2 highly abundant, its expression is strongly regulated in many tumor entities including lung adenocarcinoma and hepatocellular carcinoma as well as physiological processes, and it is associated with many RNA binding proteins and highly conserved throughout evolution. H19 large intergenic non-coding RNA (lincRNA) is one of the most highly abundant and conserved transcripts in mammalian development, being expressed in both embryonic and extra-embryonic cell lineages, yet its physiological function is unknown. Our genome-wide screens in two mammalian species reveal no more than three abundant large non-coding polyadenylated RNAs in the nucleus; the canonical large noncoding RNA XIST and NEAT1 and NEAT2. |
http://www.ncbi.nlm.nih.gov/pubmed/25493340,http://www.ncbi.nlm.nih.gov/pubmed/25186273,http://www.ncbi.nlm.nih.gov/pubmed/23234452,http://www.ncbi.nlm.nih.gov/pubmed/23402890,http://www.ncbi.nlm.nih.gov/pubmed/22693285,http://www.ncbi.nlm.nih.gov/pubmed/25802884,http://www.ncbi.nlm.nih.gov/pubmed/23255504,http://www.ncbi.nlm.nih.gov/pubmed/22499950,http://www.ncbi.nlm.nih.gov/pubmed/21131974 | Which is the molecular function of the protein CCDC40? | The coiled-coil domain containing protein CCDC40 is essential for motile cilia function and left-right axis formation and mutations in CCDC39 and CCDC40 are the major cause of primary ciliary dyskinesia with axonemal disorganization and absent inner dynein arms. |
http://www.ncbi.nlm.nih.gov/pubmed/21947558,http://www.ncbi.nlm.nih.gov/pubmed/23387883,http://www.ncbi.nlm.nih.gov/pubmed/19761698 | Can administration of the thyrotropin releasing hormone reduce fatigue in cancer patients? | yes, in cancer patients, thyrotropin releasing hormone (TRH) administration was associated with significant improvement in cancer related fatigue levels as measured by the Visual Analog Scale-Energy, fatigue and vigor subscales of the POMS, and the fatigue subscale of FACIT-F. TRH administration was safe and tolerable in the treatment of cancer-related with a positive impact on quality of life, suggesting the need for further studies investigating TRH for treatment of fatigue in cancer patients. |
http://www.ncbi.nlm.nih.gov/pubmed/22058406,http://www.ncbi.nlm.nih.gov/pubmed/11487702,http://www.ncbi.nlm.nih.gov/pubmed/20505370,http://www.ncbi.nlm.nih.gov/pubmed/17660570,http://www.ncbi.nlm.nih.gov/pubmed/11459824,http://www.ncbi.nlm.nih.gov/pubmed/23021223,http://www.ncbi.nlm.nih.gov/pubmed/15282033,http://www.ncbi.nlm.nih.gov/pubmed/9584105,http://www.ncbi.nlm.nih.gov/pubmed/18488247,http://www.ncbi.nlm.nih.gov/pubmed/12121623,http://www.ncbi.nlm.nih.gov/pubmed/12151602 | What is the role of chromomethylases in plants? | Chromomethylases (CMTs), which constitute a plant-specific DNA (cytosine-5)-methyltransferase family, are involved primarily in the maintenance of symmetrical CpNpG (N = A, T, C, or G) methylation and they also play a role in de novo methylation. CMTs are characterized by the presence of a chromatin-associated domain (chromodomain) inserted within the catalytic protein motifs I and IV. CMTs have likely evolved because of the high levels of CpNpG methylation present in plant genomes relative to animal genomes. The targeting of CMT methylation is accomplished by short interfering RNA (siRNA) pathways and histone methylation (H3K9, H3K27). It has been shown that transposons are in vivo targets of CMT-dependent methylation, suggesting that CMTs play a role in the plant genome surveillance. In Arabidopsis, CMTs play a key role in egg cell reprogramming and normal embryogenesis during the first few divisions of the zygote by mediating transposon and euchromatin epigenetic gene silencing. In tomatoes, CMTs are preferentially expressed in the pericarp during fruit development which suggests involvement of CMTs in the locus-specific control of methylation in the pericarp during fruit growth. |
http://www.ncbi.nlm.nih.gov/pubmed/25272063,http://www.ncbi.nlm.nih.gov/pubmed/25640947,http://www.ncbi.nlm.nih.gov/pubmed/26155681,http://www.ncbi.nlm.nih.gov/pubmed/25543853,http://www.ncbi.nlm.nih.gov/pubmed/25149981,http://www.ncbi.nlm.nih.gov/pubmed/24815764,http://www.ncbi.nlm.nih.gov/pubmed/25542083,http://www.ncbi.nlm.nih.gov/pubmed/25964558,http://www.ncbi.nlm.nih.gov/pubmed/24293118,http://www.ncbi.nlm.nih.gov/pubmed/25661742,http://www.ncbi.nlm.nih.gov/pubmed/24669820,http://www.ncbi.nlm.nih.gov/pubmed/25541178,http://www.ncbi.nlm.nih.gov/pubmed/24482305 | Is curcumin a phytochemical? | Yes, curcumin is a phytochemical derived from rhizome of turmeric Curcuma longa. |
http://www.ncbi.nlm.nih.gov/pubmed/12140362,http://www.ncbi.nlm.nih.gov/pubmed/21543988,http://www.ncbi.nlm.nih.gov/pubmed/10235015,http://www.ncbi.nlm.nih.gov/pubmed/26523262,http://www.ncbi.nlm.nih.gov/pubmed/24401931,http://www.ncbi.nlm.nih.gov/pubmed/26109568,http://www.ncbi.nlm.nih.gov/pubmed/22711159,http://www.ncbi.nlm.nih.gov/pubmed/8596595 | What is Cerebral Cavernous Malformation? | Cerebral cavernous malformation (CCM) is a disease of the central nervous system causing hemorrhage-prone multiple lumen vascular malformations and very severe neurological consequencesCerebral cavernous malformation (CCM) is a disease of the central nervous system causing hemorrhage-prone multiple lumen vascular malformations and very severe neurological consequences Cerebral cavernous malformations (CMs) are vascular malformations of the central nervous system, causing hemorrhagic strokes, seizures, and neurological deficits. |
http://www.ncbi.nlm.nih.gov/pubmed/12955722,http://www.ncbi.nlm.nih.gov/pubmed/9521584,http://www.ncbi.nlm.nih.gov/pubmed/10090479,http://www.ncbi.nlm.nih.gov/pubmed/12552564,http://www.ncbi.nlm.nih.gov/pubmed/23146055,http://www.ncbi.nlm.nih.gov/pubmed/20453460,http://www.ncbi.nlm.nih.gov/pubmed/20089964,http://www.ncbi.nlm.nih.gov/pubmed/24604962,http://www.ncbi.nlm.nih.gov/pubmed/19367192,http://www.ncbi.nlm.nih.gov/pubmed/19264559,http://www.ncbi.nlm.nih.gov/pubmed/11091222,http://www.ncbi.nlm.nih.gov/pubmed/11110674,http://www.ncbi.nlm.nih.gov/pubmed/25002988,http://www.ncbi.nlm.nih.gov/pubmed/10807541,http://www.ncbi.nlm.nih.gov/pubmed/15453041,http://www.ncbi.nlm.nih.gov/pubmed/9565158,http://www.ncbi.nlm.nih.gov/pubmed/21438918,http://www.ncbi.nlm.nih.gov/pubmed/12389351,http://www.ncbi.nlm.nih.gov/pubmed/16238440,http://www.ncbi.nlm.nih.gov/pubmed/21956823,http://www.ncbi.nlm.nih.gov/pubmed/15657175,http://www.ncbi.nlm.nih.gov/pubmed/12827451,http://www.ncbi.nlm.nih.gov/pubmed/9721219,http://www.ncbi.nlm.nih.gov/pubmed/22480464 | Is Fanconi anemia presented as a genetically and clinically heterogeneous disease entity? | Fanconi anemia (FA), an autosomal recessive disorder characterized by a progressive pancytopenia associated with congenital anomalies and high predisposition to malignancies, is a genetically and clinically heterogeneous disease. At least eight complementation groups (FA-A to FA-H) have been identified Fanconi anaemia (FA) is a rare, autosomal recessive, genetically complex, DNA repair deficiency syndrome in man. Patients with FA exhibit a heterogeneous spectrum of clinical features. The most significant and consistent phenotypic characteristics are stem cell loss, causing progressive bone marrow failure and sterility, diverse developmental abnormalities and a profound predisposition to neoplasia. To date, 15 genes have been identified, biallelic disruption of any one of which results in this clinically defined syndrome. |
http://www.ncbi.nlm.nih.gov/pubmed/24558442 | Which protein pathway is regulating SGK1-mediated phosphorylation of FOXO3a to control cell proliferation? | mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FOXO3a at Ser314. |
http://www.ncbi.nlm.nih.gov/pubmed/21905773,http://www.ncbi.nlm.nih.gov/pubmed/21801998,http://www.ncbi.nlm.nih.gov/pubmed/19723879,http://www.ncbi.nlm.nih.gov/pubmed/20965848,http://www.ncbi.nlm.nih.gov/pubmed/23792643 | Which drugs have been found effective for the treatment of chordoma? | Established chordoma cell lines, and patient-derived primary cell cultures, as well as chordoma tumors in vivo were found to be sensitive to treatment with bortezomib, vincristine, doxorubicin, etoposide, cisplatin, fludarabine and SD-1029 Stat3 inhibitor. Moreover, percutaneous intratumoral injection with pingyangmycin lipiodol emulsion was shown to be effective against chordoma. It should be stressed that combination treatment with the use of the above drugs was always able to increase the therapeutic potency. |
http://www.ncbi.nlm.nih.gov/pubmed/23474818,http://www.ncbi.nlm.nih.gov/pubmed/25216585,http://www.ncbi.nlm.nih.gov/pubmed/19338576,http://www.ncbi.nlm.nih.gov/pubmed/20699327,http://www.ncbi.nlm.nih.gov/pubmed/25429138,http://www.ncbi.nlm.nih.gov/pubmed/19815002,http://www.ncbi.nlm.nih.gov/pubmed/24090136,http://www.ncbi.nlm.nih.gov/pubmed/26557057,http://www.ncbi.nlm.nih.gov/pubmed/21280085,http://www.ncbi.nlm.nih.gov/pubmed/24804206,http://www.ncbi.nlm.nih.gov/pubmed/22879928,http://www.ncbi.nlm.nih.gov/pubmed/19765185 | Which components of the stress granules are known to be related to motor neuron degeneration in Amyotrophic Lateral Sclerosis? | Of note, both ALS and FTD are characterized by pathological inclusions, where some well-known SG markers localize with the ALS related proteins TDP-43 and FUS.TDP-43 and FUS have been identified as key proteins in the pathogenesis of some cases of ALS. Although their role in motor neuron degeneration is not yet known, TDP-43 and FUS have been shown to accumulate in RNA stress granules (SGs) in cell models and in spinal cord tissue from Amyotrophic Lateral Sclerosis (ALS) patients. |
http://www.ncbi.nlm.nih.gov/pubmed/22069375 | Is there evidence for de novo genesis of enhancers in vertebrates? | Yes. |
http://www.ncbi.nlm.nih.gov/pubmed/12486284,http://www.ncbi.nlm.nih.gov/pubmed/8491310,http://www.ncbi.nlm.nih.gov/pubmed/9381026,http://www.ncbi.nlm.nih.gov/pubmed/11022396,http://www.ncbi.nlm.nih.gov/pubmed/17584779,http://www.ncbi.nlm.nih.gov/pubmed/10953647,http://www.ncbi.nlm.nih.gov/pubmed/14638887,http://www.ncbi.nlm.nih.gov/pubmed/16416710,http://www.ncbi.nlm.nih.gov/pubmed/25080137 | Which could be some of the possible causes of hypersomnia? | Sleep-wake disturbances (SWD) with hypersomnia are common after traumatic brain injury (TBI), with decreased CSF levels of hypocretin-1, a wake-promoting neurotransmitter, in cases of sleep apnea, as well as in up to half the patients with dementia, particularly in vascular dementia, Korsakow syndrome, Parkinson's disease, and depression, where the alteration of sleep architecture may be pronounced, whereas in Alzheimer's disease prominent hypersomnolence or insomnia is typically only found in later stages of the diseases. |
http://www.ncbi.nlm.nih.gov/pubmed/12407171,http://www.ncbi.nlm.nih.gov/pubmed/18483489,http://www.ncbi.nlm.nih.gov/pubmed/16103108,http://www.ncbi.nlm.nih.gov/pubmed/9874792,http://www.ncbi.nlm.nih.gov/pubmed/22541691,http://www.ncbi.nlm.nih.gov/pubmed/12170777,http://www.ncbi.nlm.nih.gov/pubmed/11679590,http://www.ncbi.nlm.nih.gov/pubmed/17091579,http://www.ncbi.nlm.nih.gov/pubmed/12934068,http://www.ncbi.nlm.nih.gov/pubmed/18544666,http://www.ncbi.nlm.nih.gov/pubmed/11551979,http://www.ncbi.nlm.nih.gov/pubmed/10888847,http://www.ncbi.nlm.nih.gov/pubmed/15970694,http://www.ncbi.nlm.nih.gov/pubmed/12933355,http://www.ncbi.nlm.nih.gov/pubmed/23139158,http://www.ncbi.nlm.nih.gov/pubmed/15723613,http://www.ncbi.nlm.nih.gov/pubmed/11553704,http://www.ncbi.nlm.nih.gov/pubmed/11489831,http://www.ncbi.nlm.nih.gov/pubmed/18955972,http://www.ncbi.nlm.nih.gov/pubmed/14555221,http://www.ncbi.nlm.nih.gov/pubmed/10511707,http://www.ncbi.nlm.nih.gov/pubmed/11032171,http://www.ncbi.nlm.nih.gov/pubmed/16284213,http://www.ncbi.nlm.nih.gov/pubmed/15711100,http://www.ncbi.nlm.nih.gov/pubmed/21238939,http://www.ncbi.nlm.nih.gov/pubmed/15967022,http://www.ncbi.nlm.nih.gov/pubmed/11996667,http://www.ncbi.nlm.nih.gov/pubmed/10794589,http://www.ncbi.nlm.nih.gov/pubmed/14646471,http://www.ncbi.nlm.nih.gov/pubmed/10739653,http://www.ncbi.nlm.nih.gov/pubmed/18729734,http://www.ncbi.nlm.nih.gov/pubmed/17181147,http://www.ncbi.nlm.nih.gov/pubmed/15450935,http://www.ncbi.nlm.nih.gov/pubmed/22633487,http://www.ncbi.nlm.nih.gov/pubmed/20846841,http://www.ncbi.nlm.nih.gov/pubmed/17013363,http://www.ncbi.nlm.nih.gov/pubmed/16622074,http://www.ncbi.nlm.nih.gov/pubmed/16700650,http://www.ncbi.nlm.nih.gov/pubmed/11573949,http://www.ncbi.nlm.nih.gov/pubmed/19473994,http://www.ncbi.nlm.nih.gov/pubmed/17082813 | What is the function of caspases? | Caspases are intracellular proteases that propagate programmed cell death, proliferation, and inflammation. |
http://www.ncbi.nlm.nih.gov/pubmed/18552163,http://www.ncbi.nlm.nih.gov/pubmed/23085512,http://www.ncbi.nlm.nih.gov/pubmed/24132636,http://www.ncbi.nlm.nih.gov/pubmed/20018082,http://www.ncbi.nlm.nih.gov/pubmed/19925440,http://www.ncbi.nlm.nih.gov/pubmed/12721663,http://www.ncbi.nlm.nih.gov/pubmed/21314842,http://www.ncbi.nlm.nih.gov/pubmed/23369981,http://www.ncbi.nlm.nih.gov/pubmed/17660584,http://www.ncbi.nlm.nih.gov/pubmed/23472207,http://www.ncbi.nlm.nih.gov/pubmed/18021318 | Is TNNI3K a cardiac-specific protein? | Yes, TNNI3K is highly expressed in heart but is undetectable in other tissues. |
http://www.ncbi.nlm.nih.gov/pubmed/24462468,http://www.ncbi.nlm.nih.gov/pubmed/24656819,http://www.ncbi.nlm.nih.gov/pubmed/23809990,http://www.ncbi.nlm.nih.gov/pubmed/24685139,http://www.ncbi.nlm.nih.gov/pubmed/22850673,http://www.ncbi.nlm.nih.gov/pubmed/24634216,http://www.ncbi.nlm.nih.gov/pubmed/24879017,http://www.ncbi.nlm.nih.gov/pubmed/24532715,http://www.ncbi.nlm.nih.gov/pubmed/22279046,http://www.ncbi.nlm.nih.gov/pubmed/19948482,http://www.ncbi.nlm.nih.gov/pubmed/22850674,http://www.ncbi.nlm.nih.gov/pubmed/15342490 | How does Rif1 regulate DNA replication? | Rif1 (Rap1-interacting-factor-1), originally identified as a telomere-binding factor in yeast, is a critical determinant of the replication timing programme in human cells. Rif1 tightly binds to nuclear-insoluble structures at late-M-to-early-G1 and regulates chromatin-loop sizes. Furthermore, Rif1 colocalizes specifically with the mid-S replication foci. Thus, Rif1 establishes the mid-S replication domains that are restrained from being activated at early-S-phase. Overall, Rif1 plays crucial roles in determining the replication timing domain structures in human cells through regulating higher-order chromatin architecture. This function of Rif1 depends on its interaction with PP1 phosphatases and the PP1/Rif1 interaction is downregulated by the phosphorylation of Rif1, most likely by CDK/DDK. |
http://www.ncbi.nlm.nih.gov/pubmed/18378181,http://www.ncbi.nlm.nih.gov/pubmed/18160615,http://www.ncbi.nlm.nih.gov/pubmed/20485963,http://www.ncbi.nlm.nih.gov/pubmed/1546275,http://www.ncbi.nlm.nih.gov/pubmed/8277060 | Is factor XI deficient in Hemophilia C? | Factor XI deficiency is associated with a bleeding tendency called Hemophilia C. |
http://www.ncbi.nlm.nih.gov/pubmed/23567359,http://www.ncbi.nlm.nih.gov/pubmed/23496382,http://www.ncbi.nlm.nih.gov/pubmed/16313685,http://www.ncbi.nlm.nih.gov/pubmed/17979710,http://www.ncbi.nlm.nih.gov/pubmed/23767452,http://www.ncbi.nlm.nih.gov/pubmed/20036949 | What is known about food intolerance and gluten ? | Celiac disease, with a prevalence around 1% of the general population, is the most common genetically-induced food intolerance in the world. Triggered by the ingestion of gluten in genetically predisposed individuals.
Emerging research into a syndrome known as nonceliac gluten sensitivity suggests a heterogeneous condition with some features of celiac disease but often categorized as FGIDs, including IBS.Coeliac disease is a multifactorial disease characterized by a dysregulated immune response to ingested wheat gluten and related cereal proteins. With an incidence of about 1% of the general population, it is considered the most common food intolerance disorder.Emerging research into a syndrome known as nonceliac gluten sensitivity suggests a heterogeneous condition with some features of celiac disease but often categorized as FGIDs, including IBS. |
http://www.ncbi.nlm.nih.gov/pubmed/15834508,http://www.ncbi.nlm.nih.gov/pubmed/12631670,http://www.ncbi.nlm.nih.gov/pubmed/14633923,http://www.ncbi.nlm.nih.gov/pubmed/11471546,http://www.ncbi.nlm.nih.gov/pubmed/15294878,http://www.ncbi.nlm.nih.gov/pubmed/12574515,http://www.ncbi.nlm.nih.gov/pubmed/20009762,http://www.ncbi.nlm.nih.gov/pubmed/16145050,http://www.ncbi.nlm.nih.gov/pubmed/20633936,http://www.ncbi.nlm.nih.gov/pubmed/9035203,http://www.ncbi.nlm.nih.gov/pubmed/11434563,http://www.ncbi.nlm.nih.gov/pubmed/12355085,http://www.ncbi.nlm.nih.gov/pubmed/9094028,http://www.ncbi.nlm.nih.gov/pubmed/18693272,http://www.ncbi.nlm.nih.gov/pubmed/11484199,http://www.ncbi.nlm.nih.gov/pubmed/16618617,http://www.ncbi.nlm.nih.gov/pubmed/10664228,http://www.ncbi.nlm.nih.gov/pubmed/10792313,http://www.ncbi.nlm.nih.gov/pubmed/14669347,http://www.ncbi.nlm.nih.gov/pubmed/22132166,http://www.ncbi.nlm.nih.gov/pubmed/21915282,http://www.ncbi.nlm.nih.gov/pubmed/11302967,http://www.ncbi.nlm.nih.gov/pubmed/8852660,http://www.ncbi.nlm.nih.gov/pubmed/10964697 | Are EDNRB mutations involved in the development of Hirschsprung disease? | Although mutations in eight different genes (EDNRB, EDN3, ECE1, SOX10, RET, GDNF, NTN, SIP1) have been identified in affected individuals, it is now clear that RET and EDNRB are the primary genes implicated in the etiology of HSCR. Mutations in genes of the RET receptor tyrosine kinase and endothelin receptor B (EDNRB) signaling pathways have been shown to be associated in HSCR patients. Molecular genetic analyses have revealed that interactions between mutations in the genes encoding the RET receptor tyrosine kinase and the endothelin receptor type B (EDNRB) are central to the genesis of HSCR.Hirschsprung's disease (HSCR) is one the most common congenital intestinal disease, which leads to aganglionic megacolon in the early childhood. Several susceptibility genes have been identified, including RET protooncogene and its ligand, glial cell derived neutrophic factor (GDNF), Sox 10, Endothelin-3 (EDN3) and its receptor B (EDNRB). More specifically, EDNRB mutations are found in 5% of familial or sporadic HSCR. |
http://www.ncbi.nlm.nih.gov/pubmed/24205807,http://www.ncbi.nlm.nih.gov/pubmed/23415822,http://www.ncbi.nlm.nih.gov/pubmed/20307404 | What is known about the effectiveness of electronic food diaries ? | Electronic dietary records were better than food diaries in terms of fat percentage reduction in our trials, indicating that teledietetics increases healthy-eating awareness. |
http://www.ncbi.nlm.nih.gov/pubmed/25524600,http://www.ncbi.nlm.nih.gov/pubmed/25619640,http://www.ncbi.nlm.nih.gov/pubmed/22116711,http://www.ncbi.nlm.nih.gov/pubmed/21307199,http://www.ncbi.nlm.nih.gov/pubmed/23954445,http://www.ncbi.nlm.nih.gov/pubmed/23567751,http://www.ncbi.nlm.nih.gov/pubmed/25116390 | Can the apoptosis regulator BAX trigger the release of cytochrome c? | Yes, altered Bax conformation trigger its redistribution from the cytosol to mitochondria. Subsequently, cytochrome c is released from mitochondria to cytosol. |
http://www.ncbi.nlm.nih.gov/pubmed/10906272,http://www.ncbi.nlm.nih.gov/pubmed/8943015,http://www.ncbi.nlm.nih.gov/pubmed/15618412,http://www.ncbi.nlm.nih.gov/pubmed/21135095,http://www.ncbi.nlm.nih.gov/pubmed/21871892,http://www.ncbi.nlm.nih.gov/pubmed/24817869,http://www.ncbi.nlm.nih.gov/pubmed/23907667,http://www.ncbi.nlm.nih.gov/pubmed/17727818,http://www.ncbi.nlm.nih.gov/pubmed/11139575,http://www.ncbi.nlm.nih.gov/pubmed/16573238,http://www.ncbi.nlm.nih.gov/pubmed/21945179,http://www.ncbi.nlm.nih.gov/pubmed/20038635,http://www.ncbi.nlm.nih.gov/pubmed/12641210,http://www.ncbi.nlm.nih.gov/pubmed/22812526,http://www.ncbi.nlm.nih.gov/pubmed/11359923,http://www.ncbi.nlm.nih.gov/pubmed/17872946,http://www.ncbi.nlm.nih.gov/pubmed/23236186,http://www.ncbi.nlm.nih.gov/pubmed/16573235,http://www.ncbi.nlm.nih.gov/pubmed/20219571,http://www.ncbi.nlm.nih.gov/pubmed/12121416,http://www.ncbi.nlm.nih.gov/pubmed/16565503,http://www.ncbi.nlm.nih.gov/pubmed/22119785,http://www.ncbi.nlm.nih.gov/pubmed/11756557,http://www.ncbi.nlm.nih.gov/pubmed/15464997,http://www.ncbi.nlm.nih.gov/pubmed/23018488,http://www.ncbi.nlm.nih.gov/pubmed/15571817 | Which biological process in known as Endoplasmic Reticulum-Associated Protein Degradation (ERAD)? | Endoplasmic reticulum-associated protein degradation (ERAD) is the quality control system in the endoplasmic reticulum of eukaryotic cells which ensures that newly synthesized proteins that fail to fold into the correct conformation or unassembled orphan subunits of oligomeric proteins are rapidly eliminated by proteolytic degradation. This entails the export of proteins from the endoplasmic reticulum to the cytosol followed by their destruction by the cytosolic ubiquitin/proteasome pathway. While this mechanism effectively prevents the cellular accumulation of non-functional or unwanted endogenous proteins, it renders the cell vulnerable to certain viruses and toxins that are able to subvert this degradative mechanism for their own advantage.In the secretory pathway, quality control for the correct folding of proteins is largely occurring in the endoplasmic reticulum (ER), at the earliest possible stage and in an environment where early folding intermediates mix with terminally misfolded species. An elaborate cellular mechanism aims at dividing the former from the latter and promotes the selective transport of misfolded species back into the cytosol, a step called retrotranslocation. During retrotranslocation proteins will become ubiquitinated on the cytosolic side of the ER membrane by dedicated machineries and will be targeted to the proteasome for degradation. The entire process, from protein recognition to final degradation, has been named ER-associated protein degradation, or simply ERAD. |
http://www.ncbi.nlm.nih.gov/pubmed/24456413,http://www.ncbi.nlm.nih.gov/pubmed/21639808,http://www.ncbi.nlm.nih.gov/pubmed/24291778,http://www.ncbi.nlm.nih.gov/pubmed/23094782,http://www.ncbi.nlm.nih.gov/pubmed/23621583,http://www.ncbi.nlm.nih.gov/pubmed/22804352,http://www.ncbi.nlm.nih.gov/pubmed/24720932,http://www.ncbi.nlm.nih.gov/pubmed/23403819,http://www.ncbi.nlm.nih.gov/pubmed/23788912,http://www.ncbi.nlm.nih.gov/pubmed/23833299,http://www.ncbi.nlm.nih.gov/pubmed/22382362,http://www.ncbi.nlm.nih.gov/pubmed/22431777,http://www.ncbi.nlm.nih.gov/pubmed/23020132,http://www.ncbi.nlm.nih.gov/pubmed/25056920,http://www.ncbi.nlm.nih.gov/pubmed/22306669,http://www.ncbi.nlm.nih.gov/pubmed/25287827,http://www.ncbi.nlm.nih.gov/pubmed/24295639,http://www.ncbi.nlm.nih.gov/pubmed/23918947,http://www.ncbi.nlm.nih.gov/pubmed/24616537,http://www.ncbi.nlm.nih.gov/pubmed/25488880,http://www.ncbi.nlm.nih.gov/pubmed/22594466,http://www.ncbi.nlm.nih.gov/pubmed/25037139,http://www.ncbi.nlm.nih.gov/pubmed/24463460,http://www.ncbi.nlm.nih.gov/pubmed/22350184,http://www.ncbi.nlm.nih.gov/pubmed/23569304,http://www.ncbi.nlm.nih.gov/pubmed/22332713,http://www.ncbi.nlm.nih.gov/pubmed/23795808,http://www.ncbi.nlm.nih.gov/pubmed/23116250,http://www.ncbi.nlm.nih.gov/pubmed/22253555,http://www.ncbi.nlm.nih.gov/pubmed/25265494,http://www.ncbi.nlm.nih.gov/pubmed/24325952,http://www.ncbi.nlm.nih.gov/pubmed/24408395,http://www.ncbi.nlm.nih.gov/pubmed/24333389,http://www.ncbi.nlm.nih.gov/pubmed/24080641,http://www.ncbi.nlm.nih.gov/pubmed/23251089,http://www.ncbi.nlm.nih.gov/pubmed/22356324,http://www.ncbi.nlm.nih.gov/pubmed/22194965,http://www.ncbi.nlm.nih.gov/pubmed/24958825,http://www.ncbi.nlm.nih.gov/pubmed/24121489,http://www.ncbi.nlm.nih.gov/pubmed/23326492,http://www.ncbi.nlm.nih.gov/pubmed/21505227,http://www.ncbi.nlm.nih.gov/pubmed/22394203,http://www.ncbi.nlm.nih.gov/pubmed/25040674,http://www.ncbi.nlm.nih.gov/pubmed/24259661,http://www.ncbi.nlm.nih.gov/pubmed/22651703 | List BRAF inhibitors that have been tested in clinical trials for treatment of melanoma patients | Vemurafenib and dabrafenib are BRAF inhibitors that have been tested in clinical trials for treatment of melanoma patients. |
http://www.ncbi.nlm.nih.gov/pubmed/23990187,http://www.ncbi.nlm.nih.gov/pubmed/15929624,http://www.ncbi.nlm.nih.gov/pubmed/18221594,http://www.ncbi.nlm.nih.gov/pubmed/17652294,http://www.ncbi.nlm.nih.gov/pubmed/19850699,http://www.ncbi.nlm.nih.gov/pubmed/21475680,http://www.ncbi.nlm.nih.gov/pubmed/9761089,http://www.ncbi.nlm.nih.gov/pubmed/19791461,http://www.ncbi.nlm.nih.gov/pubmed/23500286,http://www.ncbi.nlm.nih.gov/pubmed/23867451,http://www.ncbi.nlm.nih.gov/pubmed/17162272,http://www.ncbi.nlm.nih.gov/pubmed/15856398,http://www.ncbi.nlm.nih.gov/pubmed/7787270,http://www.ncbi.nlm.nih.gov/pubmed/18033231,http://www.ncbi.nlm.nih.gov/pubmed/2482379,http://www.ncbi.nlm.nih.gov/pubmed/20118111,http://www.ncbi.nlm.nih.gov/pubmed/20132378,http://www.ncbi.nlm.nih.gov/pubmed/19419401,http://www.ncbi.nlm.nih.gov/pubmed/22762717,http://www.ncbi.nlm.nih.gov/pubmed/10957787,http://www.ncbi.nlm.nih.gov/pubmed/19699347 | which are the risk factors for sudden cardiac death in patients with hypertrophic cardiomyopathy? | The following risk factors for sudden cardiac death in patients with hypertrophic cardiomyopathy have been identified: 1) previous cardiac arrest; 2) sustained ventricular tachycardia; 3) family history of sudden cardiac death; 4) high-risk genetic mutations; 5) unexplained syncope; 6) non-sustained ventricular tachycardia; 7) hypotensive response to exercise; 8) marked left ventricular hypertrophy; 9) J-wave on ECG and 10) myocardial fibrosis using late gadolinium enhancement |
http://www.ncbi.nlm.nih.gov/pubmed/12809878,http://www.ncbi.nlm.nih.gov/pubmed/23369111,http://www.ncbi.nlm.nih.gov/pubmed/24198618,http://www.ncbi.nlm.nih.gov/pubmed/11183903,http://www.ncbi.nlm.nih.gov/pubmed/22500250,http://www.ncbi.nlm.nih.gov/pubmed/9510336,http://www.ncbi.nlm.nih.gov/pubmed/11386591 | What is known about the economic cost of urinary incontinence? | The estimated total economic cost in treating overactive bladder was 117 billion Korean Won (KRW, the currency of South Koea) in 2006 and 145 billion KRW in 2007. The estimated total cost in treating stress urinary incontinence was 122 billion KRW in 2006 and 59 billion KRW in 2007.
The estimated total economic cost of OAB was 12.02 billion dollars in 2000, with 9.17 and 2.85 billion dollars incurred in the community and institutions, respectively. Community female and male OAB costs totaled 7.37 and 1.79 billion dollars, respectively. The estimated total cost was sensitive to the estimated prevalence of OAB; therefore, we calculated the average cost per community-dwelling person with OAB, which was 267 dollars per year.
An estimated 1835628 community-dwelling women over the age of 18 years had urinary incontinence in 1998. The total annual cost of this urinary incontinence is estimated at $710.44 million, or $387 per incontinent woman, comprising $338.47 million in treatment costs and $371.97 million in personal costs. An estimated 60% of women with incontinence in 1998 were aged 40 years or over. Assuming the prevalence of incontinence remains constant and, allowing for inflation, we project that the total annual cost in 20 years' time will be $1267.85 million, 93% ($1.18 billion) of which will constitute costs associated with women aged over 40 years.
For individuals 65 years of age and older these costs are substantial, increasing from $8.2 billion (1984 dollars) to $16.4 billion (1993 dollars). The 1995 societal cost of incontinence for individuals aged 65 years and older was $26.3 billion, or $3565 per individual with urinary incontinence. |
http://www.ncbi.nlm.nih.gov/pubmed/22632831,http://www.ncbi.nlm.nih.gov/pubmed/16332960,http://www.ncbi.nlm.nih.gov/pubmed/23380592,http://www.ncbi.nlm.nih.gov/pubmed/23985334,http://www.ncbi.nlm.nih.gov/pubmed/25097035,http://www.ncbi.nlm.nih.gov/pubmed/20439427 | Which are the coactivators of the Yes-associated protein (yap)? | The Yap protein forms complex with Tead (TEA domain) transcription factors. |
http://www.ncbi.nlm.nih.gov/pubmed/21542789,http://www.ncbi.nlm.nih.gov/pubmed/23251581,http://www.ncbi.nlm.nih.gov/pubmed/20453842,http://www.ncbi.nlm.nih.gov/pubmed/23251214,http://www.ncbi.nlm.nih.gov/pubmed/23288628,http://www.ncbi.nlm.nih.gov/pubmed/18082339,http://www.ncbi.nlm.nih.gov/pubmed/21427575,http://www.ncbi.nlm.nih.gov/pubmed/16000323,http://www.ncbi.nlm.nih.gov/pubmed/23381558,http://www.ncbi.nlm.nih.gov/pubmed/23574521,http://www.ncbi.nlm.nih.gov/pubmed/19772830,http://www.ncbi.nlm.nih.gov/pubmed/21383967 | How many genes outside of the MHC locus have been genetically associated to Rheumatoid Arthritis through GWAS? | Large genome-wide association studies (GWAS) have identified more than 30 loci involved in RA pathogenesis. To date, over 30 non-MHC RA-associated loci have been identified in humans, and over 100 arthritis-associated loci have been identified in rodent models of RA. The most relevant non-HLA gene single nucleotide polymorphisms (SNPs) associated with RA include PTPN22, IL23R, TRAF1, CTLA4, IRF5, STAT4, CCR6, PADI4. Previous studies demonstrate that 6 of the established non-HLA CD and RA risk loci (out of 26 loci for each disease) are shared between both diseases. |
http://www.ncbi.nlm.nih.gov/pubmed/24491965,http://www.ncbi.nlm.nih.gov/pubmed/25108607,http://www.ncbi.nlm.nih.gov/pubmed/24005292,http://www.ncbi.nlm.nih.gov/pubmed/19581573,http://www.ncbi.nlm.nih.gov/pubmed/24965021,http://www.ncbi.nlm.nih.gov/pubmed/25303540,http://www.ncbi.nlm.nih.gov/pubmed/25678887,http://www.ncbi.nlm.nih.gov/pubmed/23340416,http://www.ncbi.nlm.nih.gov/pubmed/25012388,http://www.ncbi.nlm.nih.gov/pubmed/22698957,http://www.ncbi.nlm.nih.gov/pubmed/23871610,http://www.ncbi.nlm.nih.gov/pubmed/25710834,http://www.ncbi.nlm.nih.gov/pubmed/23637949,http://www.ncbi.nlm.nih.gov/pubmed/25451697,http://www.ncbi.nlm.nih.gov/pubmed/24573293,http://www.ncbi.nlm.nih.gov/pubmed/23143518,http://www.ncbi.nlm.nih.gov/pubmed/22890709,http://www.ncbi.nlm.nih.gov/pubmed/24590406,http://www.ncbi.nlm.nih.gov/pubmed/23406911 | Are optogenetics tools used in the study and treatment of epilepsy? | Using optogenetics tools it is possible to begin to address some of the fundamental unanswered questions in epilepsy, to dissect epileptic neuronal circuits and to develop new intervention strategies. |
http://www.ncbi.nlm.nih.gov/pubmed/16950921,http://www.ncbi.nlm.nih.gov/pubmed/22201950,http://www.ncbi.nlm.nih.gov/pubmed/20435731,http://www.ncbi.nlm.nih.gov/pubmed/20479947,http://www.ncbi.nlm.nih.gov/pubmed/20036541 | In which phase of cell cycle does stress-induced transcription-associated mutagenesis (TAM) occur? | Factors involved in RNA polymerase (RNAP) processivity or transcriptional derepression, such as Mfd (transcription coupling repair factor), contribute to the generation of stress-induced mutations. Under stress, transcription-associated mutagenesis is increased. Stress-induced transcription-associated mutations are acquired by nondividing cells, during stationary phase, and are not observed under conditions of exponential growth. |
http://www.ncbi.nlm.nih.gov/pubmed/19295128,http://www.ncbi.nlm.nih.gov/pubmed/16080193,http://www.ncbi.nlm.nih.gov/pubmed/19604397,http://www.ncbi.nlm.nih.gov/pubmed/19029937,http://www.ncbi.nlm.nih.gov/pubmed/20168079,http://www.ncbi.nlm.nih.gov/pubmed/23880940,http://www.ncbi.nlm.nih.gov/pubmed/18611248,http://www.ncbi.nlm.nih.gov/pubmed/22249256 | Which proteins are related to the loss of cell-cell adhesion during EMT (epithelial-mesenchymal transition)? | Transcriptional and post-transcriptional regulatory mechanisms mediated by several inducers of EMT, in particular the ZEB and Snail factors, downregulate the expression and/or functional organization of core polarity complexes. Functional loss of the cell-cell adhesion molecule E-cadherin is an essential event for epithelial-mesenchymal transition (EMT), a process that allows cell migration during embryonic development and tumour invasion. Recently, we found that aPKC can also phosphorylate Par6 to drive EMT and increase the migratory potential of non-small cell lung cancer cells. We propose that the regulation of EMT by SIRT1 involves modulation of, and cooperation with, the EMT inducing transcription factor ZEB1. Knockdown of Numb by shRNA in MDCK cells led to a lateral to apical translocation of E-cadherin and beta-catenin, active F-actin polymerization, mis-localization of Par3 and aPKC, a decrease in cell-cell adhesion and an increase in cell migration and proliferation. Growth factors such as TGFb and EGF have also been shown to be related to EMT. |
http://www.ncbi.nlm.nih.gov/pubmed/19959133,http://www.ncbi.nlm.nih.gov/pubmed/20015039,http://www.ncbi.nlm.nih.gov/pubmed/17401374,http://www.ncbi.nlm.nih.gov/pubmed/22045061,http://www.ncbi.nlm.nih.gov/pubmed/19581315,http://www.ncbi.nlm.nih.gov/pubmed/19933931,http://www.ncbi.nlm.nih.gov/pubmed/23678295,http://www.ncbi.nlm.nih.gov/pubmed/20163779,http://www.ncbi.nlm.nih.gov/pubmed/19131648,http://www.ncbi.nlm.nih.gov/pubmed/19519553,http://www.ncbi.nlm.nih.gov/pubmed/23922949 | Is micro RNA 1 (miR-1) implicated in cardiac arrhythmias? | Yes. miR-1 overexpression may contribute to the increased susceptibility of the heart to AVB, which provides us novel insights into the molecular mechanisms underlying ischemic cardiac arrhythmias. As miR-1 has been shown in animal models and clinical studies to contribute to arrhythmogenesis by regulating pacemaker channel genes, our finding of miR-1 up-regulation in patients with myocardial infarction indicates that it might be responsible for the higher risk for arrhythmias in these patients.Yes, changes in abundance of muscle-specific microRNA, miR-1, have been implicated in cardiac disease, including arrhythmia and heart failure. it has been shown that miR-1 over-expression in normal or infarcted rat hearts exacerbates arrhythmogenesis, while elimination of miR-1 by an antisense inhibitor in infarcted rat hearts relieved arrhythmogenesis. Thus, miR-1 may have important pathophysiological functions in the heart, and is a potential antiarrhythmic target. |
http://www.ncbi.nlm.nih.gov/pubmed/24282393,http://www.ncbi.nlm.nih.gov/pubmed/19492354,http://www.ncbi.nlm.nih.gov/pubmed/17274809,http://www.ncbi.nlm.nih.gov/pubmed/23357263,http://www.ncbi.nlm.nih.gov/pubmed/18402933 | Are there Conserved Noncoding Elements (CNEs) in invertebrate genomes? | Yes.Yes. Conserved Noncoding Elements (CNEs) have also been found in invertebrate genomes. |
http://www.ncbi.nlm.nih.gov/pubmed/17589818,http://www.ncbi.nlm.nih.gov/pubmed/21875573,http://www.ncbi.nlm.nih.gov/pubmed/22017796,http://www.ncbi.nlm.nih.gov/pubmed/19243304,http://www.ncbi.nlm.nih.gov/pubmed/11156366,http://www.ncbi.nlm.nih.gov/pubmed/24264057,http://www.ncbi.nlm.nih.gov/pubmed/20165689,http://www.ncbi.nlm.nih.gov/pubmed/25302307,http://www.ncbi.nlm.nih.gov/pubmed/22248668,http://www.ncbi.nlm.nih.gov/pubmed/11729185,http://www.ncbi.nlm.nih.gov/pubmed/20406950,http://www.ncbi.nlm.nih.gov/pubmed/23103206,http://www.ncbi.nlm.nih.gov/pubmed/22528751,http://www.ncbi.nlm.nih.gov/pubmed/23209608,http://www.ncbi.nlm.nih.gov/pubmed/19128788,http://www.ncbi.nlm.nih.gov/pubmed/18336191,http://www.ncbi.nlm.nih.gov/pubmed/22978174,http://www.ncbi.nlm.nih.gov/pubmed/18794879,http://www.ncbi.nlm.nih.gov/pubmed/24231949,http://www.ncbi.nlm.nih.gov/pubmed/23948487,http://www.ncbi.nlm.nih.gov/pubmed/22611192,http://www.ncbi.nlm.nih.gov/pubmed/12629332,http://www.ncbi.nlm.nih.gov/pubmed/15701641,http://www.ncbi.nlm.nih.gov/pubmed/23412905,http://www.ncbi.nlm.nih.gov/pubmed/20935678,http://www.ncbi.nlm.nih.gov/pubmed/12494467,http://www.ncbi.nlm.nih.gov/pubmed/21341346,http://www.ncbi.nlm.nih.gov/pubmed/20740625,http://www.ncbi.nlm.nih.gov/pubmed/22374721,http://www.ncbi.nlm.nih.gov/pubmed/11906841,http://www.ncbi.nlm.nih.gov/pubmed/19184427,http://www.ncbi.nlm.nih.gov/pubmed/17457049,http://www.ncbi.nlm.nih.gov/pubmed/21452930,http://www.ncbi.nlm.nih.gov/pubmed/8844397,http://www.ncbi.nlm.nih.gov/pubmed/9219832,http://www.ncbi.nlm.nih.gov/pubmed/15033688,http://www.ncbi.nlm.nih.gov/pubmed/20922462 | Which tumor suppressor is referred to as "the guardian of the genome"? | The major tumour suppressor protein, p53, is one of the most well-studied proteins in cell biology. It plays a crucial role in regulating the transcription of numerous genes responsible for cells cycle arrest, DNA repair, angiogenesis, cell senescence, or apoptosis in response to various stress signals, and is considered one of the most important players in the development of cancer. p53 contributes to the maintenance of genomic stability. Thus, p53 has been described as "the guardian of the genome". |