pubmed_ids
stringlengths 41
6.9k
| questions
stringlengths 13
215
| ground_truth
stringlengths 2
7.79k
|
|---|---|---|
http://www.ncbi.nlm.nih.gov/pubmed/7679743,http://www.ncbi.nlm.nih.gov/pubmed/9782260,http://www.ncbi.nlm.nih.gov/pubmed/1402806,http://www.ncbi.nlm.nih.gov/pubmed/1658026 | What is the function of a viral peplomer? | The coronavirus peplomer protein S is responsible for attachment and fusion during viral entry as well as for the induction of cell to cell fusion.
Since tissue affinities are a function of the viral peplomer-mediated attachment of virus to cells and are often directly related to pathogenicity, |
http://www.ncbi.nlm.nih.gov/pubmed/26242919 | Have toll-like receptor 2 activators been found in food? | Yes, toll-like receptor 2 activators (TLR2) have been found in food.Yes, Toll-like receptor 2 activators (TLR2) have been found in food.Yes, Toll-like receptor 2 (TLR2) activators have been found in food.toll-like receptor 2 (tlr2) ) is a widely expressed pattern recognition receptor critical for innate immunity. tlr2 activators are found in many common foodsYes, Toll-like receptor 2 activators have been found in food.Toll-like receptor 2 (TLR2) is a widely expressed pattern recognition receptor critical for innate immunity. TLR2 is also a key regulator of mucosal immunity implicated in the development of allergic disease and they are found in many common foods. Toll-like receptor 2 ( TLR2) is a widely expressed pattern recognition receptor critical for innate immunity. TLR2 is also a key regulator of mucosal immunity implicated in the development of allergic disease. TLR2 activators are found in many common foods,yes, Toll-like receptor 2 (TLR2) is a widely expressed pattern recognition receptor critical for innate immunity. TLR2 is also a key regulator of mucosal immunity implicated in the development of allergic disease. TLR2 activators are found in many common foods,Toll-like receptor 2 (TLR2) is a widely expressed pattern recognition receptor critical for innate immunity. TLR2 is also a key regulator of mucosal immunity implicated in the development of allergic disease. TLR2 activators are found in many common foods,TLR2 is also a key regulator of mucosal immunity implicated in the development of allergic disease. TLR2 activators are found in many common foods, |
http://www.ncbi.nlm.nih.gov/pubmed/28587637,http://www.ncbi.nlm.nih.gov/pubmed/27899665,http://www.ncbi.nlm.nih.gov/pubmed/30462303,http://www.ncbi.nlm.nih.gov/pubmed/30285606,http://www.ncbi.nlm.nih.gov/pubmed/28919242 | Describe the Open Targets platform | The Open Targets platform is a data integration and visualization platform that provides evidence about the association of known and potential drug targets with diseases. The platform is designed to support identification and prioritization of biological targets for follow-up. Each drug target is linked to a disease using integrated genome-wide data from a broad range of data sources. The platform provides either a target-centric workflow to identify diseases that may be associated with a specific target, or a disease-centric workflow to identify targets that may be associated with a specific disease. Users can easily transition between these target- and disease-centric workflows. The Open Targets Validation Platform is accessible at https://www.targetvalidation.org. |
http://www.ncbi.nlm.nih.gov/pubmed/11830608,http://www.ncbi.nlm.nih.gov/pubmed/2754447,http://www.ncbi.nlm.nih.gov/pubmed/11045784,http://www.ncbi.nlm.nih.gov/pubmed/23053567,http://www.ncbi.nlm.nih.gov/pubmed/27913498,http://www.ncbi.nlm.nih.gov/pubmed/25104066,http://www.ncbi.nlm.nih.gov/pubmed/25025999,http://www.ncbi.nlm.nih.gov/pubmed/7563187,http://www.ncbi.nlm.nih.gov/pubmed/2981984,http://www.ncbi.nlm.nih.gov/pubmed/25615851,http://www.ncbi.nlm.nih.gov/pubmed/1428226,http://www.ncbi.nlm.nih.gov/pubmed/25754634,http://www.ncbi.nlm.nih.gov/pubmed/26530956 | Does radiotherapy for Hodgkin disease increases risk for lung cancer? | Yes, radiotherapy for Hodgkin disease is associated with increased risk for lung cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/28499661,http://www.ncbi.nlm.nih.gov/pubmed/27432454,http://www.ncbi.nlm.nih.gov/pubmed/19553822,http://www.ncbi.nlm.nih.gov/pubmed/25900243,http://www.ncbi.nlm.nih.gov/pubmed/27844130,http://www.ncbi.nlm.nih.gov/pubmed/27370205,http://www.ncbi.nlm.nih.gov/pubmed/26936410,http://www.ncbi.nlm.nih.gov/pubmed/18801517,http://www.ncbi.nlm.nih.gov/pubmed/27629559,http://www.ncbi.nlm.nih.gov/pubmed/30293908 | Does radiotherapy for prostate cancer increase bladder cancer risk? | Yes, radiotherapy for prostate cancer is associated with increased bladder cancer risk. |
http://www.ncbi.nlm.nih.gov/pubmed/26305889,http://www.ncbi.nlm.nih.gov/pubmed/26653113 | What is ESN364? | systemic administration of an NK3R antagonist (ESN364) prolongs the LH interpulse interval in ovarectomized ewes and significantly lowers plasma LH and FSH concentrations in castrated nonhuman primates (Macaca fascicularis). Moreover, daily oral dosing of ESN364 throughout the menstrual cycle in M fascicularis lowered plasma estradiol levels in a dose-dependent manner, although nadir levels of estradiol were maintained well above menopausal levels. Nevertheless, estradiol levels during the follicular phase were sufficiently inhibited at all doses to preclude the triggering of ovulation as evidenced by the absence of the LH surge and failure of a subsequent luteal phase rise in plasma progesterone concentrations, consistent with the absence of normal cycle changes in the uterus. Apart from the point at surge, FSH levels were not altered over the course of the menstrual cycle. These effects of ESN364 were reversible upon cessation of drug treatment.
ESN364 was well-tolerated and rapidly bioavailable with linear pharmacokinetics and no drug accumulation with repeated, daily oral administration. Drug treatment dose-dependently decreased basal LH, but not FSH, and consequently decreased estradiol and progesterone (in women) as well as testosterone (in men). The hormonal changes in women corresponded to delayed ovulation, decreased endometrial thickening, impeded follicular maturation, and prolongation of the menstrual cycle. Drug effects were rapidly reversible. Oral administration of the NK3R antagonist, ESN364, suppressed the hypothalamic-pituitary-gonadal axis in healthy volunteers by selective modulation of gonadotropin secretion, leading to a restrained decrease in ovarian hormone levels in women. These results suggest that ESN364 may offer therapeutic benefit in the treatment of women's health disorders with a mitigated risk of menopausal-like adverse events. |
http://www.ncbi.nlm.nih.gov/pubmed/26808112 | Do genes with monoallelic expression contribute proportionally to genetic diversity in humans? | No, genes with monoallelic expression contribute disproportionately to genetic diversity in humans.No. Genes with monoallelic expression contribute disproportionately to genetic diversity in humans. |
http://www.ncbi.nlm.nih.gov/pubmed/28385352 | Has MLE4901 been tested in phase III clinical trials? | No, MLE4901 has been tested in phase 2, randomised, double-blind, placebo-controlled trial. |
http://www.ncbi.nlm.nih.gov/pubmed/26653113 | Does ESN364 activate the hypothalamic-pituitary-gonadal axis? | No, the NK3R antagonist, ESN364, suppressed the hypothalamic-pituitary-gonadal axis in healthy volunteers by selective modulation of gonadotropin secretion |
http://www.ncbi.nlm.nih.gov/pubmed/27060149 | Which type of variants can be called by the VarDict algorithm? | VarDict is a novel and versatile variant caller for both DNA- and RNA-sequencing data. It simultaneously calls SNV, MNV, InDels, complex and structural variants, expanding the detected genetic driver landscape of tumors. It performs local realignments on the fly for more accurate allele frequency estimation.VarDict simultaneously calls SNV, MNV, InDels, complex and structural variants, expanding the detected genetic driver landscape of tumors. It performs local realignments on the fly for more accurate allele frequency estimation. VarDict performance scales linearly to sequencing depth, enabling ultra-deep sequencing used to explore tumor evolution or detect tumor DNA circulating in blood.VarDict is a novel and versatile variant caller for both DNA- and RNA-sequencing data. It calls SNV, MNV, InDels, complex and structural variants, expanding the detected genetic driver landscape of tumors.VarDict simultaneously calls SNV, MNV, InDels, complex and structural variants, expanding the detected genetic driver landscape of tumors. |
http://www.ncbi.nlm.nih.gov/pubmed/23593142 | Has ORMD-0801 been tested in patients? | Yes, ORMD-0801 has been tested in patients. |
http://www.ncbi.nlm.nih.gov/pubmed/28515625 | Was vivotif licensed in Europe and the US at the same time? | No, vivotif was licensed in Europe in 1983 and in the US in 1989. |
http://www.ncbi.nlm.nih.gov/pubmed/25640064,http://www.ncbi.nlm.nih.gov/pubmed/22892486,http://www.ncbi.nlm.nih.gov/pubmed/28411358 | Are stem cell transplants used to treat acute kidney injury? | Yes, stem cell transplantation is becoming the treatment of choice for complicated acute kidney injury.Yes, stem cell transplantation is being used for treatment of acute kidney injury.Yes, stem cell transplants are being used for treatment of acute kidney injury.Yes, stem cell transplants are being used for acute kidney injury treatment.Yes, stem cell transplants are being used to treat acute kidney injury.Yes, Animal studies have shown that mesenchymal stromal cell (MSC) infusions improve acute kidney injury (AKI) outcomes when administered early after ischemic/reperfusion injury or within 24 hours after cisplatin administration.D |
http://www.ncbi.nlm.nih.gov/pubmed/20696838,http://www.ncbi.nlm.nih.gov/pubmed/29447171,http://www.ncbi.nlm.nih.gov/pubmed/27872142,http://www.ncbi.nlm.nih.gov/pubmed/29217591,http://www.ncbi.nlm.nih.gov/pubmed/28220956,http://www.ncbi.nlm.nih.gov/pubmed/19696148 | What is the interaction between WAPL and PDS5 proteins? | We propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. We propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. Cohesin acetylation and Wapl-Pds5 oppositely regulate translocation of cohesin along DNA. the cohesin unloading factor WAPL and its PDS5 binding partners control the length of loops. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase head ds5 and Wapl, but not Brca2, limit the distance that cohesin extends from origins, thereby determining which active genes, enhancers and silencers bind cohesin.We propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. Translocation ability is suppressed in the presence of Wapl-Pds5 and Sororin Cohesin acetylation and Wapl-Pds5 oppositely regulate translocation of cohesin along DNA. the cohesin unloading factor WAPL and its PDS5 binding partners control the length of loops. the cohesin regulators Pds5 and Wapl release cohesin from chromosomes.Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase head. Pds5 and Wapl, but not Brca2, limit the distance that cohesin extends from origins, thereby determining which active genes, enhancers and silencers bind cohesin. Using RNA-seq we find that Brca2, Pds5 and Wapl influence the expression of most genes sensitive to Nipped-B and cohesin, largely in the same direction.We propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. Translocation ability is suppressed in the presence of Wapl-Pds5 and Sororin Cohesin acetylation and Wapl-Pds5 oppositely regulate translocation of cohesin along DNA. the cohesin unloading factor WAPL and its PDS5 binding partners control the length of loops. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase headwe propose that wapl and pds5 directly modulate conformational changes of cohesin to make it competent for dissolving from chromatin during prophaseWe propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. Translocation ability is suppressed in the presence of Wapl-Pds5 and SororinWe propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. the cohesin regulators Pds5 and Wapl release cohesin from chromosomes. a requirement for ATP hydrolysis in ring opening, suggested regulation of the cohesin ATPase activity by DNA and Smc3 acetylation, and provided insights into how Pds5 and Wapl open this exit gate. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase head ds5 and Wapl, but not Brca2, limit the distance that cohesin extends from origins, thereby determining which active genes, enhancers and silencers bind cohesin. Using RNA-seq we find that Brca2, Pds5 and Wapl influence the expression of most genes sensitive to Nipped-B and cohesin, largely in the same direction.Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase head Translocation ability is suppressed in the presence of Wapl-Pds5 and Sororin We propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. Cohesin acetylation and Wapl-Pds5 oppositely regulate translocation of cohesin along DNA. the cohesin unloading factor WAPL and its PDS5 binding partners control the length of loops. the cohesin regulators Pds5 and Wapl release cohesin from chromosomes. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase head the cohesin unloading factor WAPL and its PDS5 binding partners control the length of loops. the cohesin regulators Pds5 and Wapl release cohesin from chromosomes. a requirement for ATP hydrolysis in ring opening, suggested regulation of the cohesin ATPase activity by DNA and Smc3 acetylation, and provided insights into how Pds5 and Wapl open this exit gate. Pds5, Wapl, and SA1/2 form a rigid scaffold that docks on Scc1 and anchors the N-terminal domain of Scc1 (Scc1N) to the Smc1 ATPase head ds5 and Wapl, but not Brca2, limit the distance that cohesin extends from origins, thereby determining which active genes, enhancers and silencers bind cohesin. Using RNA-seq we find that Brca2, Pds5 and Wapl influence the expression of most genes sensitive to Nipped-B and cohesin, largely in the same direction.We propose that Wapl and Pds5 directly modulate conformational changes of cohesin to make it competent for dissociation from chromatin during prophase. Nipped-B, Pds5, and the Wapl protein that interacts with Pds5 all play unique roles in cohesin chromosome binding. the cohesin regulators Pds5 and Wapl release cohesin from chromosomes. a requirement for ATP hydrolysis in ring opening, suggested regulation of the cohesin ATPase activity by DNA and Smc3 acetylation, and provided insights into how Pds5 and Wapl open this exit gate. ds5 and Wapl, but not Brca2, limit the distance that cohesin extends from origins, thereby determining which active genes, enhancers and silencers bind cohesin. Using RNA-seq we find that Brca2, Pds5 and Wapl influence the expression of most genes sensitive to Nipped-B and cohesin, largely in the same direction. |
http://www.ncbi.nlm.nih.gov/pubmed/25454820,http://www.ncbi.nlm.nih.gov/pubmed/26463438 | Is deletion at 6q24.2-26 associated with shorter survival for ovarian cancer patients? | No, the 6q24.2-26 deletion is an independent marker of favorable outcome in high-grade serous ovarian carcinoma (HGSOC) patients with potential clinical value as it can be analyzed by FISH on tumor sections and guide the selection of patients towards more conservative therapeutic strategies in order to reduce side-effects and improve quality of life.No, deletion at 6q24.2-26 predicts longer survival of high-grade serous ovarian cancer patients. |
http://www.ncbi.nlm.nih.gov/pubmed/29187526,http://www.ncbi.nlm.nih.gov/pubmed/29157894,http://www.ncbi.nlm.nih.gov/pubmed/29724125,http://www.ncbi.nlm.nih.gov/pubmed/28918129,http://www.ncbi.nlm.nih.gov/pubmed/26745528,http://www.ncbi.nlm.nih.gov/pubmed/29175418 | What is the function of a protein kinase? | Protein kinases are enzymes that add a phosphate (PO4) group to a protein, and can modulate its function. |
http://www.ncbi.nlm.nih.gov/pubmed/29018300 | Which was the first cholera vaccine approved in the US? | Vaxchora is the first vaccine approved by the Food and Drug Administration for the prophylaxis of cholera infection. |
http://www.ncbi.nlm.nih.gov/pubmed/29571563 | List 3 PD-L1 inhibitors on the market as of 2018. | Atezolizumab (Tecentriq), Avelumab (Bavencio), and Durvalumab (Imfinzi) are PD-L1 inhibitors |
http://www.ncbi.nlm.nih.gov/pubmed/1883358,http://www.ncbi.nlm.nih.gov/pubmed/8405675,http://www.ncbi.nlm.nih.gov/pubmed/25605944,http://www.ncbi.nlm.nih.gov/pubmed/8770895,http://www.ncbi.nlm.nih.gov/pubmed/2481227,http://www.ncbi.nlm.nih.gov/pubmed/9038208,http://www.ncbi.nlm.nih.gov/pubmed/2539381,http://www.ncbi.nlm.nih.gov/pubmed/2968500 | Are there negative enhancers? | Yes, negative enhancers are also called gene silencers.Yes, there are. There is a gene called the CANP mL gene, which is responsible for muscle type regulation. It is a negative enhancer.Yes, they are genomic regions that are dense in negative regulatory elements.Yes. Negative enhancers are enhancers that negatively regulate gene expression by physically blocking transcription of a subset of genes, often immobilizing transcriptional machinery.Yes. Numerous studies suggest that negative enhancers are present in eukaryotic genomes and play key roles in gene expression.Yes, there are. There is a gene called the CANP mL gene, which is responsible for muscle type regulation. It has a positive and a negative enhancer. The positive enhancer gene controls muscle type, while the negative one controls muscle growth.Yes. There are numerous studies of gene regulation in which enhancers are found to be negative enhancers, either because they negatively regulate transcription, or are absent or have a limited function. |
http://www.ncbi.nlm.nih.gov/pubmed/24055153,http://www.ncbi.nlm.nih.gov/pubmed/27797072,http://www.ncbi.nlm.nih.gov/pubmed/17141150,http://www.ncbi.nlm.nih.gov/pubmed/29447171,http://www.ncbi.nlm.nih.gov/pubmed/29217591,http://www.ncbi.nlm.nih.gov/pubmed/28424523,http://www.ncbi.nlm.nih.gov/pubmed/17112726,http://www.ncbi.nlm.nih.gov/pubmed/23034634,http://www.ncbi.nlm.nih.gov/pubmed/17113138,http://www.ncbi.nlm.nih.gov/pubmed/28475897 | What is the function of WAPL protein on cohesin? | Human Wapl is a cohesin-binding protein that promotes sister-chromatid resolution in mitotic prophase We show that the human ortholog of Wapl is a cohesin-binding protein that facilitates cohesin's timely release from chromosome arms during prophase.Wapl is a cohesin-binding protein that facilitates cohesin's timely release from chromosome arms during prophase.It promotes the release of cohesin from chromosomes during both interphase and mitosis.Human Wapl is a cohesin-binding protein that promotes sister-chromatid resolution in mitotic prophase. We show that the human ortholog of Wapl is a cohesin-binding protein that facilitates cohesin's timely release from chromosome arms during prophase. |
http://www.ncbi.nlm.nih.gov/pubmed/29191945,http://www.ncbi.nlm.nih.gov/pubmed/28548028 | What is romiplostim targeting? | Romiplostim (ROM) is a thrombopoietin (TPO)-receptor-agonist approved for treatment of adults with chronic immune thrombocytopenia (ITP). |
http://www.ncbi.nlm.nih.gov/pubmed/28337370,http://www.ncbi.nlm.nih.gov/pubmed/29725456,http://www.ncbi.nlm.nih.gov/pubmed/29680500,http://www.ncbi.nlm.nih.gov/pubmed/27655662,http://www.ncbi.nlm.nih.gov/pubmed/28416737 | Please list 3 drugs that have EGFR as their primary target. | There are a number of drugs that target EGFR. The best known targeted therapies include: Epidermal growth factor receptor (EGFR) monoclonal antibodies (cetuximab, panitumumab, zalutumumab and nimotuzumab), EGFR tyrosine kinase inhibitors (gefitinib, erlotinib, lapatinib, afatinib and dacomitinib)Cetuximab, erlotinib and gefitinib are 3 drugs that have EGFR as their primary target.The best known targeted therapies include: Epidermal growth factor receptor (EGFR) monoclonal antibodies (cetuximab, panitumumab, zalutumumab and nimotuzumab), EGFR tyrosine kinase inhibitors (gefitinib, erlotinib, lapatinib, afatinib and dacomitinib) |
http://www.ncbi.nlm.nih.gov/pubmed/18276799,http://www.ncbi.nlm.nih.gov/pubmed/12034751,http://www.ncbi.nlm.nih.gov/pubmed/27298259,http://www.ncbi.nlm.nih.gov/pubmed/26997282,http://www.ncbi.nlm.nih.gov/pubmed/15361841,http://www.ncbi.nlm.nih.gov/pubmed/21589869,http://www.ncbi.nlm.nih.gov/pubmed/28430577,http://www.ncbi.nlm.nih.gov/pubmed/19822671,http://www.ncbi.nlm.nih.gov/pubmed/29867216 | What is the role of STAG1/STAG2 proteins in differentiation? | STAG1/STAG2 proteins are tumour suppressor proteins that suppress cell proliferation and are essential for differentiation.involved in the g2-m transitionSTAG1/STAG2 proteins are tumour suppressor proteins that suppress cell proliferation and differentiation.The expression of STAG1 mRNA was induced in response to various genotoxic stresses in a p53-dependent manner; moreover, enforced expression of STAG1 led to apoptosis in several additional cancer cell lines. The simultaneous blocking of STAG1 and STAG2 significantly reduces cell proliferation. STAG1 preferentially contributes to the stabilization of topologically associating domain boundaries together with CTCF, whereas STAG2 promotes cell-type-specific contacts between enhancers and promoters independently of CTCF. |
http://www.ncbi.nlm.nih.gov/pubmed/30154186 | What can we measure with the TSA-Seq method? | Mapping 3D genome organization relative to nuclear compartments using TSA-Seq as a cytological ruler. TSA-Seq, a new mapping method capable of providing a "cytological ruler" for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several Mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling.TSA-Seq, a new mapping method capable of providing a "cytological ruler" for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several Mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling. Mapping 3D genome organization relative to nuclear compartments using TSA-Seq as a cytological ruler. TSA-Seq is a new mapping method capable of providing a "cytological ruler" for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several Mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling.mean chromosomal distances |
http://www.ncbi.nlm.nih.gov/pubmed/29315405 | Which method is behind HipMCL? | HipMCL is a high-performance parallel implementation of the Markov clustering algorithm for large-scale networks. Despite its popularity, MCL's scalability to cluster large datasets still remains a bottleneck due to high running times and memory demands.While various clustering algorithms have been proposed to find highly connected regions, Markov Clustering (MCL) has been one of the most successful approaches to cluster sequence similarity or expression networks. HipMCL is based on MPI and OpenMP and is freely available under a modified BSD license.While various clustering algorithms have been proposed to find highly connected regions, Markov Clustering (MCL) has been one of the most successful approaches to cluster sequence similarity or expression networks. Despite its popularity, MCL's scalability to cluster large datasets still remains a bottleneck due to high running times and memory demands. High-performance MCL (HipMCL) offers a parallel implementation of the original MCL algorithm that can run on distributed-memory computers. By exploiting distributed-memory environments, HipMCL clusters large-scale networks several orders of magnitude faster than MCL and enables clustering of even bigger networks. HipMCL is based on MPI and OpenMP and is freely available under a modified BSD license.While various clustering algorithms have been proposed to find highly connected regions, Markov Clustering (MCL) has been one of the most successful approaches to cluster sequence similarity or expression networks. Despite its popularity, MCL's scalability to cluster large datasets still remains a bottleneck due to high running times and memory demands. HipMCL is a high-performance parallel implementation of the Markov clustering algorithm for large-scale networks.HipMCL (HipClustering) is a high-performance parallel implementation of the Markov clustering algorithm for large-scale networks.HipMCL is a high-performance parallel implementation of the Markov clustering algorithm for large-scale networks. |
http://www.ncbi.nlm.nih.gov/pubmed/23030360,http://www.ncbi.nlm.nih.gov/pubmed/305444,http://www.ncbi.nlm.nih.gov/pubmed/23555858,http://www.ncbi.nlm.nih.gov/pubmed/1083874 | What is the function of CR elements in B-cells? | After addition of culture supernatant from BCG-activated macrophages CR- B cells cooperate with both unprimed and primed T helper cells.The SR/CR mouse phenotype, first described in 1999 in BALB/c and later bred into C57BL/6 mice, is resistant to cancer formation following high doses of cancer cells administered intraperitoneally.CR elements are subtelomeric protein complexes that repress translation of a subset of RNAs in response to abiotic stress and can mediate diverse physiological and developmental processes in B- cells. |
http://www.ncbi.nlm.nih.gov/pubmed/29129088,http://www.ncbi.nlm.nih.gov/pubmed/30660828,http://www.ncbi.nlm.nih.gov/pubmed/30486888 | What is drug target for olaparib? | Olaparib(Lynparza) is a PARP inhibitor, inhibiting poly ADP ribose polymerase (PARP), an enzyme involved in DNA repair.Olaparib is a Poly(ADP-ribose) Polymerase (PARP) Inhibitor |
http://www.ncbi.nlm.nih.gov/pubmed/22777095 | What virus is the Gardisil vaccine used for? | Gardisil is a quadrivalent HPV vaccine would have been useful in the prevention of infections with human papillomavirus.Gardisil is a 4-component vaccine against capsular HPV 16 (4C HPV16), which has recently been licensed in Europe, Canada and Australia.Gordisil is a 4-component vaccine against capsular Meningococcus serogroup B (4CMenB), which has recently been licensed in Europe, Canada and Australia.Gardisil, the quadrivalent HPV vaccine would have been useful in the prevention of 28% (13/46) of these infections Gardisil is a 16-component vaccine against human papillomavirus (HPV), which has recently been licensed in Europe, Canada and Australia.Gardisil, the quadrivalent HPV vaccine would have been useful in the prevention of 28% (13/46) of these infections |
http://www.ncbi.nlm.nih.gov/pubmed/12218105,http://www.ncbi.nlm.nih.gov/pubmed/11994452,http://www.ncbi.nlm.nih.gov/pubmed/26635029,http://www.ncbi.nlm.nih.gov/pubmed/14768939,http://www.ncbi.nlm.nih.gov/pubmed/27817026,http://www.ncbi.nlm.nih.gov/pubmed/18955544,http://www.ncbi.nlm.nih.gov/pubmed/16579866,http://www.ncbi.nlm.nih.gov/pubmed/27043411,http://www.ncbi.nlm.nih.gov/pubmed/6605224 | Which cells mature in the human thymus? | Thymus progenitor cells mature in the human thymus through differentiation into cardiomyocytes and fibroblasts.Late stages of T cell maturation in the thymus involve NF-kB and tonic type I interferon signaling. NF-kB and tonic interferon signals are involved in the final maturation of thymocytes into naive T cells.late stages of t cell maturation in the thymus involve nf-kb and tonic type i interferon signalsNF-kB and tonic interferon signals are involved in the final maturation of thymocytes into naive T cells.The mammalian thymus is an important post-translational organ that plays a pivotal role in the development of the human immune system. Thymocytes, which represent 50% of the cells in the human body, mature into cardiomyocytes and T cells.T cells mature in the human thymus; in particular, type T cells. |
http://www.ncbi.nlm.nih.gov/pubmed/30447999 | What are the eRNA-producing centers (EPCs)? | Active enhancers in mammals produce enhancer RNAs (eRNAs) that are bidirectionally transcribed, unspliced, and unstable. Enhancer regions are also enriched with long noncoding RNA (lncRNA) transcripts, which are typically spliced and substantially more stable. DNase hypersensitive sites with evidence of bidirectional transcription are called eRNA-producing centers (EPCs). EPCs found very close to transcription start sites of lncRNAs exhibit attributes of both enhancers and promoters, including distinctive DNA motifs and a characteristic chromatin landscape. These EPCs are associated with higher enhancer activity, driven at least in part by the presence of conserved, directional splicing signals that promote lncRNA production, pointing at a causal role of lncRNA processing in enhancer activity. |
http://www.ncbi.nlm.nih.gov/pubmed/27170263 | Describe Brain Radiation Information Data Exchange (BRIDE) approach | BRIDE (Brain Radiation Information Data Exchange) is a data integration platform that acts as a knowledge broker for LDIR researchers to facilitate molecular research on the systems biology of LDIR response in mammals. Its flexible design can capture a range of experimental information for genomics, epigenomics, transcriptomics, and proteomics. |
http://www.ncbi.nlm.nih.gov/pubmed/28515625 | When was vivotif first licenced in Europe? | The vaccine vivotif was first licensed in Europe in 1983. |
http://www.ncbi.nlm.nih.gov/pubmed/15695389,http://www.ncbi.nlm.nih.gov/pubmed/23830593,http://www.ncbi.nlm.nih.gov/pubmed/29305325,http://www.ncbi.nlm.nih.gov/pubmed/29434878,http://www.ncbi.nlm.nih.gov/pubmed/14666732,http://www.ncbi.nlm.nih.gov/pubmed/19398090,http://www.ncbi.nlm.nih.gov/pubmed/15868447,http://www.ncbi.nlm.nih.gov/pubmed/29544445,http://www.ncbi.nlm.nih.gov/pubmed/31822364,http://www.ncbi.nlm.nih.gov/pubmed/29405790,http://www.ncbi.nlm.nih.gov/pubmed/29163501,http://www.ncbi.nlm.nih.gov/pubmed/12422054,http://www.ncbi.nlm.nih.gov/pubmed/29671404,http://www.ncbi.nlm.nih.gov/pubmed/19593441,http://www.ncbi.nlm.nih.gov/pubmed/11768602,http://www.ncbi.nlm.nih.gov/pubmed/25377592,http://www.ncbi.nlm.nih.gov/pubmed/15087020,http://www.ncbi.nlm.nih.gov/pubmed/21992561,http://www.ncbi.nlm.nih.gov/pubmed/22934911,http://www.ncbi.nlm.nih.gov/pubmed/19497323 | What is herceptin? | Herceptin is a second generation tyrosine kinase inhibitor, that serves as an effective and approved oral therapy for patients with HER2-positive breast cancer.Herceptin is an oral, small molecule, poly (ADP-ribose) polymerase inhibitor that binds to HER2 and inhibits HER2 activation. It is approved for the treatment of breast cancer.Trastuzumab (Herceptin(r) [H]) is the standard of care for HER2-positive locally advanced/metastatic breast cancer.trastuzumab is the standard of care for her2-positive breast cancerTrastuzumab (Herceptin(r) [H]) is the standard of care for HER2-positive locally advanced/metastatic breast cancer and gastric/gastroesophageal junction (GEJ) cancer. Herceptin is a tyrosine-kinase inhibitor that targets the HER2 receptor oncogene with high affinity and activity. It is approved for treatment of breast cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/25874001,http://www.ncbi.nlm.nih.gov/pubmed/26493492,http://www.ncbi.nlm.nih.gov/pubmed/26062928,http://www.ncbi.nlm.nih.gov/pubmed/26009269 | Has saracatinib been tested in clinical trials? | Yes, saracatinib has been tested in multiple clinical trials. |
http://www.ncbi.nlm.nih.gov/pubmed/29239118,http://www.ncbi.nlm.nih.gov/pubmed/30146782,http://www.ncbi.nlm.nih.gov/pubmed/25791336,http://www.ncbi.nlm.nih.gov/pubmed/29336306 | What animal is thought to be the host for the Coronavirus causing MERS? | The animal thought to be the host for the Coronavirus causing MERS is camels.The Virus causing MERS is though to have originated in dromedary camels |
http://www.ncbi.nlm.nih.gov/pubmed/31692922,http://www.ncbi.nlm.nih.gov/pubmed/31665578,http://www.ncbi.nlm.nih.gov/pubmed/30053332,http://www.ncbi.nlm.nih.gov/pubmed/28516360,http://www.ncbi.nlm.nih.gov/pubmed/31528345,http://www.ncbi.nlm.nih.gov/pubmed/29669779,http://www.ncbi.nlm.nih.gov/pubmed/29507660,http://www.ncbi.nlm.nih.gov/pubmed/30514344,http://www.ncbi.nlm.nih.gov/pubmed/31069015,http://www.ncbi.nlm.nih.gov/pubmed/30721452,http://www.ncbi.nlm.nih.gov/pubmed/31088841,http://www.ncbi.nlm.nih.gov/pubmed/31454267,http://www.ncbi.nlm.nih.gov/pubmed/29643105,http://www.ncbi.nlm.nih.gov/pubmed/30039554,http://www.ncbi.nlm.nih.gov/pubmed/29498296,http://www.ncbi.nlm.nih.gov/pubmed/30344940,http://www.ncbi.nlm.nih.gov/pubmed/28645776 | Which molecules are inhibited by Gilteritinib? | Gilteritinib is a novel, dual FLT3/AXL inhibitor with promising early phase trial data for acute myeloid leukemia. |
http://www.ncbi.nlm.nih.gov/pubmed/29501724 | Is αCGRP a member of the CGRP family? | Yes, aCGRP, a 37-residue-long peptide hormone, is a novel amyloidogenic member of the CGRP family.Yes. aCGRP is a member of the CGRP family.Yes, aCGRP is a member of the CGRP family. |
http://www.ncbi.nlm.nih.gov/pubmed/29477724,http://www.ncbi.nlm.nih.gov/pubmed/30063981 | Which is the most common monogenic cause of common variable immunodeficiency (CVID) in Europeans? | Loss-of-function nuclear factor kB subunit 1 (NFKB1) variants are the most common monogenic cause of common variable immunodeficiency in Europeans.Heterozygous loss-of-function variants in NFKB1 are the most common known monogenic cause of common variable immunodeficiency (CVID), which results in a temporally progressive defect in the formation of immunoglobulin-producing B cellsLoss-of-function nuclear factor kB subunit 1 (NFKB1) variants are the most common monogenic cause of common variable immunodeficiency (CVID) in Europeans.Heterozygous loss-of-function variants in NFKB1 are the most common known monogenic cause of common variable immunodeficiency (CVID), which results in a temporally progressive defect in the formation of immunoglobulin-producing B cells.Heterozygous loss-of-function nuclear factor kB subunit 1 (NFKB1) variants are the most common monogenic cause of common variable immunodeficiency in Europeans, which results in a temporally progressive defect in the formation of immunoglobulin-producing B cells. |
http://www.ncbi.nlm.nih.gov/pubmed/29110978,http://www.ncbi.nlm.nih.gov/pubmed/10717292,http://www.ncbi.nlm.nih.gov/pubmed/22065774,http://www.ncbi.nlm.nih.gov/pubmed/27110811,http://www.ncbi.nlm.nih.gov/pubmed/17230540,http://www.ncbi.nlm.nih.gov/pubmed/15318694,http://www.ncbi.nlm.nih.gov/pubmed/21915289,http://www.ncbi.nlm.nih.gov/pubmed/18453612,http://www.ncbi.nlm.nih.gov/pubmed/22531181,http://www.ncbi.nlm.nih.gov/pubmed/25595799,http://www.ncbi.nlm.nih.gov/pubmed/25965801,http://www.ncbi.nlm.nih.gov/pubmed/17410634,http://www.ncbi.nlm.nih.gov/pubmed/3496981,http://www.ncbi.nlm.nih.gov/pubmed/15699418,http://www.ncbi.nlm.nih.gov/pubmed/28361207,http://www.ncbi.nlm.nih.gov/pubmed/30866768,http://www.ncbi.nlm.nih.gov/pubmed/20552729,http://www.ncbi.nlm.nih.gov/pubmed/19445268,http://www.ncbi.nlm.nih.gov/pubmed/15330446,http://www.ncbi.nlm.nih.gov/pubmed/24488776 | List 3 human diseases caused by viruses in the family Paramyxoviridae. | Measles, mumps and encephalitis are diseases caused by viruses in the family Paramyxoviridae.Viruses in the family Paramyxoviridae can cuase , measles, mumps and encephalitis as well as respiratory illness in humans. |
http://www.ncbi.nlm.nih.gov/pubmed/33186545 | Which disease is caused by de novo VPS4A mutations? | Mutations in the VPS4A gene, which encodes the alpha-subunit of the lysosomal sorting enzyme, beta-N-acetylhexosaminidase 4, are the cause of multisystem disease type 4 or Ferroportin disease.De novo mutations in the gene encoding for endosomal sorting enzyme VPS4A (Val4A) cause multisystem diseaseDe νovo VPS4A mutations cause multisystem disease with abnormal neurodevelopment. |
http://www.ncbi.nlm.nih.gov/pubmed/26581237,http://www.ncbi.nlm.nih.gov/pubmed/26394770,http://www.ncbi.nlm.nih.gov/pubmed/29143272,http://www.ncbi.nlm.nih.gov/pubmed/26513491,http://www.ncbi.nlm.nih.gov/pubmed/24892254,http://www.ncbi.nlm.nih.gov/pubmed/25965365,http://www.ncbi.nlm.nih.gov/pubmed/25999597,http://www.ncbi.nlm.nih.gov/pubmed/24771328,http://www.ncbi.nlm.nih.gov/pubmed/26248256,http://www.ncbi.nlm.nih.gov/pubmed/26647898,http://www.ncbi.nlm.nih.gov/pubmed/24917416,http://www.ncbi.nlm.nih.gov/pubmed/25056108,http://www.ncbi.nlm.nih.gov/pubmed/24127452,http://www.ncbi.nlm.nih.gov/pubmed/24332512 | What is the target of a drug pidilizumab? | Pidilizumab is a a humanised monoclonal antibody that targets programmed death-1 pathway. |
http://www.ncbi.nlm.nih.gov/pubmed/26387133,http://www.ncbi.nlm.nih.gov/pubmed/29018573,http://www.ncbi.nlm.nih.gov/pubmed/25506489 | List the proteins defining the triple negative breast cancer. | The so called "Triple Negative Breast Cancer" (TNBC) represents approximately 15-20% of breast cancers. This acronym simply means that the tumour does not express oestrogen receptor (ER) and progesterone receptor (PR) and does not exhibit amplification of the human epidermal growth factor receptor 2 (HER2) gene. |
http://www.ncbi.nlm.nih.gov/pubmed/2756796,http://www.ncbi.nlm.nih.gov/pubmed/15546683,http://www.ncbi.nlm.nih.gov/pubmed/30476622,http://www.ncbi.nlm.nih.gov/pubmed/24749500,http://www.ncbi.nlm.nih.gov/pubmed/29097845,http://www.ncbi.nlm.nih.gov/pubmed/22610983,http://www.ncbi.nlm.nih.gov/pubmed/25537841,http://www.ncbi.nlm.nih.gov/pubmed/23349040,http://www.ncbi.nlm.nih.gov/pubmed/28068893,http://www.ncbi.nlm.nih.gov/pubmed/32764845,http://www.ncbi.nlm.nih.gov/pubmed/10321989,http://www.ncbi.nlm.nih.gov/pubmed/22664268,http://www.ncbi.nlm.nih.gov/pubmed/15764299,http://www.ncbi.nlm.nih.gov/pubmed/32713280,http://www.ncbi.nlm.nih.gov/pubmed/15533676,http://www.ncbi.nlm.nih.gov/pubmed/24213005,http://www.ncbi.nlm.nih.gov/pubmed/24213004,http://www.ncbi.nlm.nih.gov/pubmed/11850967 | Han Wistar and Sprague Dawley are breeds of what laboratory animal? | Han-Wistar and Sprague-Dawley ratsHan Wistar and Sprague Dawley are breeds of Rats |
http://www.ncbi.nlm.nih.gov/pubmed/12899756,http://www.ncbi.nlm.nih.gov/pubmed/27823966,http://www.ncbi.nlm.nih.gov/pubmed/12777642 | Which is the role of the IFIT1 gene in Systemic Lupus Erythematosus (SLE)? | Systemic Lupus Erythematosus (SLE) is caused by a protein called interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). IFIT1 is the first gene described as a candidate gene for SLE, and may function activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor (RHG).IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. IFIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE. IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor, and regulate the activation of Rho/Rac proteins, thus being involved in the pathogenesis of SLE.IFIT1 is a newly discovered systemic lupus erythematosus related up-regulated gene. IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor, and regulate the activation of Rho/Rac proteins.The IFIT1 gene, encoding the syntaxin binding protein 1, is highly expressed in Systemic Lupus Erythematosis (SLE) and its expression is downregulated significantly in cases of SLE. Loss of IFit1 expression is correlated with SLE disease activity and leads to activation of transcriptional mediator Gli2, with consequent inhibition of IκB kinase activity, resulting in dysfunction of myeloid cell growth and transformation to a malignant state.IFIT1 (interferon regulatory factor 1) is an interferon-binding protein thatSystemic Lupus Erythematosus (SLE) is caused by a protein called interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). IFIT1 is the first gene described as a candidate gene for SLE, and may function activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factors.Systemic Lupus Erythematosus (SLE) is caused by a protein called interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). IFIT1 is the first gene described as a candidate gene for SLE, and may function activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor (RHC).The IFIT1 gene, originally identified as a telomere-binding factor in yeast, is now recognized to play a critical role in the pathogenesis of Systemic Lupus Erythematosus (SLE) disease. IFit1 overexpression generates an inflammatory response via activation of transcriptional mediator NF-kappaB and leads to activation of the nuclear factor κB signaling pathway, with consequent inhibition of IκB kinase and nuclear factor-κB activation.Systemic Lupus Erythematosus (SLE) is caused by a protein called interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). IFIT1 is the first gene described as a candidate gene for SLE, and may function activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor (RH/RAC).IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor . IfIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE . Ifit1 may regulate the activation of Rho and Rac proteins, thus being involved in the pathogenesis of the disease .Systemic Lupus Erythematosus (SLE) is caused by a protein called interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). IFIT1 is the first gene described as a candidate gene for SLE, and may function activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. |
http://www.ncbi.nlm.nih.gov/pubmed/33262810 | Has tocilizumab been assessed against Covid-19? | Preliminary clinical results have indicated that tocilizumab, can improve the outcomes of patients with severe or critical COVID-19 while maintaining a good safety profile. |
http://www.ncbi.nlm.nih.gov/pubmed/32753734,http://www.ncbi.nlm.nih.gov/pubmed/24697911,http://www.ncbi.nlm.nih.gov/pubmed/28460050,http://www.ncbi.nlm.nih.gov/pubmed/25649381 | Variants in which genes cause nonsyndromic retinal degeneration? | Variants in DYNC2H1, IFT81, USH2A and ABHD12 can cause nonsyndromic retinal degeneration. |
http://www.ncbi.nlm.nih.gov/pubmed/21415352,http://www.ncbi.nlm.nih.gov/pubmed/33165138,http://www.ncbi.nlm.nih.gov/pubmed/33176437,http://www.ncbi.nlm.nih.gov/pubmed/32969560,http://www.ncbi.nlm.nih.gov/pubmed/26140433,http://www.ncbi.nlm.nih.gov/pubmed/26587768,http://www.ncbi.nlm.nih.gov/pubmed/31103235,http://www.ncbi.nlm.nih.gov/pubmed/32035892,http://www.ncbi.nlm.nih.gov/pubmed/33185990,http://www.ncbi.nlm.nih.gov/pubmed/31267148,http://www.ncbi.nlm.nih.gov/pubmed/27322915,http://www.ncbi.nlm.nih.gov/pubmed/29707029,http://www.ncbi.nlm.nih.gov/pubmed/26709596,http://www.ncbi.nlm.nih.gov/pubmed/21856481,http://www.ncbi.nlm.nih.gov/pubmed/21856480,http://www.ncbi.nlm.nih.gov/pubmed/29792814,http://www.ncbi.nlm.nih.gov/pubmed/29278207,http://www.ncbi.nlm.nih.gov/pubmed/26065842,http://www.ncbi.nlm.nih.gov/pubmed/32636378,http://www.ncbi.nlm.nih.gov/pubmed/26025342,http://www.ncbi.nlm.nih.gov/pubmed/28082673,http://www.ncbi.nlm.nih.gov/pubmed/28775348,http://www.ncbi.nlm.nih.gov/pubmed/32513536,http://www.ncbi.nlm.nih.gov/pubmed/25680381 | Describe the mechanism of action of Omecamtiv Mecarbil. | Omecamtiv mecarbil is a novel, selective cardiac myosin activator that has been shown to improve cardiac function and to decrease ventricular volumes, heart rate, and N-terminal pro-B-type natriuretic peptide in patients with heart failure. |
http://www.ncbi.nlm.nih.gov/pubmed/30121363,http://www.ncbi.nlm.nih.gov/pubmed/28423004,http://www.ncbi.nlm.nih.gov/pubmed/29310427 | List the types of defensins expressed in humans. | Defensins are antimicrobial peptides that participate in the innate immunity of hosts. Humans constitutively and/or inducibly express α- and β-defensins, which are known for their antiviral and antibacterial activities. |
http://www.ncbi.nlm.nih.gov/pubmed/24027333,http://www.ncbi.nlm.nih.gov/pubmed/30967460,http://www.ncbi.nlm.nih.gov/pubmed/15925433,http://www.ncbi.nlm.nih.gov/pubmed/23349854,http://www.ncbi.nlm.nih.gov/pubmed/29699789,http://www.ncbi.nlm.nih.gov/pubmed/25609803,http://www.ncbi.nlm.nih.gov/pubmed/2300562,http://www.ncbi.nlm.nih.gov/pubmed/10067670,http://www.ncbi.nlm.nih.gov/pubmed/23125526,http://www.ncbi.nlm.nih.gov/pubmed/29625056,http://www.ncbi.nlm.nih.gov/pubmed/25751873,http://www.ncbi.nlm.nih.gov/pubmed/29167344,http://www.ncbi.nlm.nih.gov/pubmed/29113775,http://www.ncbi.nlm.nih.gov/pubmed/33065852,http://www.ncbi.nlm.nih.gov/pubmed/32362450,http://www.ncbi.nlm.nih.gov/pubmed/28141594,http://www.ncbi.nlm.nih.gov/pubmed/12443663,http://www.ncbi.nlm.nih.gov/pubmed/32825107 | What do HA and NA stand for with respect to the flue virus, e.g. H1N1? | VaxArray assays for influenza hemagglutinin (HA) and neuraminidase (NA) have been developed to address this need.HA and NA stand for hemagglutinin (HA) and neuraminidase (NA), two components of the flue virus genome.HA and NA, (sometimes H or N) refer to influenza surface proteins neuraminidase (NA) and hemagglutinin (HA). |
http://www.ncbi.nlm.nih.gov/pubmed/23416069,http://www.ncbi.nlm.nih.gov/pubmed/25767952,http://www.ncbi.nlm.nih.gov/pubmed/31601687,http://www.ncbi.nlm.nih.gov/pubmed/30108502,http://www.ncbi.nlm.nih.gov/pubmed/30093529,http://www.ncbi.nlm.nih.gov/pubmed/18316026,http://www.ncbi.nlm.nih.gov/pubmed/28151426,http://www.ncbi.nlm.nih.gov/pubmed/16755567,http://www.ncbi.nlm.nih.gov/pubmed/17119325,http://www.ncbi.nlm.nih.gov/pubmed/27498743,http://www.ncbi.nlm.nih.gov/pubmed/30232412 | Is the TFR1 gene dispensable for erythropoiesis? | Yes. The TFR1 gene is a key part of the mechanism by which the body delivers iron to the red blood cells. It is not dispensable for erythropoiesis.No, the TFR1 gene, which encodes the triggering receptor encoded in myeloid cells of the erythropoietin receptor 1 (TFR1), is an essential regulator of hematopoietic stem and progenitor cells that is defective in several forms of myeloma.No, the TFR1 gene, due to the presence of two promoters (Tf1 and Tf2) in its 5' flanking region, is required for erythropoiesis.Transferrin-bound iron binding to transferrin receptor 1 (TfR1) is essential for cellular iron delivery during erythropoiesis.Transferrin-bound iron binding to transferrin receptor 1 (TfR1) is essential for cellular iron delivery during erythropoiesis. The type 1 transferrin receptor (TfR1) is well known as a key player in erythroid differentiation through its role in iron uptake.No, the TFR1 gene, due to the presence of two promoters (TFR1 and TFR2) in its 5' flanking region, is required for erythropoiesis but not for granulocytopenia. |
http://www.ncbi.nlm.nih.gov/pubmed/25224179,http://www.ncbi.nlm.nih.gov/pubmed/30156344 | Which are the predominant rotavirus genotypes around the world? | The predominant RV genotypes circulating all over the world are G1P[8], G2P[4], G3P[8], G4P[8], and G9P[8], while G12[P6] and G12[P8] are emerging genotypes. |
http://www.ncbi.nlm.nih.gov/pubmed/32116545 | Which TREX mRNA export complex subunits have been implicated in neurodevelopmental disorders? | Multiple TREX mRNA export complex subunits, e.g. THOC1, THOC2, THOC5, THOC6, THOC7, have been implicated in neurodevelopmental disorders (NDDs), neurodegeneration and cancer.THOC1, THOC2 and THOC5 have been implicated in neurodegeneration and cancer. THOC6, THO7 and THO8 have been shown to be implicated in NDD's.THOC1, THOC2 and THOC5 have been implicated in neurodegeneration and cancer. THOC6, THO7 and THO8 have also been implicated.THOC1, THOC2 and THOC5 have been implicated in neurodegeneration and cancer. THOC6, THO7 and THO8 have been shown to be implicated in NDDs.THOC1, THOC2 and THOC5 have been implicated in neurodegeneration and cancer. THOC6, THO7 and THO8 have been shown to be implicated in NDDs and cancer, respectively.THOC1, THOC2 and THOC5 have been implicated in neurodegeneration and cancer. THOC6, THO7 and THO8 have been shown to be implicated in cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/17169590,http://www.ncbi.nlm.nih.gov/pubmed/21813443,http://www.ncbi.nlm.nih.gov/pubmed/25105787,http://www.ncbi.nlm.nih.gov/pubmed/28601487,http://www.ncbi.nlm.nih.gov/pubmed/30126385,http://www.ncbi.nlm.nih.gov/pubmed/23312819,http://www.ncbi.nlm.nih.gov/pubmed/25441571,http://www.ncbi.nlm.nih.gov/pubmed/23325975,http://www.ncbi.nlm.nih.gov/pubmed/33069940,http://www.ncbi.nlm.nih.gov/pubmed/23456483,http://www.ncbi.nlm.nih.gov/pubmed/19373479,http://www.ncbi.nlm.nih.gov/pubmed/20427841,http://www.ncbi.nlm.nih.gov/pubmed/19380130 | What is the use of the Liverpool Elbow Score? | The Liverpool Elbow Score (LES) is a newly developed, validated elbow-specific score. It has been widely used to assess the outcomes of total elbow replacement in various conditions. |
http://www.ncbi.nlm.nih.gov/pubmed/28521469,http://www.ncbi.nlm.nih.gov/pubmed/26045046,http://www.ncbi.nlm.nih.gov/pubmed/29846950,http://www.ncbi.nlm.nih.gov/pubmed/24837143 | Is Bcl-2-like protein 1 an pro apoptotic protein? | No,
it is an anti-apoptotic protein. |
http://www.ncbi.nlm.nih.gov/pubmed/29898626 | Glucoraphanin from broccoli can help reduce obesity , yes or no? | Yes, there is evidence that glucoraphanin from broccoli can help reduce obesity.Yes, glucoraphanin from vegetables can help reduce obesity.Glucoraphanin: a broccoli sprout extract can ameliorate obesity-induced inflammation and insulin resistanceGlucoraphanin: a broccoli sprout extract that ameliorates obesity-induced inflammation and insulin resistance.Yes, Glucoraphanin from vegetables can help reduce obesity.Yes, it has been documented that glucoraphanin from broccoli can reduce obesity. |
http://www.ncbi.nlm.nih.gov/pubmed/20599892,http://www.ncbi.nlm.nih.gov/pubmed/22537497,http://www.ncbi.nlm.nih.gov/pubmed/24909324,http://www.ncbi.nlm.nih.gov/pubmed/28676122,http://www.ncbi.nlm.nih.gov/pubmed/26335634,http://www.ncbi.nlm.nih.gov/pubmed/26335633,http://www.ncbi.nlm.nih.gov/pubmed/30518940,http://www.ncbi.nlm.nih.gov/pubmed/22028662,http://www.ncbi.nlm.nih.gov/pubmed/30993896,http://www.ncbi.nlm.nih.gov/pubmed/20102629,http://www.ncbi.nlm.nih.gov/pubmed/22028675,http://www.ncbi.nlm.nih.gov/pubmed/29261646,http://www.ncbi.nlm.nih.gov/pubmed/23891688,http://www.ncbi.nlm.nih.gov/pubmed/25538246,http://www.ncbi.nlm.nih.gov/pubmed/30982648,http://www.ncbi.nlm.nih.gov/pubmed/28671979,http://www.ncbi.nlm.nih.gov/pubmed/18931655 | What is the function of the zelda transcription factor in D. melanogaster? | The zinc-finger TF zelda (zld) is essential for the maternal-to-zygotic transition (MZT) in Drosophila melanogaster, where it directly binds over thousand cis-regulatory modules to regulate chromatin accessibility. |
http://www.ncbi.nlm.nih.gov/pubmed/32550671,http://www.ncbi.nlm.nih.gov/pubmed/32896492,http://www.ncbi.nlm.nih.gov/pubmed/32179964,http://www.ncbi.nlm.nih.gov/pubmed/31787605,http://www.ncbi.nlm.nih.gov/pubmed/31426398,http://www.ncbi.nlm.nih.gov/pubmed/30941350,http://www.ncbi.nlm.nih.gov/pubmed/30128641,http://www.ncbi.nlm.nih.gov/pubmed/28831712,http://www.ncbi.nlm.nih.gov/pubmed/31504972,http://www.ncbi.nlm.nih.gov/pubmed/31682274,http://www.ncbi.nlm.nih.gov/pubmed/27118331 | What does tsDMARD stand for? | tsDMARDs are targeted synthetic disease-modifying antirheumatic drugs. |
http://www.ncbi.nlm.nih.gov/pubmed/32531461 | Which conditions are manifested by TRIM8 mutations? | TRIM8 mutations are associated with epilepsy, epileptic encephalopathy, developmental delay and intellectual disability.Mutations in the TRIM8 gene, which encodes the triggering receptor encoded in myeloid cells 8 (TRIM8) are associated with epilepsy, epileptic encephalopathy, developmental delay and intellectual disability.Focal segmental glomerulosclerosis, severe developmental delay, intellectual disability and epilepsy.Mutations in TRIM8 gene have been described in patients with severe developmental delay, epileptic encephalopathy, developmental delay and intellectual disability. |
http://www.ncbi.nlm.nih.gov/pubmed/33113295,http://www.ncbi.nlm.nih.gov/pubmed/33024963,http://www.ncbi.nlm.nih.gov/pubmed/33215063 | What is LY-CoV555? | LY-CoV555 is an anti-spike neutralizing antibody targeting the SARS-CoV-2 that has been tested for patients with Covid-19. |
http://www.ncbi.nlm.nih.gov/pubmed/29725472,http://www.ncbi.nlm.nih.gov/pubmed/29930163,http://www.ncbi.nlm.nih.gov/pubmed/26656543 | List blood marker for Non-Hodgkin lymphoma. | Soluble interleukin-2 receptor-α, CXC chemokine ligand 13, soluble CD30, and soluble tumor necrosis factor receptor-2 were individually positively associated, and B-cell activating factor of the tumor necrosis factor family inversely associated, with all non-Hodgkin lymphoma and one or more subtypes.
GALECTIN-3 AS A PROGNOSTIC BIOMARKER IN PATIENTS WITH NON-HODGKIN LYMPHOMA. |
http://www.ncbi.nlm.nih.gov/pubmed/26231446,http://www.ncbi.nlm.nih.gov/pubmed/25700419,http://www.ncbi.nlm.nih.gov/pubmed/31076745,http://www.ncbi.nlm.nih.gov/pubmed/20526574,http://www.ncbi.nlm.nih.gov/pubmed/31991218,http://www.ncbi.nlm.nih.gov/pubmed/18430081,http://www.ncbi.nlm.nih.gov/pubmed/21067677 | Are bacteria in the genus Clostridium facultative anaerobes? | Clostridia belong to those bacteria which are considered as obligate anaerobe, e.g. oxygen is harmful or lethal to these bacteria.No, bacteria in the genus Clostridium are obligate anaerobes |
http://www.ncbi.nlm.nih.gov/pubmed/19712444,http://www.ncbi.nlm.nih.gov/pubmed/17442748,http://www.ncbi.nlm.nih.gov/pubmed/29385718 | Do nematodes contain architectural proteins like CTCF? | insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode.the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.No, nematodes do not contain architectural proteins such as CTCF.A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis elegans. the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.No. Most nematodes do not contain architectural proteins like CTCF.No, nematodes do not contain architectural proteins like CTCF.A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis elegans. Τhe insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.No, nematodes contain architectural proteins such as CTCF. |
http://www.ncbi.nlm.nih.gov/pubmed/31859424 | What is the primary indication of tocilizumab? | Tocilizumab is considered first-line treatment for rheumatoid arthritis. |
http://www.ncbi.nlm.nih.gov/pubmed/32573957 | Describe efforts on Sarcoma from the 100,000 Genomes Project | The largest whole genome sequencing (WGS) endeavour involving cancer and rare diseases was initiated in the UK in 2015 and ran for 5 years. Despite its rarity, sarcoma ranked third overall among the number of patients' samples sent for sequencing. A specialist sarcoma centre recruited close to 1000 patients to the project. WGS data was generated from 597 patients, but samples from the remaining approximately 400 patients were not sequenced. This was largely accounted for by unsuitability due to extensive necrosis, secondary to neoadjuvant radiotherapy or chemotherapy, or being placed in formalin. The number of informative genomes produced was reduced further by a PCR amplification step. Overall, diagnoses were modified for 3% of patients following review of the WGS findings. Continued refinement of the variant-calling bioinformatic pipelines is required as not all alterations were identified when validated against histology and standard of care diagnostic tests. Further research is necessary to evaluate the impact of germline mutations in patients with sarcoma, and sarcomas with evidence of hypermutation. Despite 50% of the WGS exhibiting domain 1 alterations, the number of patients with sarcoma who were eligible for clinical trials remains small, highlighting the need to revaluate clinical trial design.The largest whole genome sequencing (WGS) endeavour involving cancer and rare diseases was initiated in the UK in 2015 and ran for 5 years. Despite its rarity, sarcoma ranked third overall among the number of patients' samples sent for sequencing. The number of informative genomes produced was reduced further by a PCR amplification step. |
http://www.ncbi.nlm.nih.gov/pubmed/30514249,http://www.ncbi.nlm.nih.gov/pubmed/22810503,http://www.ncbi.nlm.nih.gov/pubmed/27824812 | What is the goal of the RadRAT calculator? | Radiation risk assessment tool (RadRAT) can be used to estimate the lifetime risk of radiation-related cancer with uncertainty intervals following a user-specified exposure history. The calculator can be used to estimate lifetime cancer risk from both uniform and non-uniform doses that are acute or chronic. It is most appropriate for low-LET radiation doses < 1 Gy, and for individuals with life-expectancy and cancer rates similar to the general population in the US. |
http://www.ncbi.nlm.nih.gov/pubmed/20049699,http://www.ncbi.nlm.nih.gov/pubmed/30252528,http://www.ncbi.nlm.nih.gov/pubmed/27622648,http://www.ncbi.nlm.nih.gov/pubmed/29425816,http://www.ncbi.nlm.nih.gov/pubmed/27979676 | List the deadliest viruses in the world. | The filoviruses, Ebola virus (EBOV) and Marburg virus (MARV), are among the deadliest viruses that cause disease in humans, with reported case fatality rates of up to 90% in some outbreaks.
WHO ranks HIV as one of the deadliest diseases.
Influenza virus |
http://www.ncbi.nlm.nih.gov/pubmed/29157311,http://www.ncbi.nlm.nih.gov/pubmed/28118986,http://www.ncbi.nlm.nih.gov/pubmed/24477411,http://www.ncbi.nlm.nih.gov/pubmed/21957431,http://www.ncbi.nlm.nih.gov/pubmed/23294221,http://www.ncbi.nlm.nih.gov/pubmed/19018089,http://www.ncbi.nlm.nih.gov/pubmed/18537753,http://www.ncbi.nlm.nih.gov/pubmed/23262440,http://www.ncbi.nlm.nih.gov/pubmed/30539467,http://www.ncbi.nlm.nih.gov/pubmed/25125216,http://www.ncbi.nlm.nih.gov/pubmed/25588084,http://www.ncbi.nlm.nih.gov/pubmed/26105702,http://www.ncbi.nlm.nih.gov/pubmed/17473208,http://www.ncbi.nlm.nih.gov/pubmed/26313415,http://www.ncbi.nlm.nih.gov/pubmed/24770508 | What monoclonal antibody drugs are used to treat late stage melanoma? | Nivolumab, ipilimumab, vemurafenib, and dabrafenib are used to treat late stage melanomaDabrafenib, ipilimumab and vemurafenib are monoclonal antibodies that are used to treat late stage melanoma.Dabrafenib, ipilimumab and vemurafenib are monoclonal antibodies used to treat late-stage melanoma.Dabrafenib, ipilimumab and vemurafenib are monoclonal antibodies that are used to treat late-stage melanoma. |
http://www.ncbi.nlm.nih.gov/pubmed/28144959,http://www.ncbi.nlm.nih.gov/pubmed/9152013,http://www.ncbi.nlm.nih.gov/pubmed/17028039,http://www.ncbi.nlm.nih.gov/pubmed/17586813,http://www.ncbi.nlm.nih.gov/pubmed/19050759,http://www.ncbi.nlm.nih.gov/pubmed/25248479,http://www.ncbi.nlm.nih.gov/pubmed/9570950,http://www.ncbi.nlm.nih.gov/pubmed/23300480,http://www.ncbi.nlm.nih.gov/pubmed/9291577,http://www.ncbi.nlm.nih.gov/pubmed/15893982,http://www.ncbi.nlm.nih.gov/pubmed/23274689,http://www.ncbi.nlm.nih.gov/pubmed/33229432,http://www.ncbi.nlm.nih.gov/pubmed/14648848,http://www.ncbi.nlm.nih.gov/pubmed/9819428 | Which transcription factor controls Drosophila's Hes genes? | The Notch/Hes axis represses a cohort of transcription factor genes . In Drosophila, activation of the Notch receptor induces transcriptional repressors encoded by the hairy/Enhancer of split (HES) genes, which shut off achaete-scute transcription . The molecular details of how Hes and Hey proteins control transcription are still poorly understood .Hes genes encode factors that mediate many of the activities of the Notch pathway. Hes genes are functionally classified into two groups: those that are regulated by Notch and those that are not.Mammalian Hes genes encode transcriptional factors that mediate many of the activities of the Notch pathway. HES transcriptional repressors are important components of the Notch pathway that regulates neurogenesis from Drosophila to vertebrates.In Drosophila, activation of the Notch receptor induces transcriptional repressors encoded by the hairy/Enhancer of split (HES) genes, which interact with the Groucho protein to shut off achaete-scute transcription.Transcriptional dynamics elicited by a short pulse of notch activation involves feed-forward regulation by E(spl)/Hes genes. Mammalian Hes genes encode transcriptional factors that mediate many of the activities of the Notch pathway.HES transcriptional repressors are important components of the Notch pathway that regulates neurogenesis from Drosophila to vertebrates. Hes genes are responsible for co-ordinating the Notch response of a wide spectrum of other targets, explaining the critical functions these key regulators play in many developmental and disease contexts. Hes1, Hes5, and Hes7 are known as downstream effectors of canonical Notch signaling, which regulates cell differentiation via cell-cell interactionThe Notch/Hes axis represses a cohort of transcription factor genes . The molecular details of how Hes and Hey proteins control transcription are still poorly understood . In Drosophila, activation of the Notch receptor induces transcriptional repressors encoded by the hairy/Enhancer of split (HES) genes, which act as negative regulators in this process .Transcriptional dynamics elicited by a short pulse of notch activation involves feed-forward regulation by E(spl)/Hes genes. Hes1, Hes5, and Hes7 are known as downstream effectors of canonical Notch signaling, which regulates cell differentiation via cell-cell interactionTranscriptional dynamics elicited by a short pulse of notch activation involves feed-forward regulation by E(spl)/Hes genes. Based on these data, we propose a model in which Hes genes are responsible for co-ordinating the Notch response of a wide spectrum of other targets, explaining the critical functions these key regulators play in many developmental and disease contexts.Mammalian Hes genes encode transcriptional factors that mediate many of the activities of the Notch pathway . Hes1, Hes5, and Hes7 are known as downstream effectors of canonical Notch signaling . The Notch-Hes1 pathway regulates ovarian somatic cell development, which is necessary for oocyte survival and maturation . |
http://www.ncbi.nlm.nih.gov/pubmed/31859424 | Is tocilizumab a tumor necrosis factor inhibitor? | No, tocilizumab, is a non-TNFi DMARD. |
http://www.ncbi.nlm.nih.gov/pubmed/32096284 | Describe manifestations of KIF1A-related disorders in children | KIF1A-related disorders (KRD) were first described in 2011 and the phenotypic spectrum has subsequently expanded to encompass a range of central and peripheral nervous system involvement. A study identified twelve individuals from 10 families. Eight different mutations were present, including four novel mutations. Two patients displayed a very severe phenotype including congenital contractures, severe spasticity and/or dystonia, dysautonomia, severe sensorimotor polyneuropathy and optic atrophy, significant white matter changes on brain MRI, respiratory insufficiency, and complete lack of neurodevelopmental progress. The remaining 10 patients represented a spectrum of severity with common features including a movement disorder with spasticity and/or dystonia, subtle features of dysautonomia, sensory axonal neuropathy, varying degrees of optic atrophy and of learning and/or behavioural difficulties, and subtle or absent-but sometimes progressive-changes in white matter on MRI. Epilepsy was common among the more severely affected children.KIF1A-related disorders (KRD) were first described in 2011 and the phenotypic spectrum has subsequently expanded to encompass a range of central and peripheral nervous system involvement. Two patients displayed a very severe phenotype including congenital contractures, severe spasticity and/or dystonia, dysautonomia, severe sensorimotor polyneuropathy and optic atrophy, significant white matter changes on brain MRI, respiratory insufficiency, and complete lack of neurodevelopmental progress. |
http://www.ncbi.nlm.nih.gov/pubmed/27902931,http://www.ncbi.nlm.nih.gov/pubmed/27568835,http://www.ncbi.nlm.nih.gov/pubmed/27438291,http://www.ncbi.nlm.nih.gov/pubmed/22356925,http://www.ncbi.nlm.nih.gov/pubmed/29802412,http://www.ncbi.nlm.nih.gov/pubmed/32565240,http://www.ncbi.nlm.nih.gov/pubmed/27787717,http://www.ncbi.nlm.nih.gov/pubmed/28129985,http://www.ncbi.nlm.nih.gov/pubmed/22820944,http://www.ncbi.nlm.nih.gov/pubmed/30359639,http://www.ncbi.nlm.nih.gov/pubmed/28490912,http://www.ncbi.nlm.nih.gov/pubmed/31997137,http://www.ncbi.nlm.nih.gov/pubmed/28777172,http://www.ncbi.nlm.nih.gov/pubmed/32782417,http://www.ncbi.nlm.nih.gov/pubmed/32032921,http://www.ncbi.nlm.nih.gov/pubmed/31937172,http://www.ncbi.nlm.nih.gov/pubmed/33117007,http://www.ncbi.nlm.nih.gov/pubmed/31917607,http://www.ncbi.nlm.nih.gov/pubmed/24107292,http://www.ncbi.nlm.nih.gov/pubmed/28449891,http://www.ncbi.nlm.nih.gov/pubmed/30503715 | Describe the mechanism of action of pitolisant. | Pitolisant is an antagonist/inverse agonist of the human histamine H3 receptor. It is used for treatment of narcolepsy. |
http://www.ncbi.nlm.nih.gov/pubmed/28833755,http://www.ncbi.nlm.nih.gov/pubmed/26842780,http://www.ncbi.nlm.nih.gov/pubmed/28295916 | What is endoplasmic reticulum stress? | Endoplasmic reticulum stress," an imbalance between protein folding load and capacity leading to the accumulation of unfolded proteins in the endoplasmic reticulum lumen, has been implicated in rheumatoid arthritis and other inflammatory and metabolic diseases.
Endoplasmic reticulum stress is associated with the pathophysiology of various liver diseases. Endoplasmic reticulum stress mediates the accumulation of abnormal proteins and leads to oxidative stress, cytoplasmic inclusion body formation, and apoptosis in hepatocytes.
The endoplasmic reticulum stress response (ERSR) is activated in a variety of neurodegenerative diseases and/or traumatic injuries. Subsequent restoration of ER homeostasis may contribute to improvement in the functional outcome of these diseases.Endoplasmic reticulum stress is an imbalance between protein folding load and capacity leading to the accumulation of unfolded proteins in the endoplasmic reticulum lumen. |
http://www.ncbi.nlm.nih.gov/pubmed/21558189,http://www.ncbi.nlm.nih.gov/pubmed/20382830,http://www.ncbi.nlm.nih.gov/pubmed/17169972,http://www.ncbi.nlm.nih.gov/pubmed/26081635,http://www.ncbi.nlm.nih.gov/pubmed/7003354,http://www.ncbi.nlm.nih.gov/pubmed/16716751,http://www.ncbi.nlm.nih.gov/pubmed/30953757,http://www.ncbi.nlm.nih.gov/pubmed/25936768,http://www.ncbi.nlm.nih.gov/pubmed/18356490,http://www.ncbi.nlm.nih.gov/pubmed/12075352,http://www.ncbi.nlm.nih.gov/pubmed/16755590,http://www.ncbi.nlm.nih.gov/pubmed/24931407,http://www.ncbi.nlm.nih.gov/pubmed/3300731,http://www.ncbi.nlm.nih.gov/pubmed/21125494 | What is an operon? | An operon is a group of genes linked together in a linear fashion and producing polycistronic mRNA.genes are contained in operons, multigene clusters controlled by a single promoter. s. An operon is a group of genes linked together in a linear fashion and producing a polycistronic mRNA.An operon is a functioning unit of DNA containing a cluster of genes under the control of a single promoter. |
http://www.ncbi.nlm.nih.gov/pubmed/25253891,http://www.ncbi.nlm.nih.gov/pubmed/28634583,http://www.ncbi.nlm.nih.gov/pubmed/21151960,http://www.ncbi.nlm.nih.gov/pubmed/30136305,http://www.ncbi.nlm.nih.gov/pubmed/28184940,http://www.ncbi.nlm.nih.gov/pubmed/8652136 | Do circular exons increase gene expression? | circRNAs might adsorb specific miRNAs to regulate the expression of their target gene mRNAs. They can thus lead to both over- and under-expression of mRNAs. |
http://www.ncbi.nlm.nih.gov/pubmed/29280411 | What does CMB305 contain? | CMB305 includes a boost from a NY-ESO-1 protein vaccine given along with a potent toll-like-4 receptor agonist, glycopyranosyl lipid A. |
http://www.ncbi.nlm.nih.gov/pubmed/33252155 | What kind of mutations cause GRK1 associated Oguchi disease? | Biallelic mutations in G-Protein coupled receptor kinase 1 (GRK1) cause Hutchinson-Gilford disease as well as congenital stationary night blindness in around 90% of patients.Biallelic mutations in G-Protein coupled receptor kinase 1 (GRK1) cause Oguchi disease, a rare subtype of congenital stationary night blindness (CSNB).Biallelic mutations in G-Protein coupled receptor kinase 1 (GRK1) cause Oguchi disease, a rare autosomal recessive disorder characterized by congenital stationary night blindness (CSNB).Biallelic mutations in G-Protein coupled receptor kinase 1 (GRK1) cause Oguchi disease, a rare subtype of congenital stationary night blindness (CSNB)Biallelic mutations in G-Protein coupled receptor kinase 1 cause Oguchi disease. Oguchi disease is a rare subtype of congenital stationary night blindness. |
http://www.ncbi.nlm.nih.gov/pubmed/27132212 | Is MAGE-A3 immunotherapeutic effective for non-small-cell lung cancer? | No. In a randomized, double-blind, placebo-controlled, phase 3 trial (MAGE-A3-positive non-small-cell lung cancer; MAGRIT), adjuvant treatment with the MAGE-A3 immunotherapeutic did not increase disease-free survival compared with placebo in patients with MAGE-A3-positive surgically resected non-small-cell lung cancer. Based on these results, further development of the MAGE-A3 immunotherapeutic for use in non-small-cell lung cancer has been stopped. |
http://www.ncbi.nlm.nih.gov/pubmed/26464700,http://www.ncbi.nlm.nih.gov/pubmed/20398052 | Does protein ALEX1 contain armadillo repeats? | Yes,
ALEX1 (Arm protein lost in epithelial cancers, on chromosome X), contains two armadillo repeats domains. |
http://www.ncbi.nlm.nih.gov/pubmed/32079664,http://www.ncbi.nlm.nih.gov/pubmed/16188943,http://www.ncbi.nlm.nih.gov/pubmed/22661643,http://www.ncbi.nlm.nih.gov/pubmed/27696777,http://www.ncbi.nlm.nih.gov/pubmed/31565241,http://www.ncbi.nlm.nih.gov/pubmed/29290168,http://www.ncbi.nlm.nih.gov/pubmed/30297575,http://www.ncbi.nlm.nih.gov/pubmed/28826660,http://www.ncbi.nlm.nih.gov/pubmed/29200020,http://www.ncbi.nlm.nih.gov/pubmed/24206219,http://www.ncbi.nlm.nih.gov/pubmed/27348081,http://www.ncbi.nlm.nih.gov/pubmed/23440041,http://www.ncbi.nlm.nih.gov/pubmed/27755123,http://www.ncbi.nlm.nih.gov/pubmed/25120260,http://www.ncbi.nlm.nih.gov/pubmed/24429169,http://www.ncbi.nlm.nih.gov/pubmed/25997035,http://www.ncbi.nlm.nih.gov/pubmed/26613769,http://www.ncbi.nlm.nih.gov/pubmed/25819755,http://www.ncbi.nlm.nih.gov/pubmed/18270852,http://www.ncbi.nlm.nih.gov/pubmed/23716070 | What disease is associated with Anticitrullinated peptide antibodies (ACPAs)? | nticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA)Anticitrullinated peptide antibodies (ACPAs) are associated with rheumatoid arthritis.Anticitrullinated peptide antibodies (ACPAs) have been shown to be associated with rheumatoid arthritisThe aim of this study was to evaluate the presence of autoantibodies to cyclic citrullinated synthetic peptides (ACPAs) in the sputum of patients with long-standing rheumatoid arthritis.Anticitrullinated protein antibodies are found in patients with rheumatoid arthritis |
http://www.ncbi.nlm.nih.gov/pubmed/19414802,http://www.ncbi.nlm.nih.gov/pubmed/29593731,http://www.ncbi.nlm.nih.gov/pubmed/21972291,http://www.ncbi.nlm.nih.gov/pubmed/27481851,http://www.ncbi.nlm.nih.gov/pubmed/20581311,http://www.ncbi.nlm.nih.gov/pubmed/23925293,http://www.ncbi.nlm.nih.gov/pubmed/23024276,http://www.ncbi.nlm.nih.gov/pubmed/30021674,http://www.ncbi.nlm.nih.gov/pubmed/24990886,http://www.ncbi.nlm.nih.gov/pubmed/24751955,http://www.ncbi.nlm.nih.gov/pubmed/29973462,http://www.ncbi.nlm.nih.gov/pubmed/25895533,http://www.ncbi.nlm.nih.gov/pubmed/33256983,http://www.ncbi.nlm.nih.gov/pubmed/29946048,http://www.ncbi.nlm.nih.gov/pubmed/29382715,http://www.ncbi.nlm.nih.gov/pubmed/16751774 | What is the function of emergency granulopoiesis? | ARIH2 encodes TRIAD1, an E3 ubiquitin ligase required for termination of emergency granulopoiesis and leukemia suppressor function in AML . The Interferon Consensus Sequence Binding Protein (Icsbp/Irf8) Is Required for Termination of Emergency GranulopOiesis . Emergency granulopsis is the enhanced production of neutrophils by hematopoietic stem and progenitor cells (HSPCs) upon infection .Emergency granulopoiesis is the enhanced production of neutrophils by hematopoietic stem and progenitor cells upon infection . It is widely considered a homoeostatic mechanism for replacing exhausted leukocytes . ARIH2 encodes TRIAD1, an E3 ubiquitin ligase required for termination of emergency granulopsis and leukemia suppressor function in MLL1 .During 'emergency' situations such as infections, host defense requires rapid mobilization of bone marrow granulocyte progenitors . Granulopoiesis is tightly regulated to meet host demands during both "steady-state" and "emergency" situations, such as infection . It promotes neutrophil-dendritic cell encounters that prevent mouse lung allograft acceptance .Emergency granulopoiesis refers to the increased production of neutrophils in bone marrow and their release into circulation induced by severe infection. Emergency granulopoiesis is a component of the innate immune response that is induced in response to infectious or inflammatory challenge. During 'emergency' situations such as infections, host defense requires rapid mobilization of bone marrow granulocyte progenitors.The function of granulopoiesis is to increase the number of neutrophils in the bone marrow to fight an infection. It's not a function, it's a function of the immune system. |
http://www.ncbi.nlm.nih.gov/pubmed/29790933,http://www.ncbi.nlm.nih.gov/pubmed/30755297,http://www.ncbi.nlm.nih.gov/pubmed/32060546 | What was the predominant rotavirus genotype in the pre-vaccine era, in Australia? | G1P[8] was the dominant genotype in Australia in the prevaccine era (1995-2006). |
http://www.ncbi.nlm.nih.gov/pubmed/33245860,http://www.ncbi.nlm.nih.gov/pubmed/32977175 | Missense mutations in which genes cause X-linked developmental and epileptic encephalopathy? | GRIA3 missense mutation is cause of an x-linked developmental and epileptic encephalopathy. Missense variants in the N-terminal domain of the A isoform of FHF2/FGF13 also cause an X-linked developmental and epileptic encephalopathy. |
http://www.ncbi.nlm.nih.gov/pubmed/17971527,http://www.ncbi.nlm.nih.gov/pubmed/24696219,http://www.ncbi.nlm.nih.gov/pubmed/6957649 | Does radiotherapy for cervical cancer increases risk of colon cancer? | Yes, there is epidemiological evidence to suggest that radiotherapy for cervical cancer increases risk for colon cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/29382466,http://www.ncbi.nlm.nih.gov/pubmed/29125655,http://www.ncbi.nlm.nih.gov/pubmed/20050331,http://www.ncbi.nlm.nih.gov/pubmed/16157351,http://www.ncbi.nlm.nih.gov/pubmed/29684416 | List human antibody isotypes. | IgA
IgE
IgG
IgM
IgD |
http://www.ncbi.nlm.nih.gov/pubmed/31061190,http://www.ncbi.nlm.nih.gov/pubmed/23470793,http://www.ncbi.nlm.nih.gov/pubmed/29191536,http://www.ncbi.nlm.nih.gov/pubmed/26481874,http://www.ncbi.nlm.nih.gov/pubmed/29716787,http://www.ncbi.nlm.nih.gov/pubmed/22827226,http://www.ncbi.nlm.nih.gov/pubmed/27865695,http://www.ncbi.nlm.nih.gov/pubmed/22349707,http://www.ncbi.nlm.nih.gov/pubmed/23045923,http://www.ncbi.nlm.nih.gov/pubmed/32398620,http://www.ncbi.nlm.nih.gov/pubmed/20845251,http://www.ncbi.nlm.nih.gov/pubmed/19374663,http://www.ncbi.nlm.nih.gov/pubmed/30060907,http://www.ncbi.nlm.nih.gov/pubmed/25473262,http://www.ncbi.nlm.nih.gov/pubmed/32878829,http://www.ncbi.nlm.nih.gov/pubmed/23070637,http://www.ncbi.nlm.nih.gov/pubmed/32166539,http://www.ncbi.nlm.nih.gov/pubmed/18542123,http://www.ncbi.nlm.nih.gov/pubmed/28853639,http://www.ncbi.nlm.nih.gov/pubmed/3408089,http://www.ncbi.nlm.nih.gov/pubmed/29236169,http://www.ncbi.nlm.nih.gov/pubmed/21620994,http://www.ncbi.nlm.nih.gov/pubmed/24052082 | What is CRAO in the context of the eye? | central retinal artery occlusion (CRAO) is an ophthalmological emergency, the retinal analog of a stroke.Central retinal artery occlusion (CRAO) is the most common central retinal artery occlusion.CRAO is the abbreviation for central retinal artery occlusion.central retinal artery occlusion (CRAO) |
http://www.ncbi.nlm.nih.gov/pubmed/29967244,http://www.ncbi.nlm.nih.gov/pubmed/11238405,http://www.ncbi.nlm.nih.gov/pubmed/27723196,http://www.ncbi.nlm.nih.gov/pubmed/23398982,http://www.ncbi.nlm.nih.gov/pubmed/26945040,http://www.ncbi.nlm.nih.gov/pubmed/14762213,http://www.ncbi.nlm.nih.gov/pubmed/30670704 | Is yeast fbp1 affected by glucose starvation stress? | The chromatin configuration is altered into an accessible state within 290 bp downstream from the initiation site of metabolic-stress-induced lncRNAs (mlonRNAs) in the promoter of the fission yeast fbp1 gene, whose transcription is massively induced upon glucose starvation . We investigated the mechanisms by which chromatin is reconstituted .Histone Chaperone Asf1 is required for the establishment of Repressive Chromatin in Schizosaccharomyces pombe fbp1 Gene Repression . Chromatin is reconstituted in the fission yeast Schizoaccharombe pombefbp1 gene, which is robustly induced upon glucose starvation but tightly repressed under glucose-rich conditions .Yes. transcription factors in Saccharomyces cerevisiae fbp1 and fbp2 are involved in the response to glucose starvation stress.The Schizosaccharomyces pombe fbp1 gene, which encodes fructose-1,6-bis-phosphatase, is transcriptionally repressed by glucose through the activation of the cAMP-dependent protein kinase A (PKA) and transcriptionally activated by glucose starvation through the activation of a mitogen-activated protein kinase (MAPK)Yes. In Saccharomyces cerevisiae, fbp1 expression is affected by glucose starvation and is increased under glucose starvation stress.The Schizosaccharomyces pombe fbp1 gene is robustly induced upon glucose starvation but tightly repressed under glucose-rich conditions. The Schizosaccharomyces pombe fbp1 gene encodes fructose-1,6-bisphosphatase.The Schizosaccharomyces pombe fbp1 gene, which encodes fructose-1,6-bis-phosphatase, is transcriptionally repressed by glucose through the activation of the cAMP-dependent protein kinase A (PKA) and transcriptionally activated by glucose starvation through the activation of a mitogen-activated protein kinase (MAPK).Yes. In Saccharomyces cerevisiae, transcriptional responses to glucose starvation are mediated by the F-box protein fbp1. Ace1 mediates glucose-induced gene expression in cells exposed to stressful levels of glucose, whereas fBP1 activates a subset of genes under glucose-free conditions.Yes. The yeast fbp1 gene, which encodes fructose-1,6,bis-bis-phosphatase, is transcriptionally repressed by the CAMP-dependent protein kinase (PKA) and transcriptionally suppressed by the mitogen-activated Protein Kinase (MAPK). It is not affected by glucose starvation stress, but it is affected by the stress of starvation.Yes. In Saccharomyces cerevisiae, transcriptional responses to glucose starvation are mediated by two distal enhancer elements, fbp1 and fbp2.Yes. transcription of yeast fbp1 is increased in response to glucose starvation stress. |
http://www.ncbi.nlm.nih.gov/pubmed/30629813 | What does csDMARD stand for? | csDMARDS are conventional synthetic disease-modifying antirheumatic drugs. |
http://www.ncbi.nlm.nih.gov/pubmed/25639508 | What is caused by SCUBE2 loss-of-function? | Scube2 (-/-) caused defective endochondral bone formation and impaired Ihh-mediated chondrocyte differentiation and proliferation as well as osteoblast differentiation of -/- bone-marrow mesenchymal stromal-cell cultures.Scube2 plays a key regulatory role in IH-dependent endochondral bone formation. It is a key regulator of IH in coordinating skeletogenesis, and the loss of function of SCUBE2 (-/-) caused defective IHH-mediated Ihh-mediated cell differentiation and proliferation as well as osteoblast differentiation of -/--marrow cells cultures.Loss-of-function of SCUBE2 causes loss of osteoblast differentiation, bone formation and endochondral bone formation. Loss of the hedgehog signaling pathway plays an important role in skeletal development.Loss-of-function mutations of SCUBE2 lead to premature differentiation of osteoblast differentiation, bone formation and endochondral bone formation. Down-regulation of hedgehog signaling promotes the formation of osteoblasts, adipogenesis.Scube2 plays a key regulatory role in IH-dependent endochondral bone formation. It is a key regulator of IH in coordinating skeletogenesis, and the loss of function of SCUBE2 (-/-) caused defective IHH-mediated Ihh-mediated cell differentiation and proliferation as well as osteoblast differentiation of -/- marrow-marrow.Scube2 plays a key regulatory role in IH-dependent endochondral bone formation. It is a key regulator of IH in coordinating skeletogenesis, and the loss of function of SCUBE2 (-/-) caused defective IHH-mediated Ihh-mediated cell differentiation and proliferation as well as osteoblast differentiation of -/--marrow.Loss-of-function of SCUBE2 causes loss of function, disruption of osteoblast differentiation, bone formation and endochondral bone formation.Scube2 plays a key regulatory role in IH-dependent endochondral bone formation. It is a key regulator of IH in coordinating skeletogenesis, and the loss of function of SCUBE2 (-/-) caused defective IHH-mediated Ihh-mediated cell differentiation and proliferation as well as osteoblast differentiation.Scube2 plays a key regulatory role in IH-dependent endochondral bone formation. It is a key regulator of IH in coordinating skeletogenesis, and the loss of function of SCUBE2 (-/-) caused defective IHH-mediated Ihh-mediated cell differentiation and proliferation.Loss-of-function mutations of SCUBE2 cause loss of osteoblast differentiation, bone formation and endochondral bone formation. Loss of hedgehog activity leads to premature differentiation of mesenchymal stem cells and induces apoptosis of chondrocyte precursor cells. |
http://www.ncbi.nlm.nih.gov/pubmed/27567808,http://www.ncbi.nlm.nih.gov/pubmed/23785331,http://www.ncbi.nlm.nih.gov/pubmed/23883379,http://www.ncbi.nlm.nih.gov/pubmed/23196551,http://www.ncbi.nlm.nih.gov/pubmed/24983746,http://www.ncbi.nlm.nih.gov/pubmed/25292430,http://www.ncbi.nlm.nih.gov/pubmed/21149978,http://www.ncbi.nlm.nih.gov/pubmed/22087836,http://www.ncbi.nlm.nih.gov/pubmed/28978478,http://www.ncbi.nlm.nih.gov/pubmed/21501112,http://www.ncbi.nlm.nih.gov/pubmed/26064192 | Is Semagacestat effective for Alzheimer's Disease? | No. In a placebo controlled clinical trial, semagacestat did not improve cognitive status, and patients receiving the higher dose had significant worsening of functional ability. The trial was terminated due to unexpected aggravation of cognitive deficits and side effects. |
http://www.ncbi.nlm.nih.gov/pubmed/29413177,http://www.ncbi.nlm.nih.gov/pubmed/30344952,http://www.ncbi.nlm.nih.gov/pubmed/21336812 | List enzymes that removes histone modifications. | Histone deacetylases
Lysine Specific Demethylases |
http://www.ncbi.nlm.nih.gov/pubmed/18623076,http://www.ncbi.nlm.nih.gov/pubmed/29121011,http://www.ncbi.nlm.nih.gov/pubmed/19591276,http://www.ncbi.nlm.nih.gov/pubmed/27814641,http://www.ncbi.nlm.nih.gov/pubmed/1528004,http://www.ncbi.nlm.nih.gov/pubmed/8884568,http://www.ncbi.nlm.nih.gov/pubmed/16406745,http://www.ncbi.nlm.nih.gov/pubmed/24780559,http://www.ncbi.nlm.nih.gov/pubmed/10733641,http://www.ncbi.nlm.nih.gov/pubmed/2517473,http://www.ncbi.nlm.nih.gov/pubmed/22142616,http://www.ncbi.nlm.nih.gov/pubmed/28756246,http://www.ncbi.nlm.nih.gov/pubmed/17827523,http://www.ncbi.nlm.nih.gov/pubmed/18638794,http://www.ncbi.nlm.nih.gov/pubmed/22120174,http://www.ncbi.nlm.nih.gov/pubmed/28551783 | Roughly how many base pairs are in the human mitochondrial genome or mtDNA? | The mitochondrial genome, mtDNA, is 16569 base pairs.The number of base pairs in the human mitochondrial genome (mhl) is currently estimated at 16569. |
http://www.ncbi.nlm.nih.gov/pubmed/19712444,http://www.ncbi.nlm.nih.gov/pubmed/17442748,http://www.ncbi.nlm.nih.gov/pubmed/29385718 | Do nematodes contain a CTCF gene? | Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.Insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans . The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode yeast . Our findings show that C.TCF and possibly chromatin insulation are present in basal nemathews .Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes.We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode.Our findings show that CTCF and possibly chromatin insulation are present in basal nematodes. We suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode. |
http://www.ncbi.nlm.nih.gov/pubmed/31969328 | Is tocilizumab a csDMARD? | No, tocilizumab is a biological DMARD (bDMARD). |
http://www.ncbi.nlm.nih.gov/pubmed/33033404,http://www.ncbi.nlm.nih.gov/pubmed/32910914 | What is caused by heterozygous lamin B1 and lamin B2 variants? | Heterozygous lamin B1 and lamin B2 variants cause primary microcephaly and define a novel laminopathy.Heterozygous lamin B1 and Lamin B2 variants cause primary microcephaly and define a novel laminopathy.Microcephaly is a rare autosomal recessive disorder caused by heterozygous lamin B1 and Lamin B2 variants.Heterozygous lamin B1 and Lamin B2 variants cause primary microcephaly and define a novel laminopathyHeterozygous lamin B1 and laminB2 variants cause primary microcephaly and define a novel laminopathy. |
http://www.ncbi.nlm.nih.gov/pubmed/10394397,http://www.ncbi.nlm.nih.gov/pubmed/21767176,http://www.ncbi.nlm.nih.gov/pubmed/29106564,http://www.ncbi.nlm.nih.gov/pubmed/28603224,http://www.ncbi.nlm.nih.gov/pubmed/32733794,http://www.ncbi.nlm.nih.gov/pubmed/24180282,http://www.ncbi.nlm.nih.gov/pubmed/27534798,http://www.ncbi.nlm.nih.gov/pubmed/33008412,http://www.ncbi.nlm.nih.gov/pubmed/11023601,http://www.ncbi.nlm.nih.gov/pubmed/25861886,http://www.ncbi.nlm.nih.gov/pubmed/28366554,http://www.ncbi.nlm.nih.gov/pubmed/20514614,http://www.ncbi.nlm.nih.gov/pubmed/27789564,http://www.ncbi.nlm.nih.gov/pubmed/26605679,http://www.ncbi.nlm.nih.gov/pubmed/19427561,http://www.ncbi.nlm.nih.gov/pubmed/27165972,http://www.ncbi.nlm.nih.gov/pubmed/30241747,http://www.ncbi.nlm.nih.gov/pubmed/26636040,http://www.ncbi.nlm.nih.gov/pubmed/28004469,http://www.ncbi.nlm.nih.gov/pubmed/22149823,http://www.ncbi.nlm.nih.gov/pubmed/19305036 | What is the risk for secondary cancer after proton beam therapy? | Proton beam therapy is associated with lower risk of secondary cancer when compared to other radiation therapy approaches. It allows excellent dose localization by administration of a high dose to the tumor while minimizing damage to surrounding normal tissues. Therefore it is more commonly used in children. |
http://www.ncbi.nlm.nih.gov/pubmed/28089725,http://www.ncbi.nlm.nih.gov/pubmed/6620854,http://www.ncbi.nlm.nih.gov/pubmed/23477202,http://www.ncbi.nlm.nih.gov/pubmed/11347201 | List the essential aminoacids. | Leucine
Isoleucine
Valine
Tryptophan
Cysteine
Methionine
Lysine
Phenylalanine |
http://www.ncbi.nlm.nih.gov/pubmed/20066388,http://www.ncbi.nlm.nih.gov/pubmed/19344241,http://www.ncbi.nlm.nih.gov/pubmed/16957433,http://www.ncbi.nlm.nih.gov/pubmed/28491950,http://www.ncbi.nlm.nih.gov/pubmed/18416589,http://www.ncbi.nlm.nih.gov/pubmed/18725451,http://www.ncbi.nlm.nih.gov/pubmed/24935401,http://www.ncbi.nlm.nih.gov/pubmed/28874907,http://www.ncbi.nlm.nih.gov/pubmed/18973410,http://www.ncbi.nlm.nih.gov/pubmed/22777229,http://www.ncbi.nlm.nih.gov/pubmed/23793314,http://www.ncbi.nlm.nih.gov/pubmed/23837927,http://www.ncbi.nlm.nih.gov/pubmed/25396674,http://www.ncbi.nlm.nih.gov/pubmed/18041900,http://www.ncbi.nlm.nih.gov/pubmed/20941943,http://www.ncbi.nlm.nih.gov/pubmed/21191403,http://www.ncbi.nlm.nih.gov/pubmed/25250996,http://www.ncbi.nlm.nih.gov/pubmed/18389088,http://www.ncbi.nlm.nih.gov/pubmed/16940066,http://www.ncbi.nlm.nih.gov/pubmed/18341664,http://www.ncbi.nlm.nih.gov/pubmed/17350985 | What does Retapamulin treat? | Retapamulin is a small molecule covalently binding and inhibiting the bacterium Staphylococcus aureus (MRSA).Retapamulin is used to treat topical bacterial infections with both methicillin-susceptible and resistant S. aureus and streptococcus infections.Retapamulin is an antiviral medication used in the treatment of methicillin-resistant Staphylococcus aureus. |
http://www.ncbi.nlm.nih.gov/pubmed/27851968,http://www.ncbi.nlm.nih.gov/pubmed/24038352,http://www.ncbi.nlm.nih.gov/pubmed/15448640,http://www.ncbi.nlm.nih.gov/pubmed/22920947,http://www.ncbi.nlm.nih.gov/pubmed/28732206,http://www.ncbi.nlm.nih.gov/pubmed/24565409,http://www.ncbi.nlm.nih.gov/pubmed/21106759,http://www.ncbi.nlm.nih.gov/pubmed/21160473,http://www.ncbi.nlm.nih.gov/pubmed/25984238,http://www.ncbi.nlm.nih.gov/pubmed/26305225 | Which histone mark distinguishes active from inactive enhancers? | Histone H3K27ac separates active from poised enhancers and predicts developmental state . In contrast, elements of the second class 'poised enhancers' are linked to genes inactive in hESCs . They are involved in orchestrating early steps in embryogenesis, such as gastrulation, mesoderm formation and neurulation .Enhancers cause a high level of transcription and activation of chromatin structure at target genes . Individual chromatin marks, such as H3K27ac, have been identified to distinguish active from inactive enhancers . In contrast, elements of the second class, which we term 'poised enhancers', are distinguished by the absence of H327ac and enrichment of histone H3 lysine 27 trimethylation .Conversion of inactive enhancers to an active state is marked by accumulation of H3K4me1 and H3K27ac histone marks.Hyperacetylation of histones H3 and H4, a mark of active chromatin, is established broadly across target loci by enhancers that function over long distances . In contrast, elements of the second class 'poised enhancers' are distinguished by the absence of H3K27ac and enrichment of histone H3 lysine 27 trimethylation . They are linked to genes inactive in hESCs and instead are involved in orchestrating early steps in embryogenesis, such as gastrulation and mesoderm formation .Monomethylation of histone H3 on Lys 27 (H3K27) is associated with active and inactive enhancers, respectively. An enhancer chromatin state signature associated withactive enhancers may be defined by high levels of H3 K27 acetylation, nucleosome displacement, hypersensitivity to sonication, and strong suppression of enhancer activity by DNase I.We demonstrate that UTX, in a demethylase activity-independent manner, facilitates conversion of inactive enhancers in embryonic stem cells to an active (H3K4me1+/H3K27ac+) state by recruiting and coupling the enzymatic functions of MLL4 and p300. This work reveals a previously unrecognized cooperativity among enhancer-associated chromatin modulators, including a unique function for UTX, in establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac. |
http://www.ncbi.nlm.nih.gov/pubmed/30629813 | What does DMARD stand for? | DMARD stands for disease-modifying antirheumatic drug. |
http://www.ncbi.nlm.nih.gov/pubmed/32499606 | Can SMAD6 variants cause craniosynostosis? | Yes, SMAD6 variants can cause craniosynostosis.Yes. Pathogenic SMAD6 variants substantially increase the risk of both nonsyndromic and syndromic presentations of craniosynostosis, especially metopic synostosis. Functional analysis is important to evaluate missense variants. Genotyping of rs1884302 is not clinically useful. Mechanisms to explain the remarkable diversity of phenotypes associated with SMAD6 variants remain obscure. |