322) complexity of genomic alteration of GPCR genes as well as their functional conseque |
323) er altered circadian rhythmicity of clock genes is associated with metabolic dysfunc |
324) , and TGFβ-dependent regulation of these genes is dependent on nascent RNA transcri |
325) t this system comprised of many circadian genes is implicated in epilepsy. |
326) fication of cancer-specific vulnerability genes is one of the most promising approac |
327) hed 2005-2018 and focused on ADRD-related genes or genetic factors among underrepres |
328) hanisms that increase transcription of A3 genes or induce proteasomal degradation of |
329) developing therapeutics targeting AD risk genes or risk variants to influence AD pat |
330) ear how C4A interacts with other SCZ risk genes or whether the complement system mor |
331) nduces the stable expression of antiviral genes within CD14+ cells of the placenta, |
332) l risk loci, prioritized candidate target genes within associated regions, and highl |
333) We showed that core genes within the SggT7SST05 locus are expr |
334) sion of either the collagen type I or III genes within the cultured myofibroblasts. |
335) gs, microbes and antimicrobial resistance genes (ARGs) have the potential to be tran |
336) cteria (ARB) and antimicrobial resistance genes (ARGs) of clinical importance. |
337) communities and antimicrobial resistance genes (ARGs) to soil communities. |
338) twofold up/down differentially expressed genes (DEGs) and bioinformatics analyses r |
339) a change in 119 differentially expressed genes (DEGs) between mThy1-Asyn mice and w |
340) networks of the differentially expressed genes (DEGs) were built by the Search Tool |
341) luated the impact of human IFN-stimulated genes (ISGs) on viral replication. |
342) ntly, enrichment of interferon-stimulated genes (ISGs) predicted a favorable respons |
343) Type 1 interferon response genes (ISGs) were among those that were di |
344) germline variants in cancer-predisposing genes among 15 children with SMNs after ch |
345) ects to identify differentially expressed genes among PTSD cases and controls. |
346) The differentially expressed genes among the three groups were analyzed |
347) ium tuberculosis (Mtb) EmbR, and EmbC/A/B genes cause EMB resistance. |
348) Rare pathogenic variants in sarcomere genes cause HCM, but with unexplained phen |
349) therapeutic targets, mutations in 55 GPCR genes cause about 66 inherited monogenic d |
350) s associated loci, which are enriched for genes expressed in growth plate chondrocyt |
351) control metabolism through regulation of genes expressed in the brain, or that cont |
352) owever, it remains unclear which specific genes expressed in which layers of the gro |
353) ts show that interactions between SNPs in genes from the aging pathways influence su |
354) ne coexpression networks based on the hub genes from the candidate modules were then |
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