https://transhumanist.ru/index.php?action=history&feed=atom&title=FAM13A 2026-06-13T19:07:31Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=FAM13A&diff=6527&oldid=prev 2021-05-12T15:35:20Z

<p>Новая страница: «Protein FAM13A [FAM13A1] [KIAA0914] ==Publications== {{medline-entry |title=Trade-offs in aging lung diseases: a review on shared but opposite genetic risk vari...»</p> <p><b>Новая страница</b></p><div>Protein FAM13A [FAM13A1] [KIAA0914]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Trade-offs in aging lung diseases: a review on shared but opposite genetic risk variants in idiopathic pulmonary fibrosis, lung cancer and chronic obstructive pulmonary disease.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29517586<br /> |abstract=The process of aging involves biological changes that increases susceptibility for disease. In the aging lung disease IPF, GWAS studies identified genes associated with risk for disease. Recently, several of these genes were also found to be involved in risk for COPD or lung cancer. This review describes GWAS-derived risk genes for IPF that overlap with risk genes for lung cancer or COPD. Risk genes that overlap between aging lung diseases, include [[FAM13A]], [[DSP]] and [[TERT]]. Most interestingly, disease predisposing alleles for IPF are opposite to those for COPD or lung cancer. Studies show that the alleles are associated with differential gene expression and with physiological traits in the general population. The opposite allelic effect sizes suggest the presence of trade-offs in the aging lung. For [[TERT]], the trade-off involves cellular senescence versus proliferation and repair. For [[FAM13A]] and [[DSP]], trade-offs may involve protection from noxious gases or tissue integrity. The overlap in risk genes in aging lung diseases provides evidence that processes associated with [[FAM13A]], [[DSP]] and [[TERT]] are important for healthy aging. The opposite effect size of the disease risk alleles may represent trade-offs, for which a model involving an apicobasal gene expression gradient is presented.<br /> |mesh-terms=* Aging<br /> * Alleles<br /> * Cell Proliferation<br /> * Cellular Senescence<br /> * Desmoplakins<br /> * GTPase-Activating Proteins<br /> * Genetic Variation<br /> * Humans<br /> * Idiopathic Pulmonary Fibrosis<br /> * Lung Neoplasms<br /> * Phenotype<br /> * Pulmonary Disease, Chronic Obstructive<br /> * Risk Factors<br /> * Telomerase<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5895171<br /> }}</div>

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