https://transhumanist.ru/index.php?action=history&feed=atom&title=FANCC 2026-06-09T00:55:04Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=FANCC&diff=6528&oldid=prev 2021-05-12T15:35:23Z

<p>Новая страница: «Fanconi anemia group C protein (Protein FACC) [FAC] [FACC] ==Publications== {{medline-entry |title=Fanconi Anemia complementation group C protein in metabolic d...»</p> <p><b>Новая страница</b></p><div>Fanconi anemia group C protein (Protein FACC) [FAC] [FACC]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Fanconi Anemia complementation group C protein in metabolic disorders.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29930218<br /> |abstract=Given importance of 22-Fanconi Anemia (FA) proteins together to act in a signaling pathway in preventing deleterious clinical symptoms, e.g. severe bone marrow failure, congenital defects, an early onset of aging and cancer, studies on each FA protein become increasingly attractive. However, an unbiased and systematic investigation of cellular effects resulting from each FA protein is missing. Here, we report roles of FA complementation C group protein ([[FANCC]]) in the protection from metabolic disorders. This study was prompted by the diabetes-prone feature displayed in [[FANCC]] knockout mice, which is not typically shown in patients with FA. We found that in cells expressing [[FANCC]] at different levels, there are representative alterations in metabolites associated with aging (glycine, citrulline, ornithine, L-asparagine, L-tyrosine, L-arginine, L-glutamine, L-leucine, L-isoleucine, L-valine, L-proline and L-alanine), Diabetes Mellitus (DM) (carbon monoxide, collagens, fatty acids, D-glucose, fumaric acid, 2-oxoglutaric acid, C3), inflammation (inosine, L-arginine, L-isoleucine, L-leucine, L-lysine, L-phenylalanine, hypoxanthine, L-methionine), and cancer ( L-methionine, sphingomyelin, acetyl-L-carnitine, L-aspartic acid, L-glutamic acid, niacinamide, phospho-rylethanolamine). We also found that [[FANCC]] can act in an FA-pathway-independent manner in tumor suppression. Collectively, featured-metabolic alterations are readouts of functional mechanisms underlying reduced tumorigenicity driven by [[FANCC]], demonstrating close links among cancer, aging, inflammation and DM.<br /> |mesh-terms=* Animals<br /> * Biomarkers<br /> * Breast Neoplasms<br /> * Cell Line, Tumor<br /> * Cloning, Molecular<br /> * Fanconi Anemia Complementation Group C Protein<br /> * Female<br /> * Gene Expression Regulation<br /> * Humans<br /> * Metabolomics<br /> * Principal Component Analysis<br /> |keywords=* Fanconi Anemia (FA)<br /> * aging<br /> * cancer<br /> * diabetes<br /> * inflammation<br /> * metabolites<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046246<br /> }}</div>

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