https://transhumanist.ru/index.php?action=history&feed=atom&title=CIAO1 2026-04-04T01:32:24Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=CIAO1&diff=5115&oldid=prev 2021-05-12T13:29:52Z

<p>Новая страница: «Probable cytosolic iron-sulfur protein assembly protein CIAO1 (WD repeat-containing protein 39) [CIA1] [WDR39] ==Publications== {{medline-entry |title=Inhibited...»</p> <p><b>Новая страница</b></p><div>Probable cytosolic iron-sulfur protein assembly protein CIAO1 (WD repeat-containing protein 39) [CIA1] [WDR39]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Inhibited [[PTHLH]] downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network in no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) by systems-theoretical analysis.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22955522<br /> |abstract=We analyzed the different biological processes and occurrence numbers between low expression inhibited [[PTHLH]] downstream-mediated aging gene ontology (GO) network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and the corresponding high expression (fold change ≥2) inhibited GO network of human hepatocellular carcinoma (HCC). Inhibited [[PTHLH]] downstream-mediated aging network consisted of aging, branched chain family amino acid biosynthesis, cellular metabolism, cholesterol biosynthesis, coupled to cyclic nucleotide second messenger, cytolysis, &#039;de novo&#039; GDP-l-fucose biosynthesis, detection of mechanical stimulus, glucose homeostasis, G-protein signaling, leukocyte adhesion, iron-sulfur cluster assembly, JAK-STAT cascade, Notch signaling pathway, nucleotide-sugar metabolism, peptidyl-tyrosine sulfation, protein amino acid N-linked glycosylation, protein amino acid phosphorylation, response to drug, rRNA processing, translational initiation, ubiquitin-dependent protein catabolism, homophilic cell adhesion in no-tumor hepatitis/cirrhotic tissues. We proposed inhibited [[PTHLH]] downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network. Our hypothesis was verified by the same inhibited [[PTHLH]] downstream-mediated aging GO network in no-tumor hepatitis/cirrhotic tissues with the corresponding activated GO network of HCC, or the different with the corresponding activated GO network of no-tumor hepatitis/cirrhotic tissues. Inhibited [[PTHLH]] downstream leukocyte adhesion-mediated protein amino acid N-linked glycosylation coupling Notch and JAK-STAT cascade to iron-sulfur cluster assembly-induced aging network included TSTA3, [[ALK]], [[CIAO1]], [[NOTCH3]] in no-tumor hepatitis/cirrhotic tissues from the GEO data set using gene regulatory network inference method and our programming.<br /> |mesh-terms=* Aging<br /> * Fibrosis<br /> * Gene Expression Regulation, Neoplastic<br /> * Glycosylation<br /> * Hepacivirus<br /> * Hepatitis<br /> * Hepatitis B virus<br /> * Homeostasis<br /> * Humans<br /> * Iron-Sulfur Proteins<br /> * Leukocytes<br /> * Models, Biological<br /> * Neoplasms<br /> * Oligonucleotide Array Sequence Analysis<br /> * Parathyroid Hormone-Related Protein<br /> * Phosphorylation<br /> * Receptors, Notch<br /> * Signal Transduction<br /> * Systems Theory<br /> <br /> |full-text-url=https://sci-hub.do/10.1039/c2ib20148h<br /> }}</div>

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