https://transhumanist.ru/index.php?action=history&feed=atom&title=MCM4 2026-04-09T19:18:07Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=MCM4&diff=4701&oldid=prev 2021-04-29T19:30:35Z

<p>Новая страница: «DNA replication licensing factor MCM4 (EC 3.6.4.12) (CDC21 homolog) (P1-CDC21) [CDC21] ==Publications== {{medline-entry |title=Hepatoprotective effects of hydro...»</p> <p><b>Новая страница</b></p><div>DNA replication licensing factor MCM4 (EC 3.6.4.12) (CDC21 homolog) (P1-CDC21) [CDC21]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Hepatoprotective effects of hydroxysafflor yellow A in D-galactose-treated aging mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32454116<br /> |abstract=Hydroxysafflor yellow A (HSYA) is an effective chemical component isolated from Chinese herb Carthamus tinctorius L. In present study, we aimed to evaluate the effects of HSYA on D-galactose- (D-gal-) induced aging in mice, and to elucidate the underlying mechanism. Male C57BL/6 mice were intraperitoneal injection of D-gal and HSYA for 8 weeks. The body weight gain, spleen and thymus coefficients were determined. Levels of super dismutase (SOD), catalase ([[CAT]]), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in serum and liver were measured using commercial kits. Pathological changes and the SA-β-Gal activity in liver tissues were detected by hematoxylin and eosin and SA-β-Gal staining. The expression levels of p16, [[CDK4]], [[CDK6]] and phosphorylation levels of Retinoblastoma (Rb) were detected by immunohistochemistry and western blot analysis. mRNA levels of genes regulated by p16-Rb pathway were determined by quantitative real-time PCR. In vivo, HSYA improved the aging changes including body weight, organ index and antioxidant status such as activities of SOD, [[CAT]], GSH-Px and MDA in D-gal treated aging mice. HSYA also dramatically attenuated pathologic changes of aging liver tissues induced by D-gal. Furthermore, HSYA significantly decreased the mRNA and protein level of cyclin-dependent kinase inhibitor p16, followed by increasing [[CDK4]]/6 protein expression and decreasing the phosphorylation of Retinoblastoma (pRb) which up-regulated the expression of downstream genes [[CCNE1]], [[CCNA2]], P107 and [[MCM4]]. Collectively, these data indicated that HSYA could ameliorate aging, especially hepatic replicative senescence resulting from D-gal, the mechanism could be associated with the suppression of p16-Rb pathway.<br /> <br /> |keywords=* D-galactose<br /> * Hydroxysafflor yellow A<br /> * Oxidative stress<br /> * Replicative senescence<br /> * p16<br /> |full-text-url=https://sci-hub.do/10.1016/j.ejphar.2020.173214<br /> }}<br /> {{medline-entry<br /> |title=Changes in [[MCM2]]-7 proteins at senescence.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31092751<br /> |abstract=Cellular aging is characterized by the loss of DNA replication capability and is mainly brought about by various changes in chromatin structure. Here, we examined changes in [[MCM2]]-7 proteins, which act as a replicative DNA helicase, during aging of human WI38 fibroblasts at the single-cell level. We used nuclear accumulation of p21 as a marker of senescent cells, and examined changes in [[MCM2]]-7 by western blot analysis. First, we found that senescent cells are enriched for cells with a DNA content higher than 4N. Second, the levels of [[MCM2]], [[MCM3]], [[MCM4]] and [[MCM6]] proteins decreased in senescent cells. Third, cytoplasmic localization of [[MCM2]] and [[MCM7]] was observed in senescent cells, from an analysis of [[MCM2]]-7 except for [[MCM5]]. Consistent with this finding, fragmented [[MCM2]] was predominant in these cells. These age-dependent changes in [[MCM2]]-7, a protein complex that directly affects cellular DNA replication, may play a critical role in cellular senescence.<br /> |mesh-terms=* Cell Cycle Proteins<br /> * Cellular Senescence<br /> * DNA Replication<br /> * Gene Expression Regulation<br /> * Humans<br /> * Minichromosome Maintenance Complex Component 2<br /> * Minichromosome Maintenance Complex Component 3<br /> * Minichromosome Maintenance Complex Component 4<br /> * Minichromosome Maintenance Complex Component 6<br /> * Minichromosome Maintenance Complex Component 7<br /> * Multiprotein Complexes<br /> * Single-Cell Analysis<br /> * p21-Activated Kinases<br /> |keywords=* DNA content<br /> * MCM2–7 proteins<br /> * cellular aging<br /> * cellular localization<br /> * protein degradation<br /> |full-text-url=https://sci-hub.do/10.1266/ggs.18-00062<br /> }}</div>

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