https://transhumanist.ru/index.php?action=history&feed=atom&title=MCM3 2026-05-15T11:24:59Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=MCM3&diff=4146&oldid=prev 2021-04-29T19:03:01Z

<p>Новая страница: «DNA replication licensing factor MCM3 (EC 3.6.4.12) (DNA polymerase alpha holoenzyme-associated protein P1) (P1-MCM3) (RLF subunit beta) (p102) ==Publications==...»</p> <p><b>Новая страница</b></p><div>DNA replication licensing factor MCM3 (EC 3.6.4.12) (DNA polymerase alpha holoenzyme-associated protein P1) (P1-MCM3) (RLF subunit beta) (p102)<br /> <br /> ==Publications==<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 /> }}<br /> {{medline-entry<br /> |title=Up-regulation of [[MCM3]] Relates to Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27401074<br /> |abstract=Minichromosome maintenance complex component 3, one of the minichromosome maintenance proteins, functions as a part of pre-replication complex to initiate DNA replication in eukaryotes. Minichromosome maintenance complex component 3 ([[MCM3]]) was mainly implied in cell proliferation and tumorigenesis. In addition, [[MCM3]] might play an important role in neuronal apoptosis. However, the functions of [[MCM3]] in central nervous system are still with limited acquaintance. In this study, we performed a traumatic brain injury (TBI) model in adult rats. Western blot and immunohistochemistry staining showed up-regulation of [[MCM3]] in the peritrauma brain cortex. The expression patterns of active caspase-3 and Bax, Bcl-2 were parallel with that of [[MCM3]]. Immunofluorescent staining and terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling suggested that [[MCM3]] was involved in neuronal apoptosis. In conclusion, our data indicated that [[MCM3]] might play an important role in neuronal apoptosis following TBI. Further understanding of these insights could serve as the basis for broadening the therapeutic scope against TBI.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Apoptosis<br /> * Brain Injuries, Traumatic<br /> * Cerebral Cortex<br /> * Minichromosome Maintenance Complex Component 3<br /> * Neurons<br /> * Rats, Sprague-Dawley<br /> * Transcriptional Activation<br /> * Up-Regulation<br /> |keywords=* Active caspase-3<br /> * BAX/Bcl-2<br /> * MCM3<br /> * Neuronal apoptosis<br /> * TBI<br /> |full-text-url=https://sci-hub.do/10.1007/s10571-016-0404-x<br /> }}</div>

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