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MCM3
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==Publications== {{medline-entry |title=Changes in [[MCM2]]-7 proteins at senescence. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31092751 |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. |mesh-terms=* Cell Cycle Proteins * Cellular Senescence * DNA Replication * Gene Expression Regulation * Humans * Minichromosome Maintenance Complex Component 2 * Minichromosome Maintenance Complex Component 3 * Minichromosome Maintenance Complex Component 4 * Minichromosome Maintenance Complex Component 6 * Minichromosome Maintenance Complex Component 7 * Multiprotein Complexes * Single-Cell Analysis * p21-Activated Kinases |keywords=* DNA content * MCM2–7 proteins * cellular aging * cellular localization * protein degradation |full-text-url=https://sci-hub.do/10.1266/ggs.18-00062 }} {{medline-entry |title=Up-regulation of [[MCM3]] Relates to Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27401074 |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. |mesh-terms=* Aging * Animals * Apoptosis * Brain Injuries, Traumatic * Cerebral Cortex * Minichromosome Maintenance Complex Component 3 * Neurons * Rats, Sprague-Dawley * Transcriptional Activation * Up-Regulation |keywords=* Active caspase-3 * BAX/Bcl-2 * MCM3 * Neuronal apoptosis * TBI |full-text-url=https://sci-hub.do/10.1007/s10571-016-0404-x }}
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