Редактирование: MCM3 (раздел)

==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
}}