https://transhumanist.ru/index.php?action=history&feed=atom&title=CNOT6CNOT6 - История изменений2026-04-09T20:55:06ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=CNOT6&diff=4227&oldid=prevOdysseusBot: Новая страница: «CCR4-NOT transcription complex subunit 6 (EC 3.1.13.4) (CCR4 carbon catabolite repression 4-like) (Carbon catabolite repressor protein 4 homolog) (Cytoplasmic dea...»2021-04-29T19:07:17Z<p>Новая страница: «CCR4-NOT transcription complex subunit 6 (EC 3.1.13.4) (CCR4 carbon catabolite repression 4-like) (Carbon catabolite repressor protein 4 homolog) (Cytoplasmic dea...»</p>
<p><b>Новая страница</b></p><div>CCR4-NOT transcription complex subunit 6 (EC 3.1.13.4) (CCR4 carbon catabolite repression 4-like) (Carbon catabolite repressor protein 4 homolog) (Cytoplasmic deadenylase) [CCR4] [CCR4a] [KIAA1194]<br />
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==Publications==<br />
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{{medline-entry<br />
|title=miR-29c-3p promotes senescence of human mesenchymal stem cells by targeting [[CNOT6]] through p53-p21 and p16-pRB pathways.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26792405<br />
|abstract=Mesenchymal stem cells ([[MSC]]s) are important seed cells for tissue engineering and are promising targets for cell-based therapies. However, the replicative senescence of [[MSC]]s during in vitro culture limits their research and clinical applications. The molecular mechanisms underlying the replicative senescence of [[MSC]]s are not fully understood. Evidence suggests that miRNAs play important roles in replicative senescence. A microarray analysis found that the miR-29c-3p level was significantly increased during the [[MSC]] senescence process. In our study, we investigated the roles of miR-29c-3p in senescence of [[MSC]]s. We cultured [[MSC]]s for long periods of time, up and down-regulated the miR-29c-3p expression in [[MSC]]s, and examined the senescent phenotype changes. The over-expression of miR-29c-3p led to enhanced senescence-associated-β-galactosidase (SA-β-gal) staining, senescence associated secretory phenotype (SASP), senescence associated heterochromatic foci (SAHF), reduced proliferation ability, retarded osteogenic differentiation and corresponding changes in senescence markers, whereas the miR-29c-3p down-regulation had the opposite results. Dual-luciferase reporter assays demonstrated that [[CNOT6]] is the target gene of miR-29c-3p. Knockdown of [[CNOT6]] confirmed its inhibitory effects on the senescence of [[MSC]]s. In addition, Western blot results showed that both the p53-p21 and the p16-pRB pathways were activated during the miR-29c-3p-induced senescence of [[MSC]]s. In conclusion, our results demonstrate that miR-29c-3p promotes the senescence of [[MSC]]s by targeting [[CNOT6]] through p53-p21 and p16-pRB pathways and highlight the contribution of post-transcriptional regulation to stem cell senescence. <br />
|mesh-terms=* Cells, Cultured<br />
* Cellular Senescence<br />
* Cyclin-Dependent Kinase Inhibitor p16<br />
* Cyclin-Dependent Kinase Inhibitor p21<br />
* Exoribonucleases<br />
* Gene Expression Regulation<br />
* Humans<br />
* Mesenchymal Stem Cells<br />
* MicroRNAs<br />
* Neoplasm Proteins<br />
* Retinoblastoma Protein<br />
* Signal Transduction<br />
* Tumor Suppressor Protein p53<br />
|keywords=* Mesenchymal stem cell<br />
* MicroRNA<br />
* Replicative senescence<br />
* Tissue engineering<br />
|full-text-url=https://sci-hub.do/10.1016/j.bbamcr.2016.01.005<br />
}}</div>OdysseusBot