Noncoding RNA control of cellular senescence

Senescent cells accumulate in normal tissues with advancing age and arise by long‐term culture of primary cells. Senescence develops following exposure to a range of stress‐causing agents and broadly influences the physiology and pathology of tissues, organs, and systems in the body. While many prot...

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Vydáno v:Wiley interdisciplinary reviews. RNA Ročník 6; číslo 6; s. 615 - 629
Hlavní autoři: Abdelmohsen, Kotb, Gorospe, Myriam
Médium: Journal Article
Jazyk:angličtina
Vydáno: Hoboken, USA John Wiley & Sons, Inc 01.11.2015
Wiley Subscription Services, Inc
Témata:
Animals
Cell culture
Cellular Senescence - genetics
Humans
miRNA
p53 Protein
Riboswitches
RNA, Untranslated - physiology
RNA-mediated interference
Senescence
ISSN:1757-7004, 1757-7012
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Shrnutí:Senescent cells accumulate in normal tissues with advancing age and arise by long‐term culture of primary cells. Senescence develops following exposure to a range of stress‐causing agents and broadly influences the physiology and pathology of tissues, organs, and systems in the body. While many proteins are known to control senescence, numerous noncoding (nc)RNAs are also found to promote or repress the senescent phenotype. Here, we review the regulatory ncRNAs (primarily microRNAs and lncRNAs) identified to‐date as key modulators of senescence. We highlight the major senescent pathways (p53/p21 and pRB/p16), as well as the senescence‐associated secretory phenotype (SASP) and other senescence‐associated events governed by ncRNAs, and discuss the importance of understanding comprehensively the ncRNAs implicated in cell senescence. WIREs RNA 2015, 6:615–629. doi: 10.1002/wrna.1297 This article is categorized under: RNA Interactions with Proteins and Other Molecules > RNA–Protein Complexes Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs RNA in Disease and Development > RNA in Development
Bibliografie:ark:/67375/WNG-3JHRK3F7-G
istex:31E4D5072119C3C3771A32B18D95314DF51B4D9B
NIA-IRP, NIH
ArticleID:WRNA1297
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1757-7004
1757-7012
DOI:10.1002/wrna.1297