Uncoupling of mTORC1 from E2F activity maintains DNA damage and senescence.
DNA Damage
Mechanistic Target of Rapamycin Complex 1
/ metabolism
Cellular Senescence
/ genetics
Humans
DNA Repair
E2F Transcription Factors
/ metabolism
Cyclin-Dependent Kinase Inhibitor p16
/ metabolism
Signal Transduction
Cyclin-Dependent Kinase 4
/ metabolism
Cyclin-Dependent Kinase 6
/ metabolism
Single-Cell Analysis
DNA Replication
Animals
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
24 Oct 2024
24 Oct 2024
Historique:
received:
10
09
2020
accepted:
20
09
2024
medline:
25
10
2024
pubmed:
25
10
2024
entrez:
25
10
2024
Statut:
epublish
Résumé
DNA damage is a primary trigger for cellular senescence, which in turn causes organismal aging and is a promising target of anti-aging therapies. Most DNA damage occurs when DNA is fragile during DNA replication in S phase, but senescent cells maintain DNA damage long-after DNA replication has stopped. How senescent cells induce DNA damage and why senescent cells fail to repair damaged DNA remain open questions. Here, we combine reversible expression of the senescence-inducing CDK4/6 inhibitory protein p16
Identifiants
pubmed: 39448567
doi: 10.1038/s41467-024-52820-6
pii: 10.1038/s41467-024-52820-6
doi:
Substances chimiques
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
E2F Transcription Factors
0
Cyclin-Dependent Kinase Inhibitor p16
0
Cyclin-Dependent Kinase 4
EC 2.7.11.22
Cyclin-Dependent Kinase 6
EC 2.7.11.22
CDKN2A protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
9181Subventions
Organisme : U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)
ID : R35 GM12702601
Informations de copyright
© 2024. The Author(s).
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