EEPD1 promotes repair of oxidatively-stressed replication forks.
Journal
NAR cancer
ISSN: 2632-8674
Titre abrégé: NAR Cancer
Pays: England
ID NLM: 101769553
Informations de publication
Date de publication:
Mar 2023
Mar 2023
Historique:
received:
16
10
2022
revised:
22
11
2022
accepted:
14
12
2022
entrez:
23
1
2023
pubmed:
24
1
2023
medline:
24
1
2023
Statut:
epublish
Résumé
Unrepaired oxidatively-stressed replication forks can lead to chromosomal instability and neoplastic transformation or cell death. To meet these challenges cells have evolved a robust mechanism to repair oxidative genomic DNA damage through the base excision repair (BER) pathway, but less is known about repair of oxidative damage at replication forks. We found that depletion or genetic deletion of EEPD1 decreases clonogenic cell survival after oxidative DNA damage. We demonstrate that EEPD1 is recruited to replication forks stressed by oxidative damage induced by H
Identifiants
pubmed: 36683914
doi: 10.1093/narcan/zcac044
pii: zcac044
pmc: PMC9846428
doi:
Types de publication
Journal Article
Langues
eng
Pagination
zcac044Subventions
Organisme : NIAID NIH HHS
ID : R01 AI161363
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA205224
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA241801
Pays : United States
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of NAR Cancer.
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