Impact of Replication Stress in Human Papillomavirus Pathogenesis.
ATR
DNA damage
cancer
genomic instability
papillomavirus
replication
Journal
Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724
Informations de publication
Date de publication:
15 01 2019
15 01 2019
Historique:
pubmed:
26
10
2018
medline:
23
10
2019
entrez:
26
10
2018
Statut:
epublish
Résumé
The inactivation of critical cell cycle checkpoints by the human papillomavirus (HPV) oncoprotein E7 results in replication stress (RS) that leads to genomic instability in premalignant lesions. Intriguingly, RS tolerance is achieved through several mechanisms, enabling HPV to exploit the cellular RS response for viral replication and to facilitate viral persistence in the presence of DNA damage. As such, inhibitors of the RS response pathway may provide a novel approach to target HPV-associated lesions and cancers.
Identifiants
pubmed: 30355682
pii: JVI.01012-17
doi: 10.1128/JVI.01012-17
pmc: PMC6321920
pii:
doi:
Substances chimiques
Cell Cycle Proteins
0
Papillomavirus E7 Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : R01 CA181581
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI135542
Pays : United States
Informations de copyright
Copyright © 2019 American Society for Microbiology.
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