An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress

Activation of the KRAS oncogene is a source of replication stress, but how this stress is generated and how it is tolerated by cancer cells remain poorly understood. Here we show that induction of KRAS(G12V) expression in untransformed cells triggers H3K27me3 and HP1-associated chromatin compaction...

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Detalles Bibliográficos
Autores principales: Igarashi, Taichi, Mazevet, Marianne, Yasuhara, Takaaki, Yano, Kimiyoshi, Mochizuki, Akifumi, Nishino, Makoto, Yoshida, Tatsuya, Yoshida, Yukihiro, Takamatsu, Nobuhiko, Yoshimi, Akihide, Shiraishi, Kouya, Horinouchi, Hidehito, Kohno, Takashi, Hamamoto, Ryuji, Adachi, Jun, Zou, Lee, Shiotani, Bunsyo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10435487/
https://www.ncbi.nlm.nih.gov/pubmed/37591859
http://dx.doi.org/10.1038/s41467-023-40578-2

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10435487/
https://www.ncbi.nlm.nih.gov/pubmed/37591859
http://dx.doi.org/10.1038/s41467-023-40578-2

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