SLFN11 promotes CDT1 degradation by CUL4 in response to replicative DNA damage, while its absence leads to synthetic lethality with ATR/CHK1 inhibitors

Schlafen-11 (SLFN11) inactivation in ∼50% of cancer cells confers broad chemoresistance. To identify therapeutic targets and underlying molecular mechanisms for overcoming chemoresistance, we performed an unbiased genome-wide RNAi screen in SLFN11-WT and -knockout (KO) cells. We found that inactivat...

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Detalles Bibliográficos
Autores principales: Jo, Ukhyun, Murai, Yasuhisa, Chakka, Sirisha, Chen, Lu, Cheng, Ken, Murai, Junko, Saha, Liton Kumar, Miller Jenkins, Lisa M., Pommier, Yves
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Academy of Sciences 2021
Materias:
Biological Sciences
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8017720/
https://www.ncbi.nlm.nih.gov/pubmed/33536335
http://dx.doi.org/10.1073/pnas.2015654118

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8017720/
https://www.ncbi.nlm.nih.gov/pubmed/33536335
http://dx.doi.org/10.1073/pnas.2015654118

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