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Paper Details

SLFN11 promotes CDT1 degradation by CUL4 in response to replicative DNA damage, while its absence leads to synthetic lethality with ATR/CHK1 inhibitors.
Proc Natl Acad Sci U S A
30
2021
-, -KO cells, ATPase domain, ATPase mutant, ATR, Ataxia Telangiectasia, Ataxia Telangiectasia- and Rad3-related, BRCA2, CDT1, CHK1, CPT, CUL4, CUL4CDT2, CUL4CDT2 E3 ubiquitin ligase, DDB1, E669K, M4344, M6620, RPA1, SLFN11, SLFN11 gene, SLFN11-KO cells, SLFN11-WT and -knockout (KO, SLFN11-deficient cancers, SLFN11-expressing cells, SRA737, Schlafen, Schlafen-11, camptothecin, cancer, cancer cells, cisplatin, etoposide, expressing cells, human, indotecan, replication forks, replicative DNA, retarded, talazoparib, topotecan
Author NameAffiliation
Lisa M Miller JenkinsCenter for Cancer Research, National Cancer Institute
Lisa M Miller JenkinsCenter for Cancer Research, National Cancer Institute
Yves PommierCenter for Cancer Research, National Cancer Institute
Yves PommierCenter for Cancer Research, National Cancer Institute
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