SLFN11 promotes CDT1 degradation by CUL4 in response to replicative DNA damage, while its absence leads to synthetic lethality with ATR/CHK1 inhibitors.
Ataxia Telangiectasia Mutated Proteins
/ antagonists & inhibitors
Cell Cycle Proteins
/ metabolism
Cell Line, Tumor
Checkpoint Kinase 1
/ antagonists & inhibitors
Chromosomes, Human
/ genetics
Cullin Proteins
/ metabolism
DNA Damage
/ genetics
DNA Replication
/ genetics
DNA-Binding Proteins
/ metabolism
Drug Resistance, Neoplasm
Enzyme Stability
Genome, Human
Humans
Mitosis
Models, Biological
Molecular Targeted Therapy
Nuclear Proteins
/ metabolism
Phosphorylation
Protein Binding
Protein Kinase Inhibitors
/ pharmacology
Proteolysis
RNA Interference
Signal Transduction
Synthetic Lethal Mutations
/ genetics
ATR/CHK1 inhibitor
CDT1
CUL4
SLFN11
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
09 02 2021
09 02 2021
Historique:
entrez:
4
2
2021
pubmed:
5
2
2021
medline:
24
6
2021
Statut:
ppublish
Résumé
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
Identifiants
pubmed: 33536335
pii: 2015654118
doi: 10.1073/pnas.2015654118
pmc: PMC8017720
pii:
doi:
Substances chimiques
CDT1 protein, human
0
CUL4A protein, human
0
Cell Cycle Proteins
0
Cullin Proteins
0
DDB1 protein, human
0
DNA-Binding Proteins
0
Nuclear Proteins
0
Protein Kinase Inhibitors
0
SLFN11 protein, human
0
Ataxia Telangiectasia Mutated Proteins
EC 2.7.11.1
CHEK1 protein, human
EC 2.7.11.1
Checkpoint Kinase 1
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2021 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no competing interest.
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