Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

3 Feb 2021

Abstract excerpt

Significance Schlafen-11 (SLFN11) inactivation leads to chemoresistance of a broad range of DNA-damaging agents. We uncover an expanded Ataxia Telangiectasia- and Rad3-related (ATR)-mediated signaling network that overcomes chemoresistance by an unbiased genome-wide RNAi screen in SLFN11 -knockout cells and is validated with clinically developing ATR/CHK1 inhibitors. ATR inhibition induces CDT1 phosphorylation,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer therapeutics and mechanisms
Share to Neuroblastoma Research and Treatments
Share to PARP inhibition in cancer therapy

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33536335
DOI: 10.1073/pnas.2015654118

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SLFN11 promotes CDT1 degradation by CUL4 in response to replicative DNA damage, while its absence leads to synthetic lethality with ATR/CHK1 inhibitorsPMID 33536335Read ↗

Schlafen 11 (SLFN11) Kills Cancer Cells Undergoing Unscheduled Re-replicationSemantic proximity Read ↗

SLFN11: a pan-cancer biomarker for DNA-targeted drugs sensitivity and therapeutic strategy guidanceSemantic proximity Read ↗

The crucial role of single-stranded DNA binding in enhancing sensitivity to DNA-damaging agents for Schlafen 11 and Schlafen 13Semantic proximity Read ↗

SLFN11 Inactivation Induces Proteotoxic Stress and Sensitizes Cancer Cells to Ubiquitin Activating Enzyme Inhibitor TAK-243Semantic proximity Read ↗

Precision Oncology with Drugs Targeting the Replication Stress, ATR, and Schlafen 11Semantic proximity Read ↗

SLFN11 is a general target for enhancing the sensitivity of cancer to chemotherapy (DNA-damaging agents)Semantic proximity Read ↗

Putative DNA/RNA helicase Schlafen-11 (SLFN11) sensitizes cancer cells to DNA-damaging agentsSemantic proximity Read ↗

Epigenetic silencing schlafen-11 sensitizes esophageal cancer to ATM inhibitorSemantic proximity Read ↗

Dual genome-wide CRISPR knockout and CRISPR activation screens identify common mechanisms that regulate the resistance to multiple ATR inhibitorsSemantic proximity Read ↗

Loss of Cyclin C or CDK8 provides ATR inhibitor resistance by suppressing transcription-associated replication stressSemantic proximity Read ↗

Dual genome-wide CRISPR knockout and CRISPR activation screens identify mechanisms that regulate the resistance to multiple ATR inhibitorsSemantic proximity Read ↗

SLFN11 Enhances Cisplatin Sensitivity in Pediatric Cancer via Activation of Stress-Response and Suppression of Survival PathwaysSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.