ArticleNature communications2024
DCAF15 control of cohesin dynamics sustains acute myeloid leukemia.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- A post-translational regulatory map of chronic antigen-driven human T cell dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Degrons and degradation signals beyond short linear motifs.Nature chemical biology · 2026Review
- Venetoclax resistance in preclinical KMT2A-rearranged acute lymphoblastic leukemia models is characterized by high inter- and intra-model heterogeneity.NPJ precision oncology · 2025Article
- Dcaf15-mediated EphA2 degradation triggers disruption of the blood-brain barrier during Streptococcus suis meningitis.Communications biology · 2025Article
- Targeted citrullination enables p53 binding to non-canonical sites.Molecular cell · 2025Article
- Hypomethylation-Enhanced F-Box Protein 32 Promotes Hepatocellular Carcinogenesis via Ubiquitin-Mediated PHLPP2 Degradation.MedComm · 2025Article
- CDCA5 knockdown potentiates olaparib sensitivity in BRCA1-mutated ovarian cancer through autophagy activation.Discover oncology · 2025Article
- Characterization of E1 enzyme dependencies in mutant-UBA1 human cells reveals UBA6 as a novel therapeutic target in VEXAS syndrome.Leukemia · 2025Article
- Targeted protein degradation for cancer therapy.Nature reviews. Cancer · 2025Review
- Selective translational control by PABPC1 phase separation regulates blast crisis and therapy resistance in chronic myeloid leukaemia.Nature cell biology · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The CRL4-DCAF15 E3 ubiquitin ligase complex is targeted by the aryl-sulfonamide molecular glues, leading to neo-substrate recruitment, ubiquitination, and proteasomal degradation. However, the physiological function of DCAF15 remains unknown. Using a domain-focused genetic screening approach, we reveal DCAF15 as an acute myeloid leukemia (AML)-biased dependency. Loss of DCAF15 results in suppression of AML through compromised replication fork integrity and consequent accumulation of DNA damage. Accordingly, DCAF15 loss sensitizes AML to replication stress-inducing therapeutics. Mechanistically, we discover that DCAF15 directly interacts with the SMC1A protein of the cohesin complex and destabilizes the cohesin regulatory factors PDS5A and CDCA5. Loss of PDS5A and CDCA5 removal precludes cohesin acetylation on chromatin, resulting in uncontrolled chromatin loop extrusion, defective DNA replication, and apoptosis. Collectively, our findings uncover an endogenous, cell autonomous function of DCAF15 in sustaining AML proliferation through post-translational control of cohesin dynamics.
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