ArticleMolecular and cellular biology2013
CRL4(CDT2) targets CHK1 for PCNA-independent destruction.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 78 citations in OpenAlex.
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- Hepatocyte-specific angiotensinogen deficiency inhibits Western diet-induced liver steatosis with suppression of cell division in mice.Global translational medicine · 2025Article
- DCAF2 regulates the proliferation and differentiation of mouse progenitor spermatogonia by targeting p21 and thymine DNA glycosylase.Cell proliferation · 2024Article
- XPO1 Enables Adaptive Regulation of mRNA Export Required for Genotoxic Stress Tolerance in Cancer Cells.Cancer research · 2024Article
- Function, mechanism and drug discovery of ubiquitin and ubiquitin-like modification with multiomics profiling for cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
- BRD7 suppresses tumor chemosensitivity to CHK1 inhibitors by inhibiting USP1-mediated deubiquitination of CHK1.Cell death discovery · 2023Article
- SCML2 contributes to tumor cell resistance to DNA damage through regulating p53 and CHK1 stability.Cell death and differentiation · 2023Article
- Pan-cancer analysis and experimental validation of DTL as a potential diagnosis, prognosis and immunotherapy biomarker.BMC cancer · 2023Article
- Adaptive exchange sustains cullin-RING ubiquitin ligase networks and proper licensing of DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mice lacking DCAF2 in placenta die at the gastrulation stage.Cell and tissue research · 2022Article
- miR-34a negatively regulates cell cycle factor Cdt2/DTL in HPV infected cervical cancer cells.BMC cancer · 2022Article
- Essential role of CK2α for the interaction and stability of replication fork factors during DNA synthesis and activation of the S-phase checkpoint.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- The CRL4DTL E3 ligase induces degradation of the DNA replication initiation factor TICRR/TRESLIN specifically during S phase.Nucleic acids research · 2021Article
- HDAC6 Regulates Radiosensitivity of Non-Small Cell Lung Cancer by Promoting Degradation of Chk1.Cells · 2020Article
- Direct regulation of Chk1 protein stability by E3 ubiquitin ligase HUWE1.The FEBS journal · 2020Article
- Chk1-mediated phosphorylation of Cdh1 promotes the SCFCell death & disease · 2020Article
- CRL4 ubiquitin ligase stimulates Fanconi anemia pathway-induced single-stranded DNA-RPA signaling.BMC cancer · 2019Article
- Basal CHK1 activity safeguards its stability to maintain intrinsic S-phase checkpoint functions.The Journal of cell biology · 2019Article
- SCFβ-TrCP ubiquitinates CHK1 in an AMPK-dependent manner in response to glucose deprivation.Molecular oncology · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CDT2 targets proteins involved in replication licensing (CDT1), cell cycle control (p21), and chromatin modification (SET8) for destruction by the CUL4-based E3 ligase (CRL4). CRL4(CDT2) recruits these substrates through interactions with chromatin-bound PCNA and ubiquitinates them exclusively on chromatin. Rereplication and G(2) cell cycle arrest are observed in CDT2-depleted cells. The rereplication phenotype has been attributed to an inability to destroy CDT1, but the molecular target important for G(2) cell cycle arrest in CDT2-depleted cells has not been identified. Here we identify CHK1 as a novel CRL4(CDT2) substrate and demonstrate that CHK1 activity is required for maintaining G(2) arrest in CDT2-depleted cells. We demonstrate that CRL4(CDT2) targets the activated form of CHK1 for destruction in the nucleoplasm rather than on chromatin and that this occurs in a PCNA-independent manner. Although both CRL1 and CRL4 ubiquitinate CHK1, we report that they bind CHK1 in distinct cellular compartments. Our study provides insight into how elevated CDT2 expression levels may provide tumors with a proliferative advantage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.