ArticleMolecular biology of the cell2009
Cdh1 regulates cell cycle through modulating the claspin/Chk1 and the Rb/E2F1 pathways.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- Rac1 GTPase Regulates the SCFCancers · 2026Article
- Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Integrating multi-omics analysis identifies DNA damage-related gene CLSPN as a biomarker in gastric cancer.Scientific reports · 2026Article
- Advances in the management of peritoneal malignancies.Nature reviews. Clinical oncology · 2022Review
- CDH1 overexpression predicts bladder cancer from early stage and inversely correlates with immune infiltration.BMC urology · 2022Article
- Acetylation-dependent regulation of BRAF oncogenic function.Cell reports · 2022Article
- CDC20 promotes bone formation via APC/C dependent ubiquitination and degradation of p65.EMBO reports · 2021Article
- Sirtuin 5 Is Regulated by the SCFMolecular and cellular biology · 2021Article
- Chk1-mediated phosphorylation of Cdh1 promotes the SCFCell death & disease · 2020Article
- Posttranscriptional control of the replication stress response via TTP-mediated Claspin mRNA stabilization.Oncogene · 2020Article
- Article
- Interplay between c-Src and the APC/C co-activator Cdh1 regulates mammary tumorigenesis.Nature communications · 2019Article
- Hippo signaling is intrinsically regulated during cell cycle progression by APC/CProceedings of the National Academy of Sciences of the United States of America · 2019Article
- The mTOR-S6K pathway links growth signalling to DNA damage response by targeting RNF168.Nature cell biology · 2018Article
- Phosphorylation of EZH2 by AMPK Suppresses PRC2 Methyltransferase Activity and Oncogenic Function.Molecular cell · 2018Article
- Regulation of E2F1 Transcription Factor by Ubiquitin Conjugation.International journal of molecular sciences · 2017Review
- The APC/C E3 Ligase Complex Activator FZR1 Restricts BRAF Oncogenic Function.Cancer discovery · 2017Article
- UBE2S, a novel substrate of Akt1, associates with Ku70 and regulates DNA repair and glioblastoma multiforme resistance to chemotherapy.Oncogene · 2017Article
- Multiple molecular interactions redundantly contribute to RB-mediated cell cycle control.Cell division · 2017Article
- APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway.Bioscience reports · 2016Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
APC/Cdh1 is a major cell cycle regulator and its function has been implicated in DNA damage repair; however, its exact role remains unclear. Using affinity purification coupled with mass spectrometry, we identified Claspin as a novel Cdh1-interacting protein and further demonstrated that Claspin is a novel Cdh1 ubiquitin substrate. As a result, inactivation of Cdh1 leads to activation of the Claspin/Chk1 pathway. Previously, we demonstrated that Rb interacts with Cdh1 to influence its ability to degrade Skp2. Here, we report that Cdh1 reciprocally regulates the Rb pathway through competing with E2F1 to bind the hypophosphorylated form of Rb. Although inactivation of Cdh1 in HeLa cells, with defective p53/Rb pathways, led to premature S phase entry, acute depletion of Cdh1 in primary human fibroblasts resulted in premature senescence. Acute loss of many other major tumor suppressors, including PTEN and VHL, also induces premature senescence in a p53- or Rb-dependent manner. Similarly, we showed that inactivation of the p53/Rb pathways by overexpression of SV40 LT-antigen partially reversed Cdh1 depletion-induced growth arrest. Therefore, loss of Cdh1 is only beneficial to cells with abnormal p53 and Rb pathways, which helps explain why Cdh1 loss is not frequently found in many tumors.
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Registered trials
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.