ArticleCell proliferation2011
Anaphase-promoting complex/cyclosome controls HEC1 stability.
Article in Cell proliferation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- Juvenile hormone and BMP signaling modulate fat body cell fate during the transition of previtellogenic development to vitellogenesis.BMC biology · 2025Article
- The polyglutamine-expanded androgen receptor responsible for spinal and bulbar muscular atrophy inhibits the APC/C(Cdh1) ubiquitin ligase complex.Scientific reports · 2016Article
- Insights into APC/C: from cellular function to diseases and therapeutics.Cell division · 2016Review
- Protein purification technique that allows detection of sumoylation and ubiquitination of budding yeast kinetochore proteins Ndc10 and Ndc80.Journal of visualized experiments : JoVE · 2015Article
- Polo-like kinase 1 regulates the stability of the mitotic centromere-associated kinesin in mitosis.Oncotarget · 2014Article
- Functional characterization of Anaphase Promoting Complex/Cyclosome (APC/C) E3 ubiquitin ligases in tumorigenesis.Biochimica et biophysica acta · 2014Review
- What the hec is up with mouse oocyte meiosis?Developmental cell · 2013Article
- Hec1-dependent cyclin B2 stabilization regulates the G2-M transition and early prometaphase in mouse oocytes.Developmental cell · 2013Article
- CDK-dependent phosphorylation and nuclear exclusion coordinately control kinetochore assembly state.The Journal of cell biology · 2013Article
- Processive ubiquitin chain formation by the anaphase-promoting complex.Seminars in cell & developmental biology · 2011Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveChromosome segregation during mitosis requires a physically large proteinaceous structure called the kinetochore to generate attachments between chromosomal DNA and spindle microtubules. It is essential for kinetochore components to be carefully regulated to guarantee successful cell division. Depletion, mutation or dysregulation of kinetochore proteins results in mitotic arrest and/or cell death. HEC1 (high expression in cancer) has been reported to be a kinetochore protein, depletion of which, by RNA interference, results in catastrophic mitotic exit. MATERIALS AND METHODS AND
resultsTo investigate how HEC1 protein is controlled post-translation, we analysed the role of anaphase-promoting complex/cyclosome (APC/C)-Cdh1 in degradation of HEC1 protein. In this study, we show that HEC1 is an unstable protein and can be targeted by endogenous ubiquitin-proteasome system in HEK293T cells. Results of RNA interference and in vivo ubiquitination assay indicated that HEC1 could be ubiquitinated and degraded by APC/C-hCdh1 E3 ligase. The evolutionally conserved D-box at the C-terminus functioned as the degron of HEC1, destruction of which resulted in resistance to degradation mediated by APC/C-Cdh1. Overexpression of non-degradable HEC1 (D-box destroyed) induced accumulation of cyclin B protein in vivo and triggered mitotic arrest.
conclusionAPC/C-Cdh1 controls stability of HEC1, ensuring normal cell cycle progression.
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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.