ArticleEMBO reports2024
CKAP5 stabilizes CENP-E at kinetochores by regulating microtubule-chromosome attachments.
Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Molecular Guardians of Oocyte Maturation: A Systematic Review on TUBB8, KIF11, and CKAP5 in IVF Outcomes.International journal of molecular sciences · 2025Pooled it
- Disentangling Heterogeneous Molecular Networks for Multi-Omics-Driven Cancer Driver Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decoding the Molecular Landscape of Prepubertal Oocyte Maturation: GTPBP4 as a Key Driver of In Vitro Developmental Competence.Cell proliferation · 2025Article
- Branching, crosslinking, and decentralization of microtubules accelerates intracellular assembly.Biophysical journal · 2025Article
- Machine learning-assisted multi-dimensional transcriptomic analysis of cytoskeleton-related molecules and their relationship with prognosis in hepatocellular carcinoma.Scientific reports · 2025Article
- Article
- The kinesin motor POS3 and the microtubule polymerase MOR1 coordinate chromosome congression during mitosis in Arabidopsis.The Plant cell · 2025Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Stabilization of microtubule plus end-directed kinesin CENP-E at the metaphase kinetochores is important for chromosome alignment, but its mechanism remains unclear. Here, we show that CKAP5, a conserved microtubule plus tip protein, regulates CENP-E at kinetochores in human cells. Depletion of CKAP5 impairs CENP-E localization at kinetochores at the metaphase plate and results in increased kinetochore-microtubule stability and attachment errors. Erroneous attachments are also supported by computational modeling. Analysis of CKAP5 knockout cancer cells of multiple tissue origins shows that CKAP5 is preferentially essential in aneuploid, chromosomally unstable cells, and the sensitivity to CKAP5 depletion is correlated to that of CENP-E depletion. CKAP5 depletion leads to reduction in CENP-E-BubR1 interaction and the interaction is rescued by TOG4-TOG5 domain of CKAP5. The same domain can rescue CKAP5 depletion-induced CENP-E removal from the kinetochores. Interestingly, CKAP5 depletion facilitates recruitment of PP1 to the kinetochores and furthermore, a PP1 target site-specific CENP-E phospho-mimicking mutant gets stabilized at kinetochores in the CKAP5-depleted cells. Together, the results support a model in which CKAP5 controls mitotic chromosome attachment errors by stabilizing CENP-E at kinetochores and by regulating stability of the kinetochore-attached microtubules.
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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.