ArticleThe Journal of biological chemistry2011
Mitotic centromere-associated kinesin (MCAK) mediates paclitaxel resistance.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- From Motor Proteins to Oncogenic Factors: The Evolving Role of Kinesin Superfamily Proteins in Breast Cancer Development.Molecular biotechnology · 2026Review
- SEPT9_i1 and Septin Dynamics in Oncogenesis and Cancer Treatment.Biomolecules · 2024Review
- The role of kinesin family members in hepatobiliary carcinomas: from bench to bedside.Biomarker research · 2024Review
- Article
- α-Tubulin detyrosination links the suppression of MCAK activity with taxol cytotoxicity.The Journal of cell biology · 2023Article
- Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in nasopharyngeal carcinoma.Genes & diseases · 2023Article
- Pan-cancer analysis of kinesin family members with potential implications in prognosis and immunological role in human cancer.Frontiers in oncology · 2023Article
- Spatial regulation of MCAK promotes cell polarization and focal adhesion turnover to drive robust cell migration.Molecular biology of the cell · 2021Article
- α-Tubulin detyrosination impairs mitotic error correction by suppressing MCAK centromeric activity.The Journal of cell biology · 2020Article
- Phosphatidylinositol-5-phosphate 4-kinase gamma accumulates at the spindle pole and prevents microtubule depolymerization.Cell division · 2019Article
- A monomethyl auristatin E-conjugated antibody to guanylyl cyclase C is cytotoxic to target-expressing cells in vitro and in vivo.PloS one · 2018Article
- Microtubule-Binding Proteins as Promising Biomarkers of Paclitaxel Sensitivity in Cancer Chemotherapy.Medicinal research reviews · 2016Review
- MiR-20a-5p represses multi-drug resistance in osteosarcoma by targeting the KIF26B gene.Cancer cell international · 2016Article
- Paclitaxel Through the Ages of Anticancer Therapy: Exploring Its Role in Chemoresistance and Radiation Therapy.Cancers · 2015Review
- Article
- Peloruside A is a microtubule-stabilizing agent with exceptional anti-migratory properties in human endothelial cells.Oncoscience · 2015Article
- FOXM1 mediates resistance to docetaxel in gastric cancer via up-regulating Stathmin.Journal of cellular and molecular medicine · 2014Article
- Determination of the optimal tubulin isotype target as a method for the development of individualized cancer chemotherapy.Theoretical biology & medical modelling · 2013Article
- The microtubule-binding protein Cep170 promotes the targeting of the kinesin-13 depolymerase Kif2b to the mitotic spindle.Molecular biology of the cell · 2012Article
- Kinesins and cancer.Nature reviews. Cancer · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Paclitaxel has powerful anticancer activity, but some tumors are inherently resistant to the drug, whereas others are initially sensitive but acquire resistance during treatment. To deal with this problem, it will be necessary to understand the mechanisms of drug action and resistance. Recent studies indicate that paclitaxel blocks cell division by inhibiting the detachment of microtubules from centrosomes. Here, we demonstrate that mitotic centromere-associated kinesin (MCAK), a kinesin-related protein that destabilizes microtubules, plays an important role in microtubule detachment. Depletion of MCAK altered mitotic spindle morphology, increased the frequency of lagging chromosomes, and inhibited the proliferation of WT CHO cells, confirming that it is an essential protein for cell division. In contrast, MCAK depletion rescued the proliferation of mutant paclitaxel-dependent cell lines that are unable to divide because of defective spindle function resulting from altered α-tubulin or class III β-tubulin overexpression. In concert with the correction of mitotic defects, loss of MCAK reversed an aberrantly high frequency of microtubule detachment in the mutant cells and increased their sensitivity to paclitaxel. The results indicate that MCAK affects cell sensitivity to mitotic inhibitors by modulating the frequency of microtubule detachment, and they demonstrate that changes in a microtubule-interacting protein can reverse the effects of mutant tubulin expression.
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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.