ArticleeLife2022
Pathogenic mutations in the chromokinesin KIF22 disrupt anaphase chromosome segregation.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- BTK promotes neuroinflammation after intracerebral hemorrhage involving hub genes and alterations in microglial functions.Scientific reports · 2026Article
- Novel KIF22 Variants Disrupt Mitosis in Human Chondrocytes and Expand SEMDJL2 Mechanisms.bioRxiv : the preprint server for biology · 2026Article
- A Phosphorylation Switch Governs KIF11's Mechanical Output During Mitosis.bioRxiv : the preprint server for biology · 2026Article
- Chromosome size-dependent polar ejection force impairs mammalian mitotic error correction.The Journal of cell biology · 2024Article
- Involvement of kinesins in skeletal dysplasia: a review.American journal of physiology. Cell physiology · 2024Review
- Article
- The spindle protein CKAP2 regulates microtubule dynamics and ensures faithful chromosome segregation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of the KIF18A alpha-4 helix as a therapeutic target for chromosomally unstable tumor cells.Frontiers in molecular biosciences · 2024Article
- Modification of the neck-linker of KIF18A alters Microtubule subpopulation preference.Molecular biology of the cell · 2024Article
- Chromosome size-dependent polar ejection force impairs mammalian mitotic error correction.bioRxiv : the preprint server for biology · 2023Article
- Identification of the KIF18A alpha-4 helix as a therapeutic target for chromosomally unstable tumor cells.bioRxiv : the preprint server for biology · 2023Article
- KIF22 promotes the proliferation and glycolysis of melanoma by activating EGFR/STAT3 signaling.Clinics (Sao Paulo, Brazil) · 2023Article
- ALS-associated KIF5A mutations abolish autoinhibition resulting in a toxic gain of function.Cell reports · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The chromokinesin KIF22 generates forces that contribute to mitotic chromosome congression and alignment. Mutations in the α2 helix of the motor domain of KIF22 have been identified in patients with abnormal skeletal development, and we report the identification of a patient with a novel mutation in the KIF22 tail. We demonstrate that pathogenic mutations do not result in a loss of KIF22's functions in early mitosis. Instead, mutations disrupt chromosome segregation in anaphase, resulting in reduced proliferation, abnormal daughter cell nuclear morphology, and, in a subset of cells, cytokinesis failure. This phenotype could be explained by a failure of KIF22 to inactivate in anaphase. Consistent with this model, constitutive activation of the motor via a known site of phosphoregulation in the tail phenocopied the effects of pathogenic mutations. These results suggest that the motor domain α2 helix may be an important site for regulation of KIF22 activity at the metaphase to anaphase transition. In support of this conclusion, mimicking phosphorylation of α2 helix residue T158 also prevents inactivation of KIF22 in anaphase. These findings demonstrate the importance of both the head and tail of the motor in regulating the activity of KIF22 and offer insight into the cellular consequences of preventing KIF22 inactivation and disrupting force balance in anaphase.
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