ArticleiScience2021
Inter-organelle interactions between the ER and mitotic spindle facilitates Zika protease cleavage of human Kinesin-5 and results in mitotic defects.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Host protein cleavage by Dengue and Zika virus NS3 proteases: from substrate identification to potential biological consequences.Frontiers in cellular and infection microbiology · 2026Review
- Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.Nature communications · 2025Article
- Emerging roles of cytoskeletal transport and scaffold systems in human viral propagation.Animal cells and systems · 2024Review
- Using machine learning to predict protein-protein interactions between a zombie ant fungus and its carpenter ant host.Scientific reports · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Here we identify human Kinesin-5, Kif11/HsEg5, as a cellular target of Zika protease. We show that Zika NS2B-NS3 protease targets several sites within the motor domain of HsEg5 irrespective of motor binding to microtubules. The native integral ER-membrane protease triggers mitotic spindle positioning defects and a prolonged metaphase delay in cultured cells. Our data support a model whereby loss of function of HsEg5 is mediated by Zika protease and is spatially restricted to the ER-mitotic spindle interface during mitosis. The resulting phenotype is distinct from the monopolar phenotype that typically results from uniform inhibition of HsEg5 by RNAi or drugs. In addition, our data reveal novel inter-organelle interactions between the mitotic apparatus and the surrounding reticulate ER network. Given that Kif11 is haplo-insufficient in humans, and reduced dosage results in microcephaly, we propose that Zika protease targeting of HsEg5 may be a key event in the etiology of Zika syndrome microcephaly.
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Registered trials
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