ArticleJournal of cell science2016
KIF17 regulates RhoA-dependent actin remodeling at epithelial cell-cell adhesions.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17.Journal of cell communication and signaling · 2025Article
- Identification and regulation of EMT cellsAPL bioengineering · 2025Article
- Molecular Motors in Blood-Brain Barrier Maintenance by Astrocytes.Brain sciences · 2025Review
- Vitamin DEuropean journal of cell biology · 2023Article
- The Profiles and Functions of RNA Editing Sites Associated with High-Altitude Adaptation in Goats.International journal of molecular sciences · 2023Article
- Circulating Tumor Cell-Free DNA Genes as Prognostic Gene Signature for Platinum Resistant Ovarian Cancer Diagnosis.Biomarker insights · 2022Article
- Kinesins in Mammalian Spermatogenesis and Germ Cell Transport.Frontiers in cell and developmental biology · 2022Review
- Mast Cell Proteases Tryptase and Chymase Induce Migratory and Morphological Alterations in Bronchial Epithelial Cells.International journal of molecular sciences · 2021Article
- Actin-microtubule crosstalk in cell biology.Nature reviews. Molecular cell biology · 2019Review
- Signaling by Small GTPases at Cell-Cell Junctions: Protein Interactions Building Control and Networks.Cold Spring Harbor perspectives in biology · 2018Review
- Microtubule Motors in Establishment of Epithelial Cell Polarity.Cold Spring Harbor perspectives in biology · 2018Review
- The role of microtubules in the regulation of epithelial junctions.Tissue barriers · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The kinesin KIF17 localizes at microtubule plus-ends where it contributes to regulation of microtubule stabilization and epithelial polarization. We now show that KIF17 localizes at cell-cell adhesions and that KIF17 depletion inhibits accumulation of actin at the apical pole of cells grown in 3D organotypic cultures and alters the distribution of actin and E-cadherin in cells cultured in 2D on solid supports. Overexpression of full-length KIF17 constructs or truncation mutants containing the N-terminal motor domain resulted in accumulation of newly incorporated GFP-actin into junctional actin foci, cleared E-cadherin from cytoplasmic vesicles and stabilized cell-cell adhesions to challenge with calcium depletion. Expression of these KIF17 constructs also increased cellular levels of active RhoA, whereas active RhoA was diminished in KIF17-depleted cells. Inhibition of RhoA or its effector ROCK, or expression of LIMK1 kinase-dead or activated cofilin(S3A) inhibited KIF17-induced junctional actin accumulation. Interestingly, KIF17 activity toward actin depends on the motor domain but is independent of microtubule binding. Together, these data show that KIF17 can modify RhoA-GTPase signaling to influence junctional actin and the stability of the apical junctional complex of epithelial cells.
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Registered trials
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