ArticleInternational journal of biological sciences2013
Interaction of crk with Myosin-1c participates in fibronectin-induced cell spreading.
Article in International journal of biological sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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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
3 citing papers in PubMed, 8 citations in OpenAlex.
- Diverse ancestral myosin motors generate and segregate distinct types of nanocluster-rich domains at the plasma membrane.Science advances · 2026Article
- Myosin-I molecular motors at a glance.Journal of cell science · 2016Review
- Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region.BMC genetics · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported a novel interaction between v-Crk and myosin-1c, and demonstrated that this interaction is essential for cell migration, even in the absence of p130CAS. We here demonstrate a role for Crk-myosin-1c interaction in cell adhesion and spreading. Crk-knockout (Crk ⁻/⁻) mouse embryo fibroblasts (MEFs) exhibited significantly decreased cell spreading and reduced Rac1 activity. A stroboscopic analysis of cell dynamics during cell spreading revealed that the cell-spreading deficiency in Crk⁻/⁻ MEFs was due to the short protrusion/retraction distances and long persistence times of membrane extensions. The low activity of Rac1 in Crk⁻/⁻ MEFs, which led to delayed cell spreading in these cells, is consistent with the observed defects in membrane dynamics. Reintroduction of v-Crk into Crk⁻/⁻ MEFs rescued these defects, restoring cell-spreading activity and membrane dynamics to Crk⁺/⁺ MEF levels, and normalizing Rac1 activity. Knockdown of myosin-1c by introduction of small interfering RNA resulted in a delay in cell spreading and reduced Rac1 activity to low levels, suggesting that myosin-1c also plays an essential role in cell adhesion and spreading. In addition, deletion of the v-Crk SH3 domain, which interacts with the myosin-1c tail, led to defects in cell spreading. Overexpression of the GFP-myosin-1c tail domain effectively inhibited the v-Crk-myosin-1c interaction and led to a slight decrease in cell spreading and cell surface area. Collectively, these findings suggest that the v-Crk-myosin-1c interaction, which modulates membrane dynamics by regulating Rac1 activity, is crucial for cell adhesion and spreading.
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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.