ArticleMolecular biology of the cell2003
Crk associates with a multimolecular Paxillin/GIT2/beta-PIX complex and promotes Rac-dependent relocalization of Paxillin to focal contacts.
Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 98 citations in OpenAlex.
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- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes in Spinal Cord Injury.Molecular neurobiology · 2025Review
- Dietary Polyphenols Effects on Focal Adhesion Plaques and Metalloproteinases in Cancer Invasiveness.Biomedicines · 2024Review
- The Impact of ETV6-NTRK3 Oncogenic Gene Fusions on Molecular and Signaling Pathway Alterations.Cancers · 2023Article
- Lack of Paxillin phosphorylation promotes single-cell migration in vivo.The Journal of cell biology · 2023Article
- Pseudomonas aeruginosa ExoT induces G1 cell cycle arrest in melanoma cells.Cellular microbiology · 2021Article
- A Novel Low-Risk Germline Variant in the SH2 Domain of the SRC Gene Affects Multiple Pathways in Familial Colorectal Cancer.Journal of personalized medicine · 2021Article
- AXL confers cell migration and invasion by hijacking a PEAK1-regulated focal adhesion protein network.Nature communications · 2020Article
- Ibuprofen inhibited migration of skeletal muscle cells in association with downregulation of p130cas and CrkII expressions.Skeletal muscle · 2019Article
- Arf GAPs: A family of proteins with disparate functions that converge on a common structure, the integrin adhesion complex.Small GTPases · 2019Review
- ARF GTPases and their GEFs and GAPs: concepts and challenges.Molecular biology of the cell · 2019Review
- Roles of paxillin phosphorylation in IL-3 withdrawal-induced Ba/F3 cell apoptosis.Genes & genomics · 2019Article
- The Tumor Suppressor SASH1 Interacts With the Signal Adaptor CRKL to Inhibit Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer.Cellular and molecular gastroenterology and hepatology · 2019Article
- [The role of focal adhesions in Ewing's sarcoma].Der Pathologe · 2017Article
- Role played by paxillin and paxillin tyrosine phosphorylation in hepatocyte growth factor/sphingosine-1-phosphate-mediated reactive oxygen species generation, lamellipodia formation, and endothelial barrier function.Pulmonary circulation · 2015Article
- KSHV-TK is a tyrosine kinase that disrupts focal adhesions and induces Rho-mediated cell contraction.The EMBO journal · 2015Article
- Crk1/2 and CrkL form a hetero-oligomer and functionally complement each other during podocyte morphogenesis.Kidney international · 2014Article
- Hypoxia-induced changes in Ca(2+) mobilization and protein phosphorylation implicated in impaired wound healing.American journal of physiology. Cell physiology · 2014Article
- Investigating perturbed pathway modules from gene expression data via structural equation models.BMC bioinformatics · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
We have previously demonstrated that the CrkII and CrkL adapter proteins are required for the spreading of epithelial colonies and the breakdown of adherens junctions in response to hepatocyte growth factor. When overexpressed, CrkII and CrkL promote lamellipodia formation, cell spreading, and the loss of epithelial adherens junctions in the absence of hepatocyte growth factor. The exact mechanism by which Crk proteins elicit these changes is unclear. We show that the overexpression of CrkII or CrkL, but not Src homology 2 or amino-terminal Src homology 3 domain mutant Crk proteins, promotes the relocalization of Paxillin to focal contacts throughout the cell and within lamellipodia in a Rac-dependent manner. In stable cell lines overexpressing CrkII, enhanced lamellipodia formation and cell spreading correlate with an increased association of CrkII with Paxillin, GIT2 (an ARF-GAP) and beta-PIX (a Rac1 exchange factor). Mutants of Paxillin that fail to associate with Crk or GIT2, or do not target to focal adhesions inhibit Crk-dependent cell spreading and lamellipodia formation. We conclude from these studies that the association of Crk with Paxillin is important for the spreading of epithelial colonies, by influencing the recruitment of Paxillin to focal complexes and promoting the enhanced assembly of Paxillin/GIT2/beta-PIX complexes.
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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.