ArticleMolecular and cellular biology2000
The SH3 domain directs acto-myosin-dependent targeting of v-Src to focal adhesions via phosphatidylinositol 3-kinase.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 96 citations in OpenAlex.
- The tyrosine kinase v-Src modifies cytotoxicities of anticancer drugs targeting cell division.Journal of cellular and molecular medicine · 2021Article
- Direct visualization by FRET-FLIM of a putative mechanosome complex involving Src, Pyk2 and MBD2 in living MLO-Y4 cells.PloS one · 2021Article
- Article
- The tyrosine kinase v-Src causes mitotic slippage by phosphorylating an inhibitory tyrosine residue of Cdk1.The Journal of biological chemistry · 2018Article
- Phosphatidylinositol Phosphate 5-Kinase Iγ and Phosphoinositide 3-Kinase/Akt Signaling Couple to Promote Oncogenic Growth.The Journal of biological chemistry · 2015Article
- Tropomyosin Tm5NM1 spatially restricts src kinase activity through perturbation of Rab11 vesicle trafficking.Molecular and cellular biology · 2014Article
- Endocytosis and the Src family of non-receptor tyrosine kinases.Biomolecular concepts · 2014Review
- Regulation of Src trafficking and activation by the endocytic regulatory proteins MICAL-L1 and EHD1.Journal of cell science · 2014Article
- Single-cell imaging of mechanotransduction in endothelial cells.Progress in molecular biology and translational science · 2014Review
- Expression and prognostic significance of Src family members in renal clear cell carcinoma.British journal of cancer · 2012Article
- Article
- Endosomal signaling and cell migration.Current opinion in cell biology · 2011Review
- Is there an association with phosphorylation and dephosphorylation of Src kinase at tyrosine 530 and breast cancer patient disease-specific survival.British journal of cancer · 2010Article
- mDia1 targets v-Src to the cell periphery and facilitates cell transformation, tumorigenesis, and invasion.Molecular and cellular biology · 2010Article
- NMY-2 maintains cellular asymmetry and cell boundaries, and promotes a SRC-dependent asymmetric cell division.Developmental biology · 2010Article
- Visualizing the effect of microenvironment on the spatiotemporal RhoA and Src activities in living cells by FRET.Small (Weinheim an der Bergstrasse, Germany) · 2009Article
- The spatiotemporal pattern of Src activation at lipid rafts revealed by diffusion-corrected FRET imaging.PLoS computational biology · 2008Article
- Decreased CHK protein levels are associated with Src activation in colon cancer cells.Oncogene · 2008Article
- Palladin interacts with SH3 domains of SPIN90 and Src and is required for Src-induced cytoskeletal remodeling.Experimental cell research · 2007Article
- The Rho-mDia1 pathway regulates cell polarity and focal adhesion turnover in migrating cells through mobilizing Apc and c-Src.Molecular and cellular biology · 2006Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The v-Src oncoprotein is translocated to integrin-linked focal adhesions, where its tyrosine kinase activity induces adhesion disruption and cell transformation. We previously demonstrated that the intracellular targeting of Src is dependent on the actin cytoskeleton, under the control of the Rho family of small G proteins. However, the assembly of v-Src into focal adhesions does not require its catalytic activity or myristylation-dependent membrane association. Here, we report that the SH3 domain is essential for the assembly of focal adhesions containing the oncoprotein by mediating a switch from a microtubule-dependent, perinuclear localization to actin-associated focal adhesions; furthermore, v-Src translocation to focal adhesions requires myosin activity, at least under normal conditions when the actin cytoskeleton is being dynamically regulated. Although the SH3 domain of v-Src is also necessary for its association with focal adhesion kinase (FAK), which is often considered a likely candidate mediator of focal adhesion targeting via its carboxy-terminal targeting sequence, we show here that binding to FAK is not essential for the targeting of v-Src to focal adhesions. The p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase also associates with v-Src in an SH3-dependent manner, but in this case inhibition of PI 3-kinase activity suppressed assembly of focal adhesions containing the oncoprotein. Thus, the Src SH3 domain, which binds PI 3-kinase and which is necessary for activation of Akt downstream, is required for the actin-dependent targeting of v-Src to focal adhesions.
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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.