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Updated: May 6, 2026

Aip1p Dynamics Are Altered by the R256H Mutation in Actin
Published on: July 30, 2014
v-Src's hold over actin and cell adhesions
Margaret C Frame1, Valerie J Fincham, Neil O Carragher
1The Beatson Institute for Cancer Research, Cancer Research UK Beatson Laboratories, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK. mframe@beatson..gla.ac.uk
The oncogenic protein v-Src and its cellular form, c-Src, are tyrosine kinases. These kinases regulate cell adhesion and actin cytoskeleton dynamics, impacting cell behavior and potentially driving cancer progression.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- The oncoprotein v-Src and its cellular homologue (c-Src) are tyrosine kinases.
- These kinases play crucial roles in modulating the actin cytoskeleton and cell adhesions.
Purpose of the Study:
- To elucidate the mechanisms by which v-Src and c-Src target cell adhesion sites.
- To identify key substrates and effector pathways involved in v-Src-mediated oncogenesis.
Main Methods:
- Investigating the roles of protein-interaction and kinase domains of v-Src/c-Src.
- Analyzing phosphorylation of substrates at integrin adhesions and cadherin-dependent junctions.
- Defining effector pathways mediating oncogenic effects.
Main Results:
- v-Src and c-Src are targeted to cell matrix integrin adhesions and cadherin-dependent junctions.
- Phosphorylation of substrates induces adhesion turnover and actin re-modelling.
- Key targets and effector pathways mediating v-Src's oncogenic effects have been defined.
Conclusions:
- v-Src and c-Src are critical regulators of cell adhesion and cytoskeleton dynamics.
- Understanding these pathways provides insights into v-Src-driven oncogenesis.
- Further research into v-Src targets may reveal therapeutic strategies.
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