Abstract
The oncoprotein v-Src and its cellular homologue (c-Src) are tyrosine kinases that modulate the actin cytoskeleton and cell adhesions. Through the concerted action of their protein-interaction and kinase domains, they are targeted to cell matrix integrin adhesions or cadherin-dependent junctions between epithelial cells, where they phosphorylate substrates that induce adhesion turnover and actin re-modelling. Recent experiments have defined some of the key targets and effector pathways that mediate the pleiotropic oncogenic effects of v-Src.
MeSH terms
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Actins / physiology*
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Animals
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Cadherins / physiology
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Calpain / chemistry
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Calpain / physiology
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Cell Adhesion / physiology*
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Cell Cycle / physiology
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Focal Adhesion Kinase 1
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Focal Adhesion Protein-Tyrosine Kinases
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Guanine Nucleotide Exchange Factors / physiology
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Humans
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Models, Biological
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Nuclear Proteins / physiology
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Oncogene Protein pp60(v-src) / chemistry
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Oncogene Protein pp60(v-src) / genetics
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Oncogene Protein pp60(v-src) / physiology*
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Protein-Tyrosine Kinases / physiology
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Proto-Oncogene Proteins pp60(c-src) / chemistry
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Proto-Oncogene Proteins pp60(c-src) / genetics
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Proto-Oncogene Proteins pp60(c-src) / physiology
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Repressor Proteins
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Signal Transduction
Substances
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ARHGAP35 protein, human
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Actins
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Cadherins
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Guanine Nucleotide Exchange Factors
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Nuclear Proteins
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Repressor Proteins
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Protein-Tyrosine Kinases
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Focal Adhesion Kinase 1
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Focal Adhesion Protein-Tyrosine Kinases
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Oncogene Protein pp60(v-src)
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PTK2 protein, human
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Proto-Oncogene Proteins pp60(c-src)
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Calpain