v-Src tyrosine kinase (v-Src)

v-Src tyrosine kinase is an oncogenic, constitutively active non-receptor tyrosine kinase encoded by the Rous sarcoma virus (RSV) and responsible for virus-induced cancer in chickens[5]. It is the viral homolog of the cellular proto-oncogene c-Src, but unlike c-Src, v-Src lacks the regulatory C-terminal tyrosine (Tyr-527), resulting in persistent kinase activity[5]. v-Src phosphorylates tyrosine residues on multiple cytoplasmic targets, driving signaling pathways involved in cell proliferation, cell cycle progression, cytoskeletal changes, motility, and survival[1][5][7]. It is a prototypical model for understanding oncogene-driven transformation, and its uncontrolled kinase activity induces characteristic oncogenic features such as altered morphology, increased invasiveness, and mitotic slippage, partly through phosphorylation and inhibition of Cdk1[4][5][7]. While v-Src itself is a viral protein and not a direct human drug target, the mammalian Src family kinases are important anticancer drug targets. Experimentally, Src inhibitors (such as PP2 or dasatinib) are used to study v-Src and related kinase functions[4][8]. Key structural domains include an SH3 domain, an SH2 domain, a tyrosine kinase domain, and (in c-Src) a C-terminal tail absent in v-Src[1][5]. v-Src research led to the discovery of the first proto-oncogene and elucidated fundamental mechanisms of signal transduction and cancer biology[5][6].

Other names

Viral Src tyrosine kinasev-Src oncoproteinRous sarcoma virus SrcSrc (viral)

- ATP-competitive inhibition of kinase activity - Inhibition of tyrosine phosphorylation - Blockade of downstream signaling pathways (e.g., affecting MAP kinase, AP-1, PI3 kinase activity)[4][7]