|Citation||Read, R.D., Bach, E.A., Cagan, R.L. (2004). Drosophila C-terminal Src kinase negatively regulates organ growth and cell proliferation through inhibition of the Src, Jun N-terminal kinase, and STAT pathways. Mol. Cell. Biol. 24(15): 6676--6689. (Export to RIS)|
|Publication Type||Research paper|
|PubMed Abstract||Src family kinases regulate multiple cellular processes including proliferation and oncogenesis. C-terminal Src kinase (Csk) encodes a critical negative regulator of Src family kinases. We demonstrate that the Drosophila melanogaster Csk ortholog, dCsk, functions as a tumor suppressor: dCsk mutants display organ overgrowth and excess cellular proliferation. Genetic analysis indicates that the dCsk(-/-) overgrowth phenotype results from activation of Src, Jun kinase, and STAT signal transduction pathways. In particular, blockade of STAT function in dCsk mutants severely reduced Src-dependent overgrowth and activated apoptosis of mutant tissue. Our data provide in vivo evidence that Src activity requires JNK and STAT function.|
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|Language of Publication||English|
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|Also Published As|
|Abbreviation||Mol. Cell. Biol.|
|Title||Molecular and Cellular Biology|
|Data from Reference|
|Natural transposons (1)|