High impact information on Csk

• We demonstrate that the Drosophila melanogaster Csk ortholog, dCsk, functions as a tumor suppressor: dCsk mutants display organ overgrowth and excess cellular proliferation [1].
• Csk differentially regulates Src64 during distinct morphological events in Drosophila germ cells [2].
• These results uncover novel roles for both Csk and Src64 in a dynamic event that involves adhesion, communication between cell types and control of cell motility [2].
• Drosophila Src-family kinases function with Csk to regulate cell proliferation and apoptosis [3].
• A genetic screen for modifiers of the lats tumor suppressor gene identifies C-terminal Src kinase as a regulator of cell proliferation in Drosophila [4].

Biological context of Csk

• Mutations in the Drosophila homolog of C-terminal Src kinase (dcsk) were identified as dominant modifiers of both lats gain-of-function and loss-of-function phenotypes [4].

Regulatory relationships of Csk

• The non-receptor tyrosine kinase Src is inactivated by the C-terminal Src kinase Csk [5].

References