Brk activates rac1 and promotes cell migration and invasion by phosphorylating paxillin.

@article{Chen2004BrkAR,
  title={Brk activates rac1 and promotes cell migration and invasion by phosphorylating paxillin.},
  author={H. T. Chen and C M Shen and Yuh-Tyng Tsai and Feng-Chi Lin and Y Huang and R H Chen},
  journal={Molecular and cellular biology},
  year={2004},
  volume={24 24},
  pages={10558-72}
}
Brk (for breast tumor kinase) is a nonreceptor tyrosine kinase containing SH3, SH2, and tyrosine kinase catalytic domains. Brk was originally identified from a human metastatic breast tumor, and its overexpression is frequently observed in breast cancer and several other cancer types. However, the molecular mechanism by which this kinase participates in tumorigenesis remains poorly characterized. In the present study, we not only identified paxillin as the binding partner and substrate of Brk… CONTINUE READING

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