Product Pathways - Tyrosine Kinase/ Adaptors
BRK Kinase #7703
Cell Signaling Technology offers a full line of protein kinases, substrates, antibody detection reagents and HTScan® kits. Browse our "Reagents for High-Throughput Screening" product listing or contact us at drugdiscovery@cellsignal.com.
Description
Purified recombinant kinase, supplied as a GST fusion protein.
Source / Purification
This GST-kinase fusion protein was produced using a baculovirus expression system with a construct expressing the kinase with an amino terminal GST tag. The protein was purified by one-step affinity chromatography using glutathione-agarose.
Quality Control
The purified kinase fusion protein was quality controlled for purity using SDS-PAGE followed by Coomassie or silver stain and Western blot. The specific activity of the kinase was determined using a radiometric assay.
Background
Brk (Breast tumor kinase) is a nonreceptor tyrosine kinase that is most closely related to the Frk family of kinases, and more distantly to Src family kinases. Brk was originally identified in a screen for tyrosine kinases that are overexpressed in human metastatic breast tumors (1). Unlike Src family kinases, Brk lacks an N-terminal consensus sequence for acylation and membrane association. Brk possesses sequences that are predicted to form Src homology 3 (SH3) and Src homology 2 (SH2) domains . These domains bind to proline-rich sequences and to phosphotyrosine-containing sequences, respectively. It was proposed that the C-terminal sequence of Brk (PTSpYENPT where pY is phosphotyrosine) might be a self-ligand for the SH2 domain (2). The Brk kinase activity may be regulated by by autophosphorylation and by autoinhibition (1).Brk is highly expressed in many breast carcinoma cell lines and a significant portion of breast tumor tissues but not in human mammary epithelial cells. Elevated expression of Brk has also been detected in metastatic melanoma cell lines and in some colon tumors. In prostate cancers, although the expression of Brk is not significantly altered, Brk translocates from the nucleus to the cytoplasm during the progression of tumors (3). It was demonstrated that Brk phosphorylates the cytoplasm-localized paxillin, which in turn activates a signaling pathway to promote cell migration and invasion (3). Brk probably utilizes this pathway to participate in tumor progression and metastasis. In addition to promoting cell migration and invasion, Brk has also been reported to sensitize cells to the proliferation effect of EGF (4). Thus, Brk might elicit diverse biological effects, thereby participating in the distinct stages of tumorigenesis.
- Qiu, H. and Miller, W.T. (2002) J Biol Chem 277, 34634-41.
- Hong, E. et al. (2004) J Biol Chem 279, 29700-8.
- Chen, H.Y. et al. (2004) Mol Cell Biol 24, 10558-72.
- Kamalati, T. et al. (1996) J Biol Chem 271, 30956-63.
Application References
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Companion Products
This product is for in vitro research use only and is not intended for use in humans or animals. This product is not intended for use as therapeutic or in diagnostic procedures.
