Skip to main content
. Author manuscript; available in PMC: 2013 Apr 4.
Published in final edited form as: Oncogene. 2012 Jan 9;31(40):4372–4383. doi: 10.1038/onc.2011.608

Figure 2.

Figure 2

Brk inhibits EGF-induced EGFR-Cbl association and Cbl-mediated EGFR ubiquitination. (a) Brk inhibits EGF-induced EGFR-Cbl association and EGFR ubiquitination. SUM102 cells were transiently transfected with wild-type Brk or neo control vector for 24 h. The cells were then stimulated with 10 nM EGF in 0.5% FBS medium for the indicated time periods. EGFR immunoprecipitates (I.P. α EGFR) or whole cell lysates were subjected to Western blotting with the indicated antibodies. (b) Knockdown of Brk expression enhances EGF-induced EGFR-Cbl association and EGFR ubiquitination. SUM102 cells were subjected to Brk knockdown or control siRNA treatment for 48 h. The cells were then processed and analyzed as described in (a). (c) Constitutively active Brk inhibits EGFR-Cbl association and EGFR ubiquitination. SUM102 cells were transiently transfected with wild-type Brk, constitutively active mutant Brk-Y447F, kinase-dead mutant Brk-K219M, or neo control vector for 24 h. EGFR immunoprecipitates (I.P. α EGFR) or whole cell lysates were subjected to Western blotting with the indicated antibodies.