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. Author manuscript; available in PMC: 2014 Oct 7.
Published in final edited form as: Biochem Biophys Res Commun. 2008 Feb 22;369(2):616–621. doi: 10.1016/j.bbrc.2008.02.068

Fig. 1.

Fig. 1

CD28 binding to PI3 K, Grb-2 and Vav1. (A) Jurkat T-cells were either left untreated (lane 1) or stimulated with anti-CD28 (4 μg/ml) and rabbit anti-hamster (2 μg/ml) antibodies (lanes 2–5). Cells were washed and solubilized in Triton X-100 lysis buffer containing protease and phosphatase inhibitors. Anti-CD28 immunoprecipitates and lysates were separated by SDS–PAGE gel, transferred to nitrocellulose and immunoblotted with anit-p85 (upper panel) or anti-Grb-2 (lower panel) antibodies. Lane 6 shows the position of p85 (upper panel) and Grb-2 (lower panel) in cell lysates. Cell lysates blotted for p85 (upper panel) and Grb-2 (lower panel) served as loading controls. (B, upper panel): Jurkat cells were lysed, immunoprecipitated with anti-Vav1 (lane 1) or anti-Grb-2 (lane 2) antibodies and blotted with anti-Vav1. Lower panel: Jurkat cells were lysed, immunoprecipitated with rabbit anti-mouse (lane 1) or anti-CD28 (lane 2) antibodies and blotted for associated Vav1 with anti-Vav1 mAb. Lane 3 shows the position of Vav1 in cell lysates.

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