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. Author manuscript; available in PMC: 2008 Feb 17.
Published in final edited form as: Circ Res. 2007 Jul 5;101(4):420–428. doi: 10.1161/CIRCRESAHA.107.156463

Figure 5. Association of CAS with CrkII and formation of protein complex containing CrkII are attenuated in Abl-deficient arteries upon PE stimulation.

Figure 5

Untreated arteries or arteries that had been treated with plasmids encoding Luc shRNA, or Abl shRNA were stimulated with PE, or left unstimulated. (A) Blots of CAS immunoprecipitates from these arteries were probed with antibodies against CAS and CrkII. The immunoblots illustrate the effects of Abl silencing on CAS/CrkII coupling. (B) Blots of CrkII immunoprecipitates from these arteries were probed with antibodies against CrkII, N-WASP, and Arp2. Abl silencing inhibits the complex formation. (C) Individual protein ratios are normalized to protein ratios in corresponding unstimulated arteries. *Significantly lower protein ratios in response to PE stimulation compared to corresponding PE-induced protein ratios in untreated arteries or arteries producing Luc shRNA (n = 3, P < 0.05). Values are mean ± SE.