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. Author manuscript; available in PMC: 2016 Jan 21.
Published in final edited form as: Oncogene. 2014 Sep 8;34(27):3536–3546. doi: 10.1038/onc.2014.281

Figure 4.

Figure 4

Mechanism of YAP/TAZ activation by vGPCR. (a, b) Knockdown of Gq/11 or G12/13 suppresses YAP/TAZ activation by vGPCR. shRNAs were used to stably knockdown Gq/11 or G12/13 in the control or vGPCR expressing HEK293A cells. (c, d, g) HEK293A stable control and vGPCR expressing cells were transfected with the indicated plasmids. (e) vGPCR decreases Lats1 phosphorylation. Endogenous Lats1 was immunoprecipitated from control and vGPCR-expressing cells. Lats1 phosphorylation on the activation loop (S909) and hydrophobic motif (T1079) were detected by phosphor antibodies as indicated. (f) vGPCR expression inhibits Lats kinase activity. Lats1 was immunoprecipitated with a control IgG or Lats1 specific antibody as indicated. Kinase activity was determined in vitro using GST-YAP as a substrate. Phosphorylation of GST-YAP was detected by phosphor-specific antibody. (g) Overexpression of Lats2 suppresses the effect of vGPCR on TAZ protein accumulation and CTGF expression. (h) vGPCR does not affect MST1 activity. MST1 was immunoprecipitated from control or vGPCR expressing cells. In vitro kinase activity was measured using GST-Mob as a substrate.