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. 2022 Apr 29;15(4):dmm049320. doi: 10.1242/dmm.049320

Fig. 5.

Fig. 5.

ARCND2-associated PLCB4 mutants interfere with SRE activity in a dominant-negative manner. (A) Schematic of the signaling pathway that stimulates SRE:luc2p transcription. Gq p.Gln209Leu activates the Raf-MEK/ERK pathway through PLCB, resulting in activation of the serum response element (SRE). (B) Relative luminescence from cells co-transfected with SRE:luc2p, Gq p.Gln209Leu and wild-type or mutant PLCB4. Luminescence is expressed as the fold change relative to cells expressing wild-type PLCB4. Data points are individual experiments [n=3 for all samples except wild type and p.Arg621His (n=4)]. Error bars represent s.e.m. Significance versus wild type was calculated using Prism and an unpaired two-tailed t-test (p.Arg621His, P<0.0001; p.Tyr623Cys, P=0.0008; p.Glu358Val, P=0.0002; p.Asp360Val, P<0.0001; p.Pro838Ala;p.Arg621His, P=0.36). ***P<0.001, ****P<0.0001; ns, not significant.