Fig. 4: Xinβ interacts with NF2 to modulate the Hippo-YAP signaling in the heart.
From: Intercalated disc protein Xinβ is required for Hippo-YAP signaling in the heart
a Western blots of indicated proteins using heart samples from P7.5 XinβKO and control mice. b Quantification of p-NF2 and p-YAP protein levels in P7.5 XinβKO and control hearts. N = 3 biologically independent samples, *P < 0.05. c Immunohistochemistry detecting p-NF2 in P7.5 XinβKO and control hearts. DAPI marks nuclei, cTnT labels cardiomyocytes. Scale bars = 20 µm. d Immunohistochemistry detecting total YAP (t-YAP) in P7.5 XinβKO and control hearts. DAPI marks nuclei, α-actinin labels cardiomyocytes. Scale bars = 20 µm. Quantification of nuclear located YAP-positive cardiomyocytes is shown in the right panel. N = 5 and 4 biologically independent samples, respectively, *P < 0.05. e Immunohistochemistry detecting NF2 and Xinβ expression in the intercalated discs of adult cardiomyocytes. Scale bars = 20 µm. Quantification is presented in the right panel. N = 11 biologically independent samples, Data are presented as mean values ± SEM. f Co-immunoprecipitation assays detecting interactions between GFP-tagged NF2 and Flag-tagged Xinβ protein fragments. 5% cell lysate was used as input to demonstrate the expression of tagged proteins. g Co-immunoprecipitation assay detecting the interaction between GFP-tagged NF2 and Flag-tagged Xinβ protein fragment (amino acids 334-680). Five percent cell lysate was used as input to demonstrate the expression of tagged proteins. h Co-immunoprecipitation assays detecting the interaction between GFP-tagged NF2 and Flag-tagged Xinβ protein fragment (amino acids 334-1075) using antibodies to Flag (top) and GFP (bottom). Five percent cell lysate was used as the input to demonstrate the expression of tagged proteins. i Summary of the Xinβ domains that interact with NF2. j Interaction of endogenous Xinβ with NF2 protein. k qRT-PCR of human Xinβ (hXinβ) and cardiomyopathy marker genes NPPA and NPPB in heart samples from dilated cardiomyopathy (DCM) and control patients. N = 5 biologically independent samples, *P < 0.05.
