Extended Data Fig. 5: CCM3 attenuates the FAK/phospho-Paxillin pathway in focal adhesions to regulate coupling between the actomyosin network and the mechanical ECM.

a-b, Immunofluorescence analysis of siRNA transfected HN-CAFs and Cer-CAFs stained for (a) pY397-FAK (green), paxillin (red), and DAPI (blue) and (b) pY118-paxillin (green), F-actin (red), and DAPI (blue). Scale bars, 50 μm. c, Morphometric analysis of focal adhesion size, number per cell, and length, based on the pY118-paxillin staining. Left histogram (n: cells. HN-CAF, 20; V-CAF, 21; Cer-CAF: siCtr, 20; siCCM3, 23); middle histogram (n: individual focal adhesions. HN-CAF: siCtr, 562; siCCM3, 557. V-CAF: siCtr, 1207; siCCM3, 1211. Cer-CAF: siCtr, 402; siCCM3, 464); right histogram (n: individual focal adhesions. HN-CAF: siCtr, 562; siCCM3, 584. V-CAF: siCtr, 1206; siCCM3, 1179. Cer-CAF: siCtr, 402; siCCM3, 526). Line and error bars indicate mean ± s.d.; Kruskal–Wallis non-parametric tests, following up multiple-comparison post-hoc test. d–f, Immunofluorescence analysis of siRNA transfected V-CAFs stained for (d) pY397-FAK (green), vinculin (red), and DAPI (blue), (e) pY118-paxillin (green), talin (red), and DAPI (blue), and (f) pY118-paxillin (green), α-actinin (red), and DAPI (blue). Scale bars, 50 μm. Statistical data are provided in the source data.