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. 2017 Jun 29;37(14):e00675-16. doi: 10.1128/MCB.00675-16

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FIG 5 — CD99-induced PKA activation results in β1 integrin inactivation via regulation of the SHP2/MAPK/ERK signaling pathway. (A, F) In situ PLAs performed to assess the interactions between the pairs of molecules indicated in MCF-7 cells. Numerical values are the average intensities (±SD) of red spots in eight randomly selected fields. (B) Coimmunoprecipitation (Co-IP) assay performed to assess the physical interaction of PKA with SHP2. Immunoprecipitates (IP) and whole-cell lysates (input) were separated by SDS-PAGE and analyzed by Western blotting with the antibodies indicated. (C to E) Western blot analysis was carried out to assess the phosphorylation of ERK1/2 and FAK Y397 and the knockdown efficiency of PKA siRNA. β-Actin was used as a loading control. FN, fibronectin; RCPs, rolling-circle products.

FIG 5 — CD99-induced PKA activation results in β1 integrin inactivation via regulation of the SHP2/MAPK/ERK signaling pathway. (A, F) In situ PLAs performed to assess the interactions between the pairs of molecules indicated in MCF-7 cells. Numerical values are the average intensities (±SD) of red spots in eight randomly selected fields. (B) Coimmunoprecipitation (Co-IP) assay performed to assess the physical interaction of PKA with SHP2. Immunoprecipitates (IP) and whole-cell lysates (input) were separated by SDS-PAGE and analyzed by Western blotting with the antibodies indicated. (C to E) Western blot analysis was carried out to assess the phosphorylation of ERK1/2 and FAK Y397 and the knockdown efficiency of PKA siRNA. β-Actin was used as a loading control. FN, fibronectin; RCPs, rolling-circle products.