Fig. 6 | Cell Death & Differentiation

Fig. 6

From: RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke

Fig. 6The alternative text for this image may have been generated using AI.

RGMa forms a complex with ALK5 and Smad2/3 to facilitate Smad2/3 phosphorylation by ALK5. a Interaction of ALK5 with Smad2/3 and RGMa in astrocytes analyzed by a co-immunoprecipitation assay. ALK5 was isolated by immunoprecipitation from astrocytes infected with rAd-shRGMa or rAd-HK before exposure to TGFβ1 (10 ng/ml for 3 days), and ALK5-associated proteins were analyzed by Western blot with the indicated antibodies (top panels). Controls of protein levels in whole-cell lysates are displayed on the bottom. Similar results were obtained using two additional cell batches. b Association of RGMa with Smad2/3 and ALK5 in primary cultured astrocytes infected with rAd-shRGMa or rAd-HK, followed by TGFβ1 (10 ng/ml for 3 days) stimulation. Smad2/3 and ALK5 that associated with RGMa were isolated by co-immunoprecipitation with anti-RGMa and detected by western blot with the indicated antibodies on the top panels. Controls of protein expression in whole-cell lysates are shown on the bottom. Similar results were obtained using two additional cell batches

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