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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: RGS6 drives cardiomyocyte death following nucleolar stress by suppressing Nucleolin/miRNA-21

Fig. 1

RGS6 forms a complex with Nucleolin in VCM. A Co-immunoprecipitation (Co-IP) of RGS6 with Nucleolin from human AC-16 cardiomyocytes. B In silico modeling of the RGS6-Nucleolin supports direct interaction.The best docking pose for the RGS6-Nucleolin (NCL) complex predicted using the ZDOCK webserver. The residues present on the protein–protein interaction interface are highlighted in red. C Co-IP of Nucleolin with RGS6 deletion constructs transfected into human AC-16 cardiomyocytes. D–F Mice VCM were transduced with RGS6-pEGFP (RGS6 OE) or RGS6 specific shRNA (RGS6 KD) or vector control and harvested 36 hours after transduction. D Representative immunoblots and quantification for RGS6, Nucleolin, Nucleophosmin (n = 8). E Fold change in Nucleolin and Nucleophosmin mRNA (n = 3). F Immunoblots and quantification for Nucleolin pT76 and Nucleolin pT84 (n = 4). β-Actin serves as a loading control for immunoblots. Data were analyzed by one-way ANOVA with Sidak’s post-hoc test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns = not significant. Data are presented as mean ± SEM

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