Fig. 6From: Abnormal expression of PRKAG2-AS results in dysfunction of cardiomyocytes through regulating PRKAG2 transcription by interacting with PPARGPRKAG2-AS regulated PRKAG2b and PRKAG2d by directly interacting with PPARĪ³. A The top ten positive relative proteins between PRKAG2 and these 58 proteins in the GSE57338 and GSE79962 datasets were used to construct a network by STRING and Cytoscape, in which PPARG and HDAC1 occupied a pivotal position. BāD Overexpression of PPARG promoted the transcription of PRKAG2b and PRKAG2d in AC16 cells. EāF The PPARĪ³ agonist rosiglitazone significantly up-regulated the expression of PRKAG2b and PRKAG2d in cardiomyocytes. G-H The effects of rosiglitazone on PRKAG2b and PRKAG2d transcription were mediated by PRKAG2-ASBack to article page