Orphan receptor that acts as transcription activator in the absence of bound ligand. Binds specifically to an estrogen response element and activates reporter genes controlled by estrogen response elements. Induces the expression of PERM1 in the skeletal muscle. Homodimer. Interacts with NRIP1, NCOA1 and NCOR2 (By similarity). Binds TLE1, PNRC1 and PNRC2 (By similarity). Binds GRIP1. Highly expressed in the heart, brain and kidney and low expression in the liver. Acetylated by PCAF/KAT2 (in vitro). Sumoylation on Lys-40 is enhanced by phosphorylation at Ser-45 and represses transcriptional activity. Phosphorylation on Ser-45 enhances sumoylation on Lys-40 thus repressing transcriptional activity. Cardiomyocyte-specific double konckout for ESRRA and ESRRG are slower at gaining weight, smaller and shorter from 5 to 7 days of age compared to controls. They show decreased absolute weight of most internal organs except the heart. They have about 70% decreased plasma IGF1 levels but normal plasma growth hormone levels. At 14-15 days, mutants develop lethal dilated cardiomyopathy and heart failure. No physiological activating ligand is known for this orphan receptor, but 4-hydroxytamoxifen and diethylstilbestrol act as inverse agonists and deactivate ESRRG. Belongs to the nuclear hormone receptor family. NR3 subfamily. Extended N-terminus.