High impact information on Zfpm2_predicted

• These findings demonstrate that FOG-2 represses hypertrophic responses in cardiac myocytes and that p300 is involved in these repressive effects [1].
• We show here that exogenous FOG-2 represses phenylephrine-induced hypertrophic responses such as myofibrillar organization, increases in cell size, and hypertrophy-associated gene transcription [1].
• In addition, RXR alpha was found to bind FOG-2, in a 9-cis-RA-dependent manner [2].
• Retinoid X receptor alpha represses GATA-4-mediated transcription via a retinoid-dependent interaction with the cardiac-enriched repressor FOG-2 [2].
• These data reveal a novel mechanism by which retinoids regulate cardiogenic gene expression through direct interaction with GATA-4 and its co-repressor, FOG-2 [2].

Anatomical context of Zfpm2_predicted

• Co-transfection of liganded RXR alpha and the known cardiac-enriched GATA-4 repressor, FOG-2, resulted in additive repression of GATA-4 activity in ventricular myocytes [2].
• These competitors, along with the GATA-4 cofactor FOG-2 (friend of GATA-2), were used to specifically modulate endogenous GATA-4 activity in Sertoli cells [3].
• Furthermore, the coregulator of GATA, FOG2, markedly suppresses the GATA-induced increase in myocytes, but enhances it in PC12 cells [4].

Analytical, diagnostic and therapeutic context of Zfpm2_predicted

• Using immunoprecipitation Western blotting, we demonstrate that FOG-2 physically interacted with p300 and reduced the binding of GATA-4 to p300 [1].

References