ASC-2: An important co-activator of different nuclear receptors

ASC-2, also known as Nuclear Receptor Co-Activator 6, directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. It is involved in the co-activation of different nuclear receptors, such as for steroids (GR and ERs), retinoids (RARs and RXRs), thyroid hormone (TRs), vitamin D3 (VDR) and prostanoids (PPARs). It is believed to function as a general co-activator, rather than just a nuclear receptor co-activator. It may also be involved in the co-activation of the NF-kappa-B pathway and co-activate expression via remodeling of chromatin and its interaction with histone acetyltransferase proteins. Diseases associated with ASC-2 include thyroiditis and AIDS dementia complex. Among its related super-pathways are Regulation of Lipid Metabolism by Peroxisome proliferator-activated receptor alpha (PPARalpha) and Metabolic pathways.

Using Novus NB200-336 ASC-2 antibody, Surapureddi’s group has revealed that Nuclear Receptor Co-Activator 6 mediates the synergistic activation of human cytochrome P-450 2C9 by the constitutive androstane receptor (CAR) and hepatic nuclear factor-4alpha (HNF4alpha). (1) A group of researchers using the same Novus antibody in their study characterized ASC-2 as an antiatherogenic transcriptional co-activator of liver X receptors in macrophages. They have shown that suppression of the LXR-specific activity of ASC-2 results in both defective cholesterol metabolism in macrophages and accelerated atherogenesis, suggesting that ASC-2 is an antiatherogenic co-activator of LXRs in macrophages. (2)

Immunohistochemistry-Paraffin: NCOA6 Antibody [NB200-336]

ASC-2 is enriched in liver cancer cells and associates with many transcription factors that are active in hepatocytes. Data from Kong HJ’s group has shown that Hepatitis B virus X protein (HBx) which plays a significant role in the regulation of genes involved in inflammation and cell survival, stabilizes the cellular co-activator ASC-2 through direct protein-protein interaction, affecting the regulation of genes actively transcribed in liver cancer cells. (3)

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