Browse our anti-NCOA6 (NCOA6) Antibodies

Human Nuclear Receptor Coactivator 6 (NCOA6) interaction partners

1. The retinoid x receptor does not interact with the NR box-1 of ASC-2, but functions as an allosteric activator of LXR binding to NR box-2 of ASC-2.

2. diverse physiological function of NCOA6 may be mediated by multiple isoforms expressed in different tissues and localized in different subcellular compartments

3. NCOA6 is responsible for the synergistic activation of CYP2C9 by HNF4alpha and pregnane X receptor and NCOA6 differentially regulates CYP2C9 and CYP3A4 gene expression though both the genes are regulated by the same nuclear receptors.

4. we show that ASC-2 belongs to a steady-state complex of approximately 2 MDa (ASC-2 complex [ASCOM]) in HeLa nuclei. ASCOM contains retinoblastoma-binding protein RBQ-3, alpha/beta-tubulins, and trithorax group proteins ALR-1, ALR-2, HALR, and ASH2.

5. The activation of DNA-PK in the absence of DNA ends by the coactivator TRBP suggests a novel mechanism of coactivator-stimulated DNA-PK phosphorylation in transcriptional regulation.

6. ASC-2 is a physiologically important transcriptional coactivator of LXRs and demonstrate its pivotal role in the liver lipid metabolism

7. ASC-2 appears to contain at least three distinct nuclear receptor interaction domains; also, Rb and ASC-2 have roles in androgen receptor transactivation

8. ASC-2 has a role in inducing target gene transcription during granulocytic differentiation through binding to ATF2

9. results suggest that ASC-2 is a novel coactivator for HSF1 and heat shock stress may contribute to the strong active transcription complex through sequential recruitment of HSF1 and ASC-2.

10. ASC-2 is a bona fide coactivator of the xenobiotic nuclear receptor CAR and mediate the specific xenobiotic response by CAR in vivo.

11. interaction between RAP250, Smad2, and Smad3 constitutes an important bridging mechanism linking LXR and TGF-beta signaling pathways.

12. AIB3 contributes to the maintenance of beta-cell function in nondiabetic children and regulates gene expression in INS-1 cells.

13. The coactivator NCOA6 mediates the mechanism of the synergistic activation of the CYP2C9 gene by CAR and HNF4alpha.

14. Promoter analysis showed that PRIP acted through serum-responsive factor to regulate FOS gene expression.

15. ASCOM-MLL3 and ASCOM-MLL4 play redundant but essential roles in FXR transactivation via their histone 3 lysine 4 trimethylation activity.

Mouse (Murine) Nuclear Receptor Coactivator 6 (NCOA6) interaction partners

1. PRIP deficiency impairs osteoclast differentiation, particularly at the early stages, and PRIP stimulates osteoclast differentiation through calcium-calcineurin-NFATc1 signaling via regulating intracellular Ca(2+)

2. The results suggest that NCOA6 stimulates insulin secretion, at least partially, by modulating Nampt expression in pancreatic beta-cells.

3. These results indicate that PRIP is implicated in BMP-induced osteoblast differentiation by the negative regulation of Smad phosphorylation, through the methylation of inhibitory Smad6.

4. The results indicate that PRIP negatively regulates UCP1-mediated thermogenesis in brown adipocytes.

5. Two independent mouse models of NCOA6 dysfunction develop severe dilated cardiomyopathy with impaired mitochondrial function and reduced activity of peroxisome proliferator-activated receptor delta.

6. The NCOA6 controls E(2) sensitivity and uterine receptivity by regulating multiple E(2)-signaling components.

7. ASC-2 negatively affects hepatic insulin sensitivity, at least in part, through induction of the insulin signalling inhibitors SOCS1 and SOCS3.

8. PRIP is implicated in the negative regulation of bone formation

9. diverse physiological function of NCOA6 may be mediated by multiple isoforms expressed in different tissues and localized in different subcellular compartments

10. methylation of transporter promoters by MLL3 as part of activating signal cointegrator-2 -containing complex is essential for activation of bile salt export pump

11. The apoptotic-like processes in the transgenic lens were both p53-dependent and p53-independent. Lens-specific deletion of Ncoa6 also resulted in disrupted lens fiber cell differentiation.

12. These results suggest that AIB3 is required for PPARgamma function in placental development and for normal heart development.

13. role as modulator of placental, cardiac, hepatic, and embryonic development

14. Our results demonstrate that RAP250 is necessary for placental development and thus essential for embryonic development

15. AIB3 mRNA and protein are preferentially expressed in specific cell types, suggesting that AIB3 may support the function of nuclear receptors in a cell type-specific manner.

16. PRIP, like PPARgamma-binding protein, is a downstream regulator of PPARgamma-mediated adipogenesis and that both these coactivators are required for the successful completion of adipogenic program

17. peroxisome proliferator-activated receptor-interacting protein (PRIP)is important for normal mammary gland development

18. Overexpressed ASC-2 increased glucose-elicited insulin secretion, whereas insulin secretion was decreased in islets from ASC-2+/- mice.

19. Results show that PRIP is not essential for nuclear translocation of constitutive androstane receptor.

20. Results suggest that ASC-2 confers target gene specificity to MLL3 and MLL4 H3K4MT complexes and that recruitment of H3K4MTs to their target genes involves interactions between integral components of H3K4MT complexes and transcription factors.