Language:
  
[Sign in] [Register]   

EIAab logo

EIAab news detail, please contact eiaab@eiaab.com if you have any questions about online orders and payment.
AMP-activated protein kinase suppresses the expression of LXR/SREBP-1 signaling-induced ANGPTL8 in HepG2 cells
Update time:2015-09-28 18:40:28   【 Font: Large  Medium Small

 

Abstract
ANGPTL8 is a liver-derived secretory protein that leads to elevated serum triglyceride and the level of circulating ANGPTL8 is strongly associated with obesity and diabetes. Here we investigated the mechanisms of activation and inhibition of ANGPTL8 expression in hepatocytes.

The expression of ANGPTL8 was significantly increased in HepG2 cells exposed to palmitic acid, tunicamycin, or T0901317, and was reversed in cells treated with AICAR. Palmitic acid, tunicamycin, and T0901317 increased LXRα and SREBP-1c mRNA expression. The inhibitory effect of AICAR on the expression of T0901317-induced ANGPTL8 was most strongly evident in cells that were transfected with SREBP-1 siRNA. AICAR increased phosphorylation of PPARα and the effect of AICAR was not observed in cells treated with PPARα inhibitor. Metformin had a similar effect on ANGPTL8 expression to that of AICAR. These data suggest that AMPK can suppress the expression of LXR/SREBP-1 signal-induced ANGPTL8 in HepG2 cells.

Cited products
Source:Molecular and Cellular Endocrinology      by Lee J, Hong SW, Park SE, et al.
Hot Genes
ALCAM ACE KSR2 ASPRO C19orf80 Gdf5 Trap1a Atf2
Top Searches
Asprosin Ubiquitin ELISA Ubiquitin-protein ligase TRAP1A metalloproteinase Tumor necrosis vitamin d
Why choose EIAAB
Our products have been quoted by many publications in famous journals such as Cell; Cell Metabolism; Hepatology; Biomaterials.more
Further Information
About us Protein center Bank account Distributors Terms & Conditions Career eiaab.cn

Copyright & copy www.eiaab.com2006-2016 All Rights Reserved    EIAab         Email:eiaab@eiaab.com

Twitter