Biological functions of CREB/ATF bZIP transcription factor in metabolism and cell growth.
- Author:
Yu-Xiao LIU
1
;
Wei-Tong SU
1
;
Yu LI
2
Author Information
1. CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
2. CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. liyu@sibs.ac.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Basic-Leucine Zipper Transcription Factors/metabolism*;
Cell Cycle;
Cell Proliferation;
Diet, High-Fat;
Hepatocytes;
Insulin Resistance;
Lipid Metabolism;
Liver;
Mice;
Mice, Inbred C57BL;
Mice, Knockout;
Signal Transduction
- From:
Acta Physiologica Sinica
2021;73(5):761-771
- CountryChina
- Language:Chinese
-
Abstract:
Nutrient overload-caused deregulation of glucose and lipid metabolism leads to insulin resistance and metabolic disorders, which increases the risk of several types of cancers. CREB/ATF bZIP transcription factor (CREBZF), a novel transcription factor of the ATF/CREB family, has emerged as a critical mechanism bridging the gap between metabolism and cell growth. CREBZF forms a heterodimer with other proteins and functions as a coregulator for gene expression. CREBZF deficiency in the liver attenuates hepatic steatosis in high fat diet-induced insulin-resistant mice, while the expression levels of CREBZF are increased in the livers of obese mice and humans with hepatic steatosis. Intriguingly, CREBZF also regulates cell proliferation and apoptosis via interaction with several transcription factors including STAT3, p53 and HCF-1. Knockout of CREBZF in hepatocytes results in enhanced cell cycle progression and proliferation capacity in mice. Here we highlight how the CREBZF signaling network contributes to the deregulation of metabolism and cell growth, and discuss the potential of targeting these molecules for the treatment of insulin resistance, diabetes, fatty liver disease and cancer.
