[Biological functions of CREB/ATF bZIP transcription factor in metabolism and cell growth].
Sheng Li Xue Bao
; 73(5): 761-771, 2021 Oct 25.
Article
en Zh
| MEDLINE
| ID: mdl-34708233
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.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Resistencia a la Insulina
/
Factores de Transcripción con Cremalleras de Leucina de Carácter Básico
/
Hígado
Límite:
Animals
Idioma:
Zh
Revista:
Sheng Li Xue Bao
Año:
2021
Tipo del documento:
Article
País de afiliación:
China