scholarly journals Cannabinoid Receptor Type 1 (CB1R) Signaling Regulates Hepatic Gluconeogenesis via Induction of Endoplasmic Reticulum-bound Transcription Factor cAMP-responsive Element-binding Protein H (CREBH) in Primary Hepatocytes

2011 ◽  
Vol 286 (32) ◽  
pp. 27971-27979 ◽  
Author(s):  
Dipanjan Chanda ◽  
Don-Kyu Kim ◽  
Tiangang Li ◽  
Yong-Hoon Kim ◽  
Seung-Hoi Koo ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Cannabinoid Receptor ◽  
Receptor Type ◽  
Primary Hepatocytes ◽  
Hepatic Gluconeogenesis ◽  
Element Binding Protein ◽  
Responsive Element ◽  
Camp Responsive Element Binding

scholarly journals Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)–ATF composite site to regulate Gadd153 expression during the stress response

1999 ◽  
Vol 339 (1) ◽  
pp. 135-141 ◽  
Author(s):  
Timothy W. FAWCETT ◽  
Jennifer L. MARTINDALE ◽  
Kathryn Z. GUYTON ◽  
Tsonwin HAI ◽  
Nikki J. HOLBROOK
Keyword(s):  
Transcription Factor ◽  
Pc12 Cells ◽  
Protein C ◽  
Binding Protein ◽  
Enhancer Binding Protein ◽  
Element Binding Protein ◽  
Activating Transcription Factor ◽  
Responsive Element ◽  
Camp Responsive Element Binding ◽  
Gadd153 Expression

Gadd153, also known as chop, encodes a member of the CCAAT/enhancer-binding protein (C/EBP) transcription factor family and is transcriptionally activated by cellular stress signals. We recently demonstrated that arsenite treatment of rat pheochromocytoma PC12 cells results in the biphasic induction of Gadd153 mRNA expression, controlled in part through binding of C/EBPβ and two uncharacterized protein complexes to the C/EBP–ATF (activating transcription factor) composite site in the Gadd153 promoter. In this report, we identified components of these additional complexes as two ATF/CREB (cAMP-responsive-element-binding protein) transcription factors having differential binding activities dependent upon the time of arsenite exposure. During arsenite treatment of PC12 cells, we observed enhanced binding of ATF4 to the C/EBP–ATF site at 2 h as Gadd153 mRNA levels increased, and enhanced binding of ATF3 complexes at 6 h as Gadd153 expression declined. We further demonstrated that ATF4 activates, while ATF3 represses, Gadd153 promoter activity through the C/EBP–ATF site. ATF3 also repressed ATF4-mediated transactivation and arsenite-induced activation of the Gadd153 promoter. Our results suggest that numerous members of the ATF/CREB family are involved in the cellular stress response, and that regulation of stress-induced biphasic Gadd153 expression in PC12 cells involves the ordered, sequential binding of multiple transcription factor complexes to the C/EBP–ATF composite site.

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