A cotton dehydration responsive element binding protein functions as a transcriptional repressor of DRE-mediated gene expression

2006 ◽  
Vol 343 (4) ◽  
pp. 1023-1031 ◽  
Author(s):  
Bo Huang ◽  
Jin-Yuan Liu
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Transcriptional Repressor ◽  
Protein Functions ◽  
Element Binding Protein ◽  
Responsive Element

scholarly journals Carbohydrate-Responsive Element-Binding Protein (ChREBP) Is a Negative Regulator of ARNT/HIF-1  Gene Expression in Pancreatic Islet  -Cells

Diabetes ◽  
2009 ◽  
Vol 59 (1) ◽  
pp. 153-160 ◽  
Author(s):  
N. A. Noordeen ◽  
T. K. Khera ◽  
G. Sun ◽  
E. R. Longbottom ◽  
T. J. Pullen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Binding Protein ◽  
Negative Regulator ◽  
Pancreatic Islet Cells ◽  
Element Binding Protein ◽  
Responsive Element

Abstract 540: Very Low Density Lipoprotein Assembly is Required for cAMP Responsive Element-binding Protein H Processing and Hepatic Apolipoprotein A-IV Expression in Mouse Models of Acute Steatosis

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Dongmei Cheng ◽  
Xu Xu ◽  
Elena Boudyguina ◽  
Trang Simon ◽  
Zhiyong Deng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Models ◽  
Ketogenic Diet ◽  
Binding Protein ◽  
Apolipoprotein A ◽  
Vldl Secretion ◽  
Element Binding Protein ◽  
Vldl Assembly ◽  
Responsive Element ◽  
Camp Responsive Element Binding

Background: Our previous studies have demonstrated that hepatic expression of apolipoprotein A-IV (apoA-IV) is increased in mouse models of chronic steatosis and is closely correlated with hepatic triglyceride (TG) content. We have also shown that steatosis-induced hepatic apoA-IV gene expression is regulated by processing of the nuclear transcription factor cAMP responsive element-binding protein H (CREBH). Herein, we explored the mechanisms that mediate steatosis-induced CREBH processing. Methods: We measured hepatic CREBH processing, apoA-IV gene expression, and lipid content in several mouse models of attenuated or enhanced VLDL assembly that were subjected to acute steatosis induced by a 16 hour overnight fast or by feeding a ketogenic diet for 6 days. Results: Both fasting and the ketogenic diet induced acute hepatic TG accumulation associated with increased CREBH processing and apoA-IV gene expression, which were associated with hepatic TG content in C57BL/6 mice. All mouse models of attenuated VLDL secretion (shRNA-induced apoB knock down, liver specific microsomal triglyceride transfer protein (MTP) knockout, treatment with the MTP inhibitor BMS212122, and comparative gene identification-58 (CGI-58) deficiency) had increased hepatic TG accumulation, but displayed repressed CREBH processing and reduced apoA-IV gene expression compared to controls. When deficient VLDL assembly in liver-specific MTP knockout mice was reconstituted by adenoviral infection with a human MTP transgene, steatosis-induced CREBH processing and apoA-IV expression were restored. In a mouse model of enhanced VLDL assembly (transgenic overexpression of human MTP), apoA-IV gene expression correlated with bulk hepatic TG accumulation, but not with VLDL secretion rate, indicating that other steatosis-related factors participate in apoA-IV gene regulation. Conclusions: Taken together, these data provide compelling evidence that VLDL assembly and secretion is required for hepatic CREBH processing and enhanced apoA-IV gene expression in the setting of acute steatosis. These data further suggest that CREBH and apoA-IV play central roles in VLDL-mediated hepatic lipid efflux.

scholarly journals Degradation of Transcriptional Repressor ATF4 during Long-Term Synaptic Plasticity

2020 ◽  
Vol 21 (22) ◽  
pp. 8543
Author(s):  
Spencer G. Smith ◽  
Kathryn A. Haynes ◽  
Ashok N. Hegde
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Transcriptional Repressor ◽  
Long Term Potentiation ◽  
Long Term Memory ◽  
Activating Transcription Factor 4 ◽  
Element Binding Protein ◽  
Activating Transcription Factor ◽  
Responsive Element

Maintenance of long-term synaptic plasticity requires gene expression mediated by cAMP-responsive element binding protein (CREB). Gene expression driven by CREB can commence only if the inhibition by a transcriptional repressor activating transcription factor 4 (ATF4; also known as CREB2) is relieved. Previous research showed that the removal of ATF4 occurs through ubiquitin-proteasome-mediated proteolysis. Using chemically induced hippocampal long-term potentiation (cLTP) as a model system, we investigate the mechanisms that control ATF4 degradation. We observed that ATF4 phosphorylated at serine-219 increases upon induction of cLTP and decreases about 30 min thereafter. Proteasome inhibitor β-lactone prevents the decrease in ATF4. We found that the phosphorylation of ATF4 is mediated by cAMP-dependent protein kinase. Our initial experiments towards the identification of the ligase that mediates ubiquitination of ATF4 revealed a possible role for β-transducin repeat containing protein (β-TrCP). Regulation of ATF4 degradation is likely to be a mechanism for determining the threshold for gene expression underlying maintenance of long-term synaptic plasticity and by extension, long-term memory.

scholarly journals Iron-responsive element-binding protein. Phosphorylation by protein kinase C.

1993 ◽  
Vol 268 (36) ◽  
pp. 27363-27370
Author(s):  
R S Eisenstein ◽  
P T Tuazon ◽  
K L Schalinske ◽  
S A Anderson ◽  
J A Traugh
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Phosphorylation ◽  
Binding Protein ◽  
Iron Responsive Element ◽  
Kinase C ◽  
Element Binding Protein ◽  
Responsive Element
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