Antisense‐induced knockdown of cAMP response element‐binding protein downregulates Per1 gene expression in the shell region of nucleus accumbens resulting in reduced alcohol consumption in mice

2021 ◽  
Author(s):  
Rishi Sharma ◽  
Vaibhav Mishra ◽  
Meet Parikh ◽  
Anshul Soni ◽  
Pradeep Sahota ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nucleus Accumbens ◽  
Alcohol Consumption ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Element Binding Protein ◽  
Shell Region

scholarly journals Inhibition of cAMP Response Element-Binding Protein or Dynorphin in the Nucleus Accumbens Produces an Antidepressant-Like Effect

2002 ◽  
Vol 22 (24) ◽  
pp. 10883-10890 ◽  
Author(s):  
Samuel S. Newton ◽  
Johannes Thome ◽  
Tanya L. Wallace ◽  
Yukihikko Shirayama ◽  
Lee Schlesinger ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Element Binding Protein

scholarly journals Induction of Human NF-IL6β by Epidermal Growth Factor Is Mediated through the p38 Signaling Pathway and cAMP Response Element-binding Protein Activation in A431 Cells

2005 ◽  
Vol 16 (7) ◽  
pp. 3365-3376 ◽  
Author(s):  
Ju-Ming Wang ◽  
Joseph T. Tseng ◽  
Wen-Chang Chang
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Binding Activity ◽  
A431 Cells ◽  
Base Pairs ◽  
Camp Response Element ◽  
Response Element ◽  
Element Binding Protein ◽  
Epidermal Growth

The CCAAT/enhancer binding protein δ (C/EBPδ, CRP3, CELF, NF-IL6β) regulates gene expression and plays functional roles in many tissues, such as in acute phase response to inflammatory stimuli, adipocyte differentiation, and mammary epithelial cell growth control. In this study, we examined the expression of human C/EBPδ (NF-IL6β) gene by epidermal growth factor (EGF) stimulation in human epidermoid carcinoma A431 cells. NF-IL6β was an immediate-early gene activated by the EGF-induced signaling pathways in cells. By using 5′-serial deletion reporter analysis, we showed that the region comprising the –347 to +9 base pairs was required for EGF response of the NF-IL6β promoter. This region contains putative consensus binding sequences of Sp1 and cAMP response element-binding protein (CREB). The NF-IL6β promoter activity induced by EGF was abolished by mutating the sequence of cAMP response element or Sp1 sites in the –347/+9 base pairs region. Both in vitro and in vivo DNA binding assay revealed that the CREB binding activity was low in EGF-starved cells, whereas it was induced within 30 min after EGF treatment of A431 cells. However, no change in Sp1 binding activity was found by EGF treatment. Moreover, the phosphatidylinositol 3 (PI3)-kinase inhibitor (wortmannin) and p38MAPK inhibitor (SB203580) inhibited the EGF-induced CREB phosphorylation and the expression of NF-IL6β gene in cells. We also demonstrated that CREB was involved in regulating the NF-IL6β gene transcriptional activity mediated by p38MAPK. Our results suggested that PI3-kinase/p38MAPK/CREB pathway contributed to the EGF activation of NF-IL6β gene expression.

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