scholarly journals On the Role of the cAMP Response Element Binding Protein in Long-Term Cardiac Memory

2003 ◽  
Vol 93 (9) ◽  
Author(s):  
Kornelis W. Patberg ◽  
Michael R. Rosen
Keyword(s):  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Cardiac Memory ◽  
Element Binding Protein

scholarly journals p300/cAMP-response-element-binding-protein ('CREB')-binding protein (CBP) modulates co-operation between myocyte enhancer factor 2A (MEF2A) and thyroid hormone receptor-retinoid X receptor

2003 ◽  
Vol 369 (3) ◽  
pp. 477-484 ◽  
Author(s):  
Antonio De LUCA ◽  
Anna SEVERINO ◽  
Paola De PAOLIS ◽  
Giuliano COTTONE ◽  
Luca De LUCA ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Creb Binding Protein ◽  
Camp Response Element ◽  
Response Element ◽  
Adenovirus E1a ◽  
Element Binding Protein ◽  
Enhancer Factor

Thyroid hormone receptors (TRs) and members of the myocyte enhancer factor 2 (MEF2) family are involved in the regulation of muscle-specific gene expression during myogenesis. Physical interaction between these two factors is required to synergistically activate gene transcription. p300/cAMP-response-element-binding-protein ('CREB')-binding protein (CBP) interacting with transcription factors is able to increase their activity on target gene promoters. We investigated the role of p300 in regulating the TR—MEF2A complex. To this end, we mapped the regions of these proteins involved in physical interactions and we evaluated the expression of a chloramphenicol acetyltransferase (CAT) reporter gene in U2OS cells under control of the α-myosin heavy chain promoter containing the thyroid hormone response element (TRE). Our results suggested a role of p300/CBP in mediating the transactivation effects of the TR—retenoid X receptor (RxR)—MEF2A complex. Our findings showed that the same C-terminal portion of p300 binds the N-terminal domains of both TR and MEF2A, and our in vivo studies demonstrated that TR, MEF2A and p300 form a ternary complex. Moreover, by the use of CAT assays, we demonstrated that adenovirus E1A inhibits activation of transcription by TR—RxR—MEF2A—p300 but not by TR—RxR—MEF2A. Our data suggested that p300 can bind and modulate the activity of TR—RxR—MEF2A at TRE. In addition, it is speculated that p300 might modulate the activity of the TR—RxR—MEF2A complex by recruiting a hypothetical endogenous inhibitor which may act like adenovirus E1A.

An Essential Role of cAMP Response Element Binding Protein in Ginsenoside Rg1-Mediated Inhibition of Na+/Glucose Cotransporter 1 Gene Expression

2015 ◽  
Vol 88 (6) ◽  
pp. 1072-1083 ◽  
Author(s):  
Chun-Wen Wang ◽  
Shih-Chieh Su ◽  
Shu-Fen Huang ◽  
Yu-Chuan Huang ◽  
Fang-Na Chan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Essential Role ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Ginsenoside Rg1 ◽  
Camp Response Element ◽  
Response Element ◽  
Element Binding Protein

scholarly journals Long-Term Memory Is Facilitated by cAMP Response Element-Binding Protein Overexpression in the Amygdala

2001 ◽  
Vol 21 (7) ◽  
pp. 2404-2412 ◽  
Author(s):  
Sheena A. Josselyn ◽  
Chanjun Shi ◽  
William A. Carlezon ◽  
Rachael L. Neve ◽  
Eric J. Nestler ◽  
...  
Keyword(s):  
Binding Protein ◽  
Camp Response Element Binding ◽  
Long Term Memory ◽  
Protein Overexpression ◽  
Camp Response Element ◽  
Response Element ◽  
Term Memory ◽  
Element Binding Protein

ROLE OF CAMP-RESPONSE ELEMENT-BINDING PROTEIN PHOSPHORYLATION IN HEPATIC APOPTOSIS UNDER PROTEIN KINASE C ?? SUPPRESSION DURING SEPSIS

Shock ◽  
2005 ◽  
Vol 24 (4) ◽  
pp. 357-363 ◽  
Author(s):  
Ya-Ching Hsieh ◽  
Yen-Hsu Chen ◽  
Hsiao-Ching Jao ◽  
Hseng-Kuang Hsu ◽  
Li-Ju Huang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Phosphorylation ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Kinase C ◽  
Element Binding Protein

CREB: A Multifaceted Target for Alzheimer’s Disease

2021 ◽  
Vol 18 ◽  
Author(s):  
Vivek Kumar Sharma ◽  
Thakur Gurjeet Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Signaling ◽  
Camp Response Element ◽  
Response Element ◽  
Term Memory ◽  
Element Binding Protein

: Alzheimer’s disease (AD) is a persistent neuropathological stipulation manifested in the form of neuronal/synapse demise, the formation of senile plaques, hyperphosphorylated tau tangles, neuroinflammation, and apoptotic cell death. The absence of a therapeutic breakthrough for AD has continued the quest to find a suitable intervention. Apart from various candidates, the cyclic AMP-protein kinase A-cAMP response element-binding protein (cAMP/PKA/CREB) pathway is the most sought-after drug target AD as the bulk of quality literature documents that there is downregulation of cAMP signaling and CREB mediated transcriptional cascade in AD. cAMP signaling is evolutionarily conserved and can be found in all species. cAMP response element-binding protein (CREB) is a ubiquitous and integrally articulated transcription aspect that regulates neuronal growth, neuronal differentiation/proliferation, synaptic plasticity, neurogenesis, maturation of neurons, spatial memory, long-term memory formation as well as ensures neuronal survival. CREB is a central part of the molecular machinery that has a role in transforming short-term memory to long-term. Besides AD, impairment of CREB signaling has been well documented in addiction, Parkinsonism, schizophrenia, Huntington’s disease, hypoxia, preconditioning effects, ischemia, alcoholism, anxiety, and depression. The current work highlights the role and influence of CREB mediated transcriptional signaling on major pathological markers of AD (amyloid β, neuronal loss, inflammation, apoptosis, etc.). The present work justifies the continuous efforts being made to explore the multidimensional role of CREB and related downstream signaling pathways in cognitive deficits and neurodegenerative complications in general and AD particularly. Moreover, it is reaffirmed that cyclic nucleotide signaling may have vast potential to treat neurodegenerative complications like AD.

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