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CAMP responsive element -mediated

Shaw-Lutchman TZ, Barrot M, Wallace T, et al Regional and cellular mapping of cAMP response element-mediated transcription during naltrexone-precipitated morphine withdrawal. J Neurosci 22 3663-3672, 2002 Shreeram SS, McDonald T, Dennison S Psychosisafterultrarapidopiatedetoxification (letter). Am J Psychiatry 158 970, 2001... [Pg.107]

Thome J., Sakain N., Shin K. et al. (2000). cAMP response element-mediated gene transcription in upregulated by chronic antidepressant. J. Neurosci. 20, 4030-6. [Pg.460]

Thome J, SakaiN, Shin KH, Steffen C, Zhang Y-J, Impey S, Storm DR, Diunan RS (2000) cAMP response element-mediated gene transcription is upregulated by chronic antidepressant treatment. J Nemosci 20 4030-4036... [Pg.334]

Obrietan, K., Impey, S., Smith, D., Athos,J., and Storm, D. R. (1999). Circadian regulation of cAMP response element-mediated gene expression in the suparachiasmatic nuclei. J. Biol. Chem. 274, 17748-17756. [Pg.217]

The cAMP responsive element binding factor (CREB) is also activated by phosphorylation. Depending on the stimuli, CREB is the target of a cAMP dependent protein kinase or of kinases called MAPKs, RSK, and CamKIV. As in AP-1, CREB carries a basic leucine zipper motif (bZDP), which mediates homo dimerization of CREB when bound to the CRE. [Pg.1227]

Impey S, Smith DM, Obrietan K, Donahue R, Wade C, Storm DR (1998) Stimulation of cAMP response element (CRE)-mediated transcription during contextual learning. Nat Neurosci 1 595-601... [Pg.330]

Das S, Tosaki A, Bagchi D, Maulik N, Das DK (2005b) Resveratrol-mediated activation of cAMP response element-binding protein through adenosine A3 receptor by Akt-dependent and -independent pathways. J Pharmacol Exp Ther 314(2) 762-769... [Pg.69]

Papadia S., Stevenson P., Hardingham N. R., Bading H., and Hardingham G. E. (2005). Nuclear Ca2+ and the cAMP response element-binding protein family mediate a late phase of activity-dependent neuroprotection. J. Neurosci. 25 4279 1287. [Pg.101]

This mechanism may account partially for the stimulatory action of NO on transmitter release in hippocampal synapses (Schuman et al. 1994). Last but not least, NO may modulate cellular functions by S-nitrosylation of various proteins. For example, S-nitrosylation of nuclear proteins associated with cAMP response element (CRE) binding protein is involved in regulation of its DNA binding and, hence, CRE-mediated gene expression (Riccio et al. 2006). S-nitrosylation has also been reported to modify the function of various ion channels (Broillet and Firestein 1996, 1997 Xu et al. 1998 Jaffrey et al. 2001). [Pg.537]

The Role of cAMP Response Element—Binding Proteins in Mediating Stress-Induced Vulnerability to Drug Abuse... [Pg.451]

Fig. 7. Model for activation by coactivators (A) and inhibition by corepressors (B) of transcription. Abbreviations CBP/p300, cAMP response element binding protein SRC-1, steroid receptor coactivator 1 TBP, TATA-binding protein TAF, TBP-associated factor pol II, RNA polymerase II N-CoR, nuclear receptor corepressor SMRT, silencing mediator of retinoic and thyroid hormone receptors. Fig. 7. Model for activation by coactivators (A) and inhibition by corepressors (B) of transcription. Abbreviations CBP/p300, cAMP response element binding protein SRC-1, steroid receptor coactivator 1 TBP, TATA-binding protein TAF, TBP-associated factor pol II, RNA polymerase II N-CoR, nuclear receptor corepressor SMRT, silencing mediator of retinoic and thyroid hormone receptors.
As indicated in Chapters 5, 7 and 8, transcription can be switched on by a variety of signalling pathways. Thus, cAMP-mediated pathways generate phosphorylated CREB proteins that activate expression of particular proteins by binding to promoters called cAMP response elements (GREs). Similarly, Ca2+-dependent PKC activation results in phosphorylation of transcription factors that bind to and activate tetradecanoylphorbol ester response element (TRE) promoters. In the immune response bacterial lipopolysaccharide (LPS) and particular cytokines can switch on signalling pathways resulting in activation of transcription factors such as NFkB (Chapter 7) with resultant expression of proteins such as cytokines,... [Pg.341]

Figure 16.31. The Promoter of the Phosphoenolpyruvate Carhoxykinase Gene. This promoter is approximately 500 bp in length and contains regulatory sequences (response elements) that mediate the action of several hormones. IRE, insulin response element GRE, glucocorticoid response element TRE, thyroid hormone response element CREI and CREII, cAMP response elements. [After M. M. McGrane, J. S Jun, Y. M. Patel, and R. W. Hanson. Trends Biochem. Sci. 17(1992) 40.]... Figure 16.31. The Promoter of the Phosphoenolpyruvate Carhoxykinase Gene. This promoter is approximately 500 bp in length and contains regulatory sequences (response elements) that mediate the action of several hormones. IRE, insulin response element GRE, glucocorticoid response element TRE, thyroid hormone response element CREI and CREII, cAMP response elements. [After M. M. McGrane, J. S Jun, Y. M. Patel, and R. W. Hanson. Trends Biochem. Sci. 17(1992) 40.]...
Corbett GT, Roy A, Pahan K (2013) Sodium phenylbutyrate enhances astrocytic neuro-trophin synthesis via protein kinase C (PKC)-mediated activation of cAMP-response element-binding protein (CREB) Implications for Alzheimer disease therapy. J Biol Chem 288 8299-8312... [Pg.545]


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