Cyclic adenosine monophosphate response element

Cyclic adenosine monophosphate, 25f Cyclic adenosine monophosphate response element binding, 83, 88 Cytochrome P450 enzymes, 171... 

Minor sites of action inhibits activation of the transcription factors cyclic adenosine monophosphate response element-binding protein and nuclear factor kappa-B. 

Antidepressant treatment has, in recent studies, been shown to upregulate the cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) cascade and expression of BDNF [59]. This upregulation of CREB and BDNF raises the possibility that antidepressant treatment could oppose the cell death pathway, possibly via increased expression of the oncogene Bcl-2. Studies are necessary to determine if antidepressant treatment increases Bcl-2 expression. Increased expression of Bcl-2 in brain and cultured cells, and inhibition of apoptosis of cultured cerebellar granule neurons have been reported with lithium treatment [57]. Mice lacking the BDNF TrkB receptor fail to show behavioral and neurogenic responses to antidepressants. 

Meyer, T.E. and Habener, J.E (1993) Cyclic adenosine 3, 5 -monophosphate response element-binding protein (CREB) and related transcription-activating deoxyribonucleic acid-binding proteins. Endocr Rev 14 269-290. 

Fig. 8.1 A schematic diagram illustrating the involvement of NF-k I in gpl20, ROS, NO, PG, IL-1/3 and TNF-a-mediated neurotoxicity. NMDA-R, N-Methyl-D-aspartate receptor, cPLA2, cytosolic phospholipase A2 lyso-PtdCho, lysophosphatidylcholine AA, arachidonic acid cAMP, cyclic adenosine monophosphate PKA, protein kinase A TNF-a, tumor necrosis factor-a TNF-a-R, TNF-a-receptor IL-1/8, interleukin-1 /3 IL-l/i-R, IL-1/8-receptor, IL-6, interleukin-6 MARK, mitogen-activated protein kinase NO, nitric oxide PG, prostaglandins EP-R, prostaglandin receptors NF-kB, nuclear factor-icB NF-kB-RE, nuclear factor-/cB-response element I/cB, inhibitory subunit of NF-icB HIV-1, human immunodeficiency virus type 1 gpl20, HIV-1 coat glycoprotein COX-2, cyclooxygenase-2 iNOS, inducible nitric oxide synthase SPLA2, secretory phospholipase A2 SOD, superoxide dismutase MMP, matrix metalloproteinase and VCAM-1, vascular adhesion molecule-1...

Fig. 4 Assays for G-protein-coupled receptors. The two main ciasses are binding and functional assays. Binding assays detect compounds that are ligands of the receptor. Functional assays probe the signaling of the receptor within the cell. Gs/i and Gq/i, G-proteins PLC, phospholipase C AC, adenylyl cyclase DAG, diacylglycerol cAMP, cyclic adenosine monophosphate PKC, protein kinase C PKA, protein kinase A (PKA) lns(l,4,5)P3, inositol phosphates P-CREB, phosphorylated cAMP response element binding protein CRE, cAMP regulatory element.

Figure 2.5. A schematic of a p-lactamase reporter cell line that is coupled through a seven transmembrane G-protein—coupled receptor whose second messenger signaling pathway operates through cyclic adenosine monophosphate (cAMP). The G-protein, Gas, activates adenyl cyclase, increasing the concentration of cAMP, which stimulates the production of p-lactamase through cAMP response element.

Brain-derived neurotrophic factor Cyclic adenosine monophosphate (cAMP)-response element-binding protein... 

Recent studies demonstrate that chronic antidepressant treatment targets pathways involved in the production of factors associated with cell survival and plasticity such as cyclic adenosine monophosphate (cAMP)-response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF). 

Figure 109.4 The effect of low thyroid function on peripheral vasculature. The figure is a schemafic represenfafion of fhe principal pathophysiological mechanisms responsible for fhe increased vascular resistance activated by a hypothyroid state. CRE Cyclic Adenosine Monophosphate (CAMP) response element CREB Cyclic Monophosphate (CAMP) response element binding protein.

Most human CKRs preferentially activate Gaj/o proteins, resulting in the inhibition of cyclic adenosine monophosphate (cAMP) production by the enzyme adenylyl cyclase (AC). cAMP activates exchange proteins activated by cAMP (Epac) and protein kinase A (PKA) and the latter subsequently activates the transcription factor cAMP-responsive element (CRE). The released CPy subunits activate phosphoHpase C-P (PLC-P), resulting in the formation of inositol 1,4,5-triphosphate (IP3) and diacylglycerol (DAG) from phosphatidylinositol-4,5-bisphosphate (PIP2)- IP3 subsequently increases intracellular Ca release from endoplasmic reticulum (ER) stores, which results in the activation of protein kinase C (PKC) and the transcription factor nuclear factor of activated T cells (NFAT) (Neptune Bourne, 1997 Patel et al., 2013). Furthermore, CKRs are phosphorylated on their intracellular domains by G protein-coupled receptor kinases (GRKs) and subsequently recruit P-arrestins (Fig. 12). 

Figure 12 CKR signaling. CKRs preferentially signal via Gai/o proteins and recruit p-arrestin upon receptor activation. Abbreviations AC, adenylyl cyclase ATP, adenosine triphosphate cAMP, cyclic adenosine monophosphate CRE, cAMP-responsive element DAG, diacylglycerol Epac, exchange proteins activated by cAMP GRK, G protein-coupled receptor kinase IP3, inositol 1,4,5-triphosphate NFAT, nuclear factor of activated T-cells PIP2, phosphatidylinositol-4,5-bisphosphate PKA, protein kinase A PKC, protein kinase C PLC-p, phospholipase C-p.

Fig. 16.6 Prosthetic gene networks. (A) Selfsufficient synthetic circuit to control blood-urate homeostasis. (B) Obesity treatment. (C) Diabetic ketoacidosis treatment (D) Artificial insemination. cAMP, cyclic adenosine monophosphate CREBl, cAMP-responsive element binding protein 1 KRAB, Kriippel associated box LHR, luteinizing hormone receptor TtgR-specific operator promoter activated by CREBl human cytomegalovirus promoter hEFia elongation factor 1 alpha promoter, P, simian virus 40 promoter PPARa, human...

Quantitatively, the binding of Ca2+ to the glycocalyx is of secondary importance compared to that bound by phospholipid elements. The glycocalyx does play a significant role in the determination of myocardial cell Ca2+ permeability (20, 21). Upon arrival of the appropriate electrical stimulus T ction potential), Ca2+ crosses the sarcolemma and is the principal cation responsible for a current called the "slow inward current" (lsi) (3-2, 22, 23, 24). Calcium is conducted across the sarcolemma through channels or pores which are controlled by the phosphorylation of sarcolemmal and sarcotubular proteins. Cardiac sarcolemma and sarcoplasmic reticulum are phosphorylated by exogenous and endogenous cyclic adenosine 5 -5 - monophosphate (cAMP)-dependent protein kinases (25, ... 

Clem, B. F., Hudson, E. A., and Clark, B. J. (2005). Cyclic adenosine 3 ,5 -monophosphate (cAMP) enhances cAMP-responsive element binding (CREB) protein phosphorylation and phospho-CREB interaction with the mouse steroidogenic acute regulatory protein gene promoter. Endocrinology 3, 1348-1356. 

Rozman, D., M. Fink, G.M. Fimia, P. Sassone-Corsi, and M.R. Waterman (1999). Cyclic adenosine 3, 5 -monophosphate(cAMP)/ cAMP-responsive element modulator (CREM)-depend-ent regulation of cholesterogenic lanosterol 14a-demethylase (CYP51) in spermatids. Mol. Endocrinol. 13, 1951-1962. 

Basic-leucine zipper Cyclic AMP, or 3 -5Lcyclic adenosine monophosphate CRE cAMP-responsive element... 

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