CAMP-response element binding monophosphate

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. 

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.

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. 

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.

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, ... 

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