Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

CAMP cyclic adenosine

A/J A Jackson inbred mouse strain ALP Anti-leukoprotease ALS Amyotrophic lateral sclerosis cAMP Cyclic adenosine monophosphate also known as adenosine 3, 5 -phosphate AM Alveolar macrophage AML Acute myelogenous leukaemia AMP Adenosine monophosphate AMVN 2,2 -azobis (2,4-dimethylvaleronitrile)... [Pg.279]

CAH Chronic active hepatitis CALLA Common lymphoblastic leukaemia antigen CALX Conjunctival associated lymphoid tissue CaM Calmodulin cAMP Cyclic adenosine monophosphate also knomt as adenosine 3, 5 -phosphate CAM CeU adhesion molecule CAP57 Cationic protein from neutrophils CAT Catalase CatG Cathepsin G... [Pg.280]

Gs Noradrenaline and fi2 Dopamine Di and D5 Histamine H2 Serotonin 5-HT4 Stimulates adenylate cyclase increasing the concentration of cAMP (cyclic-adenosine-3, 5 -monophosphate)... [Pg.23]

Fig. 3. Mechanisms of vasocontraction and vasorelaxation in endothelial and smooth muscle cells. COX cyclooxygenase, eNOS endothelial nitric oxide synthase, HO-1 heme oxygenase-1, EET epoxyeicosatrienoic acid, EDHF endothelium-derived hyperpolariz-ing factor, PGI2 prostaglandin I2, NO nitric oxide, CO carbon monoxide, PLC phospholipase C, IP3 inositol 1,4,5-trisphosphate, DAG diacylglycerol, ER/SR endo-plasmic/sarcoplasmic reticulum, AC adenylyl cyclase, cAMP cyclic adenosine monophosphate, sGC soluble guanylyl cyclase, cGMP cyclic guanosine monophosphate. Fig. 3. Mechanisms of vasocontraction and vasorelaxation in endothelial and smooth muscle cells. COX cyclooxygenase, eNOS endothelial nitric oxide synthase, HO-1 heme oxygenase-1, EET epoxyeicosatrienoic acid, EDHF endothelium-derived hyperpolariz-ing factor, PGI2 prostaglandin I2, NO nitric oxide, CO carbon monoxide, PLC phospholipase C, IP3 inositol 1,4,5-trisphosphate, DAG diacylglycerol, ER/SR endo-plasmic/sarcoplasmic reticulum, AC adenylyl cyclase, cAMP cyclic adenosine monophosphate, sGC soluble guanylyl cyclase, cGMP cyclic guanosine monophosphate.
Figure 8-1. Hormonal regulation of fat metabolism. A Control of fatty acid synthesis by reversible phosphorylation of acetyl CoA carboxylase. B Regulation of tri-acylglycerol degradation by reversible phosphorylation of hormone-sensitive lipase. cAMP, cyclic adenosine monophosphate HS, hormone-sensitive. Figure 8-1. Hormonal regulation of fat metabolism. A Control of fatty acid synthesis by reversible phosphorylation of acetyl CoA carboxylase. B Regulation of tri-acylglycerol degradation by reversible phosphorylation of hormone-sensitive lipase. cAMP, cyclic adenosine monophosphate HS, hormone-sensitive.
Figure 8-6. Hormonal regulation of cholesterol synthesis by reversible phosphorylation of HMG CoA reductase. Availability of mevalonic acid as the fundamental building block of the sterol ring system controls flux through the pathway that follows. cAMP, cyclic adenosine monophosphate HMG CoA, hydroxymethylglutary I CoA. Figure 8-6. Hormonal regulation of cholesterol synthesis by reversible phosphorylation of HMG CoA reductase. Availability of mevalonic acid as the fundamental building block of the sterol ring system controls flux through the pathway that follows. cAMP, cyclic adenosine monophosphate HMG CoA, hydroxymethylglutary I CoA.
Note. cAMP = cyclic adenosine monophosphate MHPG phenylglycol. [Pg.29]

Abbreviations INR, international normalized ratio cAMP, cyclic adenosine monophosphate. [Pg.117]

Figure 1.10 Model of a G protein-coupled receptor with 7 membrane-spanning domains. Binding of an agonist to the receptor causes GDP to exchange with GTP. The a-GTP complex then dissociates from the receptor and the py complex and interacts with intercellular en mes or ion channels. The Py complex can activate an ion channel or possibly also interact with intercellular enzymes. GDP, guanine diphosphate GTP, guanine triphosphate cAMP, cyclic adenosine monophosphate PKC, protein kinase C PLC, phospholipase C DAG, diacylglycerol. Figure 1.10 Model of a G protein-coupled receptor with 7 membrane-spanning domains. Binding of an agonist to the receptor causes GDP to exchange with GTP. The a-GTP complex then dissociates from the receptor and the py complex and interacts with intercellular en mes or ion channels. The Py complex can activate an ion channel or possibly also interact with intercellular enzymes. GDP, guanine diphosphate GTP, guanine triphosphate cAMP, cyclic adenosine monophosphate PKC, protein kinase C PLC, phospholipase C DAG, diacylglycerol.
ACPD, fra/7S-l-amino-cyclopentyl-l,3-dicarboxylate AMPA, DL-tt-amino-3-hydroxy-5-methylisoxazole-4-propionate cAMP, cyclic adenosine monophosphate CQNX, 6-cyano-7-nitroquinoxaline-2,3-dione DAG, diacylglycerol IP3, inositol trisphosphate LSD, lysergic acid diethylamide MCPG, a-methyl-4-carboxyphenylglycine. [Pg.461]

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. 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...
FIGURE 52.5 The actions of glipizide. ATP = adenosine triphosphate ADP = adenosine diphosphate cAMP = cyclic adenosine monophosphate. [Pg.506]

Mechanisms of action of dipyridamole. Abbreviations ADR adenosine diphosphate AMP, adenosine monophosphate cAMP, cyclic adenosine monophosphate cGMR guanosine cyclic monophosphate NO, nitric oxide. [Pg.71]

Mechanisms of action of cilostazol. Abbreviations cAMP, cyclic adenosine monophosphate cGMP, guanosine cyclic monophosphate HGF, hepatocyte growth factor MCP-I, monocyte chemoattractant protein-1 NO, nitric oxide. [Pg.73]

When the odorant binds to the odorant receptor it changes the receptor structure and activates an olfactory protein called a G protein. This in turn converts ATP (adenosine triphosphate) to cAMP (cyclic adenosine monophosphate) that allows opening of ion channels, causing the receptor to become depolarized. Depolarization is an electrical change that triggers a nerve impulse. Impulses from the nasal receptors are sent along the olfactory nerve to the brain. [Pg.111]

Adenylate cyclase is considered as a second messenger that catalyzes the formation of cAMP (cyclic adenosine monophosphate) from ATP this results in alterations in intracellular cAMP levels that change the activity of certain enzymes—that is, enzymes that ultimately mediate many of the changes caused by the neurotransmitter. For example, there are protein kinases in the brain whose activity is dependent upon these cyclic nucleotides the presence or absence of cAMP alters the rate at which these kinases phosphorylate other proteins (using ATP as substrate). The phosphorylated products of these protein kinases are enzymes whose activity to effect certain reactions is thereby altered. One example of a reaction that is altered is the transport of cations (e.g., Na+, K+) by the enzyme adenosine triphosphatase (ATPase). [Pg.366]


See other pages where CAMP cyclic adenosine is mentioned: [Pg.473]    [Pg.909]    [Pg.434]    [Pg.60]    [Pg.243]    [Pg.789]    [Pg.504]    [Pg.245]    [Pg.168]    [Pg.307]    [Pg.368]    [Pg.194]    [Pg.88]    [Pg.113]    [Pg.215]    [Pg.1371]    [Pg.223]    [Pg.44]    [Pg.212]    [Pg.109]    [Pg.598]    [Pg.637]    [Pg.166]    [Pg.82]    [Pg.170]    [Pg.343]    [Pg.605]    [Pg.444]    [Pg.413]    [Pg.106]    [Pg.473]    [Pg.909]   


SEARCH



CAMP

CAMP (cyclic adenosine monophosphate action

CAMP—See Cyclic adenosine

CAMP—See Cyclic adenosine monophosphate

Calcium/cyclic adenosine monophosphate cAMP)

Cyclic adenosine

Cyclic adenosine monophosphate cAMP response element binding protein

Cyclic adenosine monophosphate cAMP)

Cyclic adenosine monophosphate cAMP)-stimulated acid secretion

© 2024 chempedia.info