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Stimulation signals

A platelet-activating-factor-stimulated signal-transduction pathway is a major component of the kainic-acid-induced cyclooxygenase-2 expression in hippocampus 584... [Pg.575]

Chatterjee, S., 1994, Neutral sphingomyehnase achon stimulates signal transduction of tumor necrosis factor-alpha in the synthesis of cholesteryl esters in human fibroblasts. /. Biol. Chem. 269 879-882... [Pg.241]

Fig. 7.21. Activation of glycogen-bound protein phosphatase I by insulin. Insulin has a stimulating effect on glycogen synthesis by initiating the dephosphorylation and activation of glycogen synthase and the dephosphorylation and inhibition of glycogen phosphorylase. Both enzymes (substrate S in the figure) are dephosphorylated by protein phosphatase PPIG. Insulin mediates the activation of a protein kinase (insulin-sensitive protein kinase) within an insulin-stimulated signal pathway, which phosphorylates and thus activates protein phosphatase PPIG at the PI site. Fig. 7.21. Activation of glycogen-bound protein phosphatase I by insulin. Insulin has a stimulating effect on glycogen synthesis by initiating the dephosphorylation and activation of glycogen synthase and the dephosphorylation and inhibition of glycogen phosphorylase. Both enzymes (substrate S in the figure) are dephosphorylated by protein phosphatase PPIG. Insulin mediates the activation of a protein kinase (insulin-sensitive protein kinase) within an insulin-stimulated signal pathway, which phosphorylates and thus activates protein phosphatase PPIG at the PI site.
Triethanolamine has been clinically tested with other model irritant compoimds for potency to stimulate signal release of proinflammatory mediators in hrnnan skin in order to find biomarkers of irritancy. Neat or aqueous triethanolamine was applied to the lower arm of 12 male volimteers after 24 h, suction blister fluid specimens were taken from the site of treated skin. Triethanolamine caused no significant increase in arachidonic acid and prostaglandin concentrations in suction blister fluid samples, in... [Pg.390]

E) The bound ATP is hydrolyzed to await the next stimulation signal. [Pg.224]

Pmax+ state of polarization when the stimulating signal reaches its maximum value - positive saturation... [Pg.59]

In all systems studied thus far, olfactory-stimulated signal transduction is mediated by G-protein-coupled receptor (GPCR) pathways involving the synthesis of second messengers such as cyclic AMP (cAMP) and/or inositol 1,4,5-triphosphate (IP3) (Boekhoff et al., 1994 Reed, 1992). Moreover, several proteins that are involved in fundamental aspects of olfactory signal transduction have... [Pg.372]

Imaging assays (DiscoveRx PathHunter, Bioimage) Can use recombinant green fluorescent or yellow fluorescent fusion proteins to measure kinase-stimulated signalling events such as protein translocation to nucleus or membrane to cytosolic translocations Biological assay can present kinase in native form examines functional consequences of test compound Difficult to develop lower throughput Nickischer (2006) Traskjr (2006)... [Pg.5]

Schlaepfer DD, Broome MA, Hunter T. Fibronectin-stimulated signaling from a focal adhesion kinase-c-Src complex involvement of the Grb2, pl30cas, and Nek adaptor proteins. Mol. Cell. [Pg.781]

Standstill It can be assumed that fibrogenesis will initially come to a standstill upon cessation of the causative factors or stimulating signals. When the extracellular matrix is only moderately increased, the lobular structure, the vascular supply and the bile flow from the periportal fields are undisturbed. A balance between the stimulation and inhibition of fibrogenesis can develop, stopping liver fibrosis at the point which has been reached. [Pg.404]

Activation of the chemokine receptor leads to rapid activation of phosphoinositide-spe-cific phospholipases, which leads to inositol-1,4,5-triphosphate formation and a transient rise in intracellular calcium (18). Phospholipase C (PLC) isoforms that are involved in chemokine receptor activation become activated by direct interaction with the J3y subunits. In addition to its interaction with PLCs, the j3y subunits also interact with the type phosphoinositol 3 kinase y (PISKy), and activation of this enzyme results in the formation of PtdIns(3,4,5)P3 (17). Mice that do not express PI3Ky have severely impaired chemo-kine-stimulated signal transduction, and PKB is not activated, suggesting an important role for this pathway in the chemotactic process (27-29). Although leukocytes isolated from these mice showed a decrease in cell chemo-taxis, the response is not completely lost, and under conditions of complete PI3Ky inhibition, neutrophils can still chemotax in response to chemokines (30). [Pg.134]

Jones CR, Aral T, Rapoport SI. Evidence for the involvement of docosahexaenoic acid in cholinergic stimulated signal transduction at the synapse. Neurochem Res 1997 22 663-670. [Pg.141]

Remarkably, the KSHV GPCR stimulates signalling pathways linked to cell proliferation in a constitutively active (agonist-independent) manner (Arvanitakis et al.,... [Pg.231]

Scheme 3. Structures of some of the components of the complex oviposition stimulant signal of Citrus unshiu. Narirutin [1], hesperidin [2], rutin [3], vicenin-2 [4], 5-hydroxy-A/ Scheme 3. Structures of some of the components of the complex oviposition stimulant signal of Citrus unshiu. Narirutin [1], hesperidin [2], rutin [3], vicenin-2 [4], 5-hydroxy-A/<j-methyltryptamine [5], adenosine [6], and MN-dimethylprolinium ion [7].
FIGURE 1A4-1 The cell biology of extracellular acidification. When a receptor is stimulated, signal transduction pathways are Induced. Adenosine triphosphate (ATP) consumption is then compensated by the increased uptake and metabolism of glucose, which results m an increase in the excretion of acid waste products. The extracellular acidification is measured by the LAPS. (From F. Hafner. Biosens. 8/betecfron., 2000. 15. 149. With permission.)... [Pg.758]

Warmka, J.K., et al.. Extracellular signal-regulated kinase transmits palytoxin-stimulated signals leading to altered gene expression on mouse keratinocytes, Toxicol Appl Pharmacol, 185, 8, 2002. [Pg.711]


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