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Signaling receptor-mediated transduction

B. Goldstein, Kinetic proofreading in receptor-mediated transduction of cellular signals receptor aggregation, partially activated receptors, and cytosolic messengers, Bull. Math. Biol. 2002, 64, 887-911. [Pg.1079]

Figure 1. Simplified schematic of receptor-mediated signal transduction in neutrophils. Binding of ligand to the receptor activates a guanine-nucleotide-binding protein (G protein), which then stimulates phospholipase C. Phosphatidylinositol 4,5-bis-phosphate is cleaved to produce diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3). DAG stimulates protein kinase C. IP3 causes the release of Ca from intracellular stores, which results in an increase in the cytosolic Ca concentration. This increase in Ca may stimulate protein kinase C, calmodulin-dependent protein kinases, and phospholipase A2. Protein phosphorylation events are thought to be important in stimulating degranulation and oxidant production. In addition, ionic fluxes occur across the plasma membrane. It is possible that phospholipase A2 and ionic channels may be governed by G protein interactions. ... Figure 1. Simplified schematic of receptor-mediated signal transduction in neutrophils. Binding of ligand to the receptor activates a guanine-nucleotide-binding protein (G protein), which then stimulates phospholipase C. Phosphatidylinositol 4,5-bis-phosphate is cleaved to produce diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3). DAG stimulates protein kinase C. IP3 causes the release of Ca from intracellular stores, which results in an increase in the cytosolic Ca concentration. This increase in Ca may stimulate protein kinase C, calmodulin-dependent protein kinases, and phospholipase A2. Protein phosphorylation events are thought to be important in stimulating degranulation and oxidant production. In addition, ionic fluxes occur across the plasma membrane. It is possible that phospholipase A2 and ionic channels may be governed by G protein interactions. ...
Felder CC, Briley EM, Axelrod J, Simpson JT, Mackie K, Devane WA. Anandamide, an endogenous cannabimimetic eicosanoid, binds to the cloned human cannabinoid receptor and stimulates receptor-mediated signal transduction. Proc Natl Acad Sci USA 1993 90 7656-7660. [Pg.150]

Developmental exposure to Pb or Mm affect signal transduction process, possibly related to the modulation of nitric oxide as well as alterations in receptor-mediated phosphoinositide hydrolysis and protein kinase C (rats)... [Pg.366]

Noradrenaline acts on three types of receptor. The ai receptors mediate the main excitatory effects of noradrenaline upon wake-active neurons in the dorsal raphe, basal forebrain, and elsewhere (Vandermaelen Aghajanian, 1983 Nicoll, 1988 Fort et al., 1995 Brown et al., 2002). The a2 receptors mediate inhibitory effects of noradrenaline, e.g. on noradrenaline neurons themselves and on cholinergic brainstem neurons (Williams et al., 1985 Williams Reiner, 1993). The (3-receptors modulate neurons in a more subtle fashion, increasing excitability via blockade of afterhyperpolarizations in hippocampal and cortical neurons (Haas Konnerth, 1983). Activation of (3-receptors also promotes synaptic plasticity via activation of the cyclic-AMP-dependent kinase (PKA) and cyclic AMP response element binding protein (CREB) signal transduction pathway (Stanton Sarvey, 1987 Cirelli et al., 1996). [Pg.34]

Geng, Y. et al., Effects of nicotine on the immune response. I. Chronic exposure to nicotine impairs antigen receptor-mediated signal transduction in lymphocytes, Toxicol. Appl. Pharmacol., 135, 268-287, 1995. [Pg.539]

Diveu C, Venereau E, Froger J, et al Molecular and functional characterization of a soluble form of oncostatin M/interleukin-31 shared receptor. J Biol Chem 2006 281 36673-36682. Stress C, Radtke S, Clahsen T, et al Oncostatin M receptor-mediated signal transduction is negatively regulated by SOCS3 through a receptor tyrosine-independent mechanism. J Biol Chem 2006 281 8458-8468. [Pg.91]

Rebois, R. V., and Hebert, T. E. (2003) Protein complexes involved in heptahelical receptor-mediated signal transduction. Receptors Channels. 9, 169-194. [Pg.100]

Smooth muscle effects. The opposing effects on smooth muscle (A) of a-and p-adrenoceptor activation are due to differences in signal transduction (p. 66). This is exemplified by vascular smooth muscle (A). ai-Receptor stimulation leads to intracellular release of Ca + via activation of the inositol tris-phosphate (IP3) pathway. In concert with the protein calmodulin, Ca + can activate myosin kinase, leading to a rise in tonus via phosphorylation of the contractile protein myosin. cAMP inhibits activation of myosin kinase. Via the former effector pathway, stimulation of a-receptors results in vasoconstriction via the latter, P2-receptors mediate vasodilation, particularly in skeletal muscle - an effect that has little therapeutic use. [Pg.84]

Dennler, S. et al. (2002). Transforming growth factor-/) signal transduction. J. Leukocyte Biol. 71(5), 731-740. Derynck, R. (1994). TGF-jS-receptor-mediated signalling. Trends Biochem. Sci. 19, 548-553. [Pg.301]

Figure 1. Schematic representations of significant biological functions displayed by host-guest complexation in homogeneous solutions or at membrane surfaces, (a) Separation (e.g., antibody-antigen complex formation), (b) Transformation (e.g., enzymatic reaction), (c) Translocation (e.g., carrier- or channel-mediated transport), (d) Transduction (e.g., receptor-mediated transmembrane signaling). Figure 1. Schematic representations of significant biological functions displayed by host-guest complexation in homogeneous solutions or at membrane surfaces, (a) Separation (e.g., antibody-antigen complex formation), (b) Transformation (e.g., enzymatic reaction), (c) Translocation (e.g., carrier- or channel-mediated transport), (d) Transduction (e.g., receptor-mediated transmembrane signaling).
Collaborative signaling integrin-mediated cell adhesion modulates signal transduction by other receptors (e.g., receptor tyrosine kinases). [Pg.373]


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See also in sourсe #XX -- [ Pg.219 , Pg.220 ]




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