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Pertussis Toxin Pathway

Functionally, the Dl-like receptors (Dl, D5) are coupled to the G protein Gas and thus can stimulate adenylyl cyclase. The D2-like receptors (D2, D3, and D4) couple to pertussis toxin sensitive G proteins (Gai/0), and consequently inhibit adenylyl cyclase activity. While the Dl-like receptors almost exclusively signal through Gas-mediated activation of adenylyl cyclase, the D2-like receptors have been reported to modulate the activity of a plethora of signaling molecules and pathways. Many of these actions are mediated through the G(3y subunit. Some of these molecules and pathways include the calcium channels, potassium channels, sodium-hydrogen exchanger, arachidonic acid release, and mitogen-activated protein kinase pathways. [Pg.440]

Secondly, treatment of neutrophils with pertussis toxin, which ADP-ribosylates a neutrophil G protein and causes a loss of cell responsiveness via receptor-mediated pathways (40,41), has minimal effect on the response to HCH (Figure 11, lower panel). Thus it can be concluded that HCH activation of neutrophils is independent of receptor-mediated activation of G proteins. [Pg.39]

Number of papers to date have shown that the CXCR4 receptors expressed in both neuronal and glial cells are functional and coupled to multiple intracellular pathways (Lazarini et al. 2003). The CXCR4 through pertussis toxin (PTX)- sensitive G proteins is coupled to at least two distinct signaling pathways (1) the first pathway, involving the activation of phosphatidylinositol- 3 (PI-3) kinase and extracellular signal... [Pg.273]

Activation of neutrophils with PAF occurs through a G-protein-linked receptor, and the subsequent transmembrane signalling involves the stimulation of inositol phosphate metabolism. Within 30 s of addition of PAF (0.01-100 nM), intracellular Ca2+ levels increase and Ca2+ transport from the external medium is enhanced. It seems that phospholipase C-dependent and -independent activation pathways are involved in Ca2+ mobilisation. This indirectly suggests that two receptors may be involved in PAF activation. The first of these is pertussis-toxin-insensitive and may be linked to a... [Pg.87]

Sillard, R., Harii, K. and Takuwa, Y., 1999, The novel sphingosine 1-phosphate receptor AGR16 is coupled via pertussis toxin-sensitive and -insensitive G-proteins to multiple signaling pathways. Biochem. J. 337 67-75. [Pg.262]

This reaction is reversible when conducted in vitro, but under the conditions of pH and nicotinamide concentration that exist in the cell, it is irreversible. Thus, diphtheria toxin kills cells by irreversibly destroying the ability of EF-2 to participate in the translocation step of protein synthesis elongation. A number of other protein toxins have subsequently been found to ADP-ribosylate and inactivate cellular proteins involved in other essential cellular pathways. For example, cholera and pertussis toxins ADP-ribosylate and inactivate proteins important to cAMP metabolism. [Pg.752]

Beaumont V, Zucker RS (2000) Enhancement of synaptic transmission by cyclic AMP modulation of presynaptic Ih channels. Nat Neurosci 3 133 41 Beech DJ, Bernheim L, Hille B (1992) Pertussis toxin and voltage dependence distinguish multiple pathways modulating calcium channels of rat sympathetic neurons. Neuron 8 97-106 Benfenati F, Bahler M, Jahn R et al (1989a) Interactions of synapsin I with small synaptic vesicles distinct sites in synapsin I bind to vesicle phospholipids and vesicle proteins. J Cell Biol 108 1863-72... [Pg.243]

Presynaptic H3 receptors also are uniform in their signal transduction. They couple to Gi/o proteins and decrease the depolarization-induced release of neurotransmitters by inhibiting multiple calcium channels (e.g., Arrang et al. 1985 Schlicker et al. 1994 Endou et al. 1994 Brown and Haas 1999 see Stark et al. 2004). For comparison, the signal transduction of soma-dendritic H3 autoreceptors in histamin-ergic neurons also involves a pertussis toxin-sensitive G-protein with subsequent inhibition of N- and P-type Ca2+ channels (Takeshita et al. 1998). The few exceptions to this signal transduction pathway are discussed in the corresponding subsections below (see Sections 3.1, 3.3, and 3.9). [Pg.306]

In the calyx of Held synapse in the auditory brainstem of rats the 5-HTib receptor inhibition of glutamate release was fully explained by inhibition of Ca2+ entry through voltage-dependent channels (Mizutani et al. 2006). In rat nucleus accumbens, in contrast, the analogous 5-HTib effect did not involve inhibition of Ca2+ channels (Muramatsu et al. 1998). In rat amygdala, the 5-HTia inhibition operated via a cyclic AMP pathway and apparently inhibition of Ca2+ entry an unexplained observation was the failure of pertussis toxin to abolish the 5-HTia inhibition (Cheng et al. 1998). [Pg.322]

Like the other 5-Hrl receptors, the major signaling pathway of the 5-HT1D receptor is to the inhibition of AC through pertussis toxin-sensitive G proteins in the substantia nigra (153), in MDCK cells (154), and in transfected C6 glioma and NIH-3T3 fibroblast cells (116,134,155,156). [Pg.158]

Abdel-Baset H, Bozovic V, Szyf M, Albert PR. Conditional transformation mediated via a pertussis toxin-sensitive receptor signalling pathway. Mol Endocrinol 1992 6 730-740. [Pg.183]


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See also in sourсe #XX -- [ Pg.297 ]




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