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1 MCH with high affinity, and signals through Gq protein.
2 tors are also coupled to phospholipase C via Gq proteins.
3 o receptors to couple to the Gs, Gi, Go, and Gq proteins.
4 ly of G proteins; some forms can also act on Gq proteins.
7 orresponding to the C-terminal domain of the Gq protein alpha subunit (Galphaq-Ct peptide) and charac
8 f severe cardiomyopathy, which overexpresses Gq protein and hematopoietic progenitor kinase-/germinal
9 nic M3 receptors, which couple to endogenous Gq protein and mediate a stimulatory effect of carbachol
11 ogenous agonists, which causes activation of Gq proteins and phospholipase C, and generation of inosi
12 meabilized cells, contraction was blocked by Gq-protein antibodies, but not by other G-protein antibo
14 tion, alpha1B-adrenergic receptors couple to Gq proteins, calcium signaling and protein kinase C acti
17 ndent mechanism may provide the link between Gq protein-coupled CCK receptor stimulation and Ras acti
19 FAP-hM3Dq mice) that expresses an engineered Gq protein-coupled receptor (Gq-GPCR) known as hM3Dq DRE
25 lular mechanisms that require the following: Gq-protein-coupled 5-HT2 receptor activation, new BDNF s
26 ooth muscle cell (VSMC) growth by activating Gq-protein-coupled AT1 receptors, which leads to elevati
29 ansmitters, autacoids, or hormones acting on Gq-protein-coupled receptors may serve as physiological
32 onformational states of the CCK2R activating Gq-protein-dependent pathway (CCK2R(G)) or recruiting be
34 yze this effect anatomically, we manipulated Gq-protein-dependent signaling selectively in neurons be
35 e precise impact and underlying mechanism of Gq-protein-dependent signals remain poorly understood.
37 ecular mechanism and functional relevance of Gq-protein-driven signals in striatal circuits under nor
38 ecular mechanism and functional relevance of Gq-protein-driven signals in striatal circuits under nor
39 fluoxetine can stimulate egg laying via the Gq protein EGL-30, independent of SER-1, SER-4, or 5HT.
40 lly, we find that the presence of noncognate Gq protein enhances cAMP stimulated by two Gs-coupled re
42 use FR to investigate whether inhibition of Gq proteins is an effective post-receptor strategy to ta
45 ng in the NTS depresses the baroreflex via a Gq protein-mediated activation of phospholipase C, which
47 ology, we found that sustained activation of Gq-protein signaling impairs the functionality of striat
49 triatal circuits can be "turned on" by acute Gq-protein signaling or "turned off" by sustained Gq-pro
53 IL3), bound NKB but impaired dissociation of Gq-protein subunits from the receptor compared with WT N
54 3-acetylcholine (M3-ACh) receptor as well as Gq-protein subunits with high spatiotemporal resolution
55 he receptor predominantly interacts with the Gq protein, thereby activating phospholipase C and incre
56 f full-length receptors, whereas coupling of Gq protein was abolished in the T310 truncated mutant de
57 ino acid residues, respectively, couple with Gq protein with an efficiency similar to that of full-le
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