This is the first report characterizing a functional role of DGKζ in the in vivo mouse heart. Molecular, gravimetric, and morphological analyses clearly showed that cardiac-specific overexpression of DGKζ abrogated cardiac hypertrophy in response to GPCR agonists such as angiotensin II and phenylephrine by regulating the DAG-PKC signaling in transgenic mouse hearts.. DGKζ-TG mice were indistinguishable in appearance from WT mice, and no baseline cardiac effects were observed in physiological or histological analyses. In addition, we found that isolated cardiomyocyte function and in vivo cardiac function evaluated by echocardiography were normal in DGKζ-TG mice. Blood pressure and heart rate after subcutaneous infusion of angiotensin II and phenylephrine were not different among DGKζ-TG-High, DGKζ-TG-Low, and WT mice, indicating that the overexpression of DGKζ does not affect hemodynamic regulations in response to angiotensin II and phenylephrine. Consistent with previous works,2,3,31,32 ...
BioTek Application Notes, 05-Oct-18, Thapsigargin-induced Cellular Stress Response and Inhibition of Gq-dependent Calcium Signaling
The heart initially compensates for hypertension-mediated pressure overload by enhancing its contractile force and developing hypertrophy without dilation. Gq protein-coupled receptor pathways become activated and can depress function, leading to cardiac failure. Initial adaptation mechanisms to reduce cardiac damage during such stimulation remain largely unknown. Here we have shown that this initial adaptation requires regulator of G protein signaling 2 (RGS2). Mice lacking RGS2 had a normal basal cardiac phenotype, yet responded rapidly to pressure overload, with increased myocardial Gq signaling, marked cardiac hypertrophy and failure, and early mortality. Swimming exercise, which is not accompanied by Gq activation, induced a normal cardiac response, while Rgs2 deletion in Gαq-overexpressing hearts exacerbated hypertrophy and dilation. In vascular smooth muscle, RGS2 is activated by cGMP-dependent protein kinase (PKG), suppressing Gq-stimulated vascular contraction. In normal mice, but not ...
Importantly, this work underscores the significance of ERK-dependent signaling in TAA development in MFS. ERK-dependent signaling has been demonstrated previously to contribute to aortic dilation in MFS (18, 20). ANG stimulates ERK1/2 activation via the AT1aR and both Gq proteins as well as βarr2. ERK activated via these different transducers is both spatially and temporally distinct (3) with unique functional outcomes (22, 34). Whereas βarr2-dependent ERK activation appears to lead to TGF-β-independent, proaneurysmal signaling, ANG-stimulated activation of TGF-β signaling has been reported previously to involve Gq proteins (35). Interestingly, G protein- and βarr2-dependent ERK1/2 activation has been shown to require EGFR transactivation in VSMC (21), suggesting the EGFR could serve as a mediator of AT1aR-mediated pathogenic signaling in MFS. This hypothesis is supported by our preliminary work demonstrating a reduction in aortic dilation in FbnC1039G/+ mice treated with the EGFR inhibitor ...
The new compound relieves these spasms - and is supposedly more effective and has a more prolonged action than the most common asthma drug salbutamol.. "However, we have so far only tested the substance in asthmatic mice," explained junior professor Daniela Wenzel. Wenzel is doing research in respiratory diseases at the Institute of Physiology I at the University of Bonn; she was the leader of the study.. The idea to test FR900359 came from the Institute of Pharmaceutical Biology. There, the scientists managed to isolate and characterize the active pharmaceutical substance from the leaves of the coralberry.. "This compound inhibits critical signaling molecules in our cells, the Gq proteins," explained Wenzel. Gq proteins exert key functions in many processes in the body - including control of the airway tone.. Normally, interaction of various signaling pathways induces narrowing of the airways. Inhibition of individual signaling pathways can reduce the contraction of the respiratory tract. ...
In cardiac fibroblasts and MEFs, our data indicate that the α1ARs make the primary contribution to ERK activation, supporting the dominant roles of these receptor subtypes in cardiac remodeling.34 Consistent with previous studies,35 stimulation of the α1ARs with Phe induces the classic Gq-dependent activation of PLC and PKC, leading to ERK activation through Raf-MEK1 kinase cascade. Under this signaling cascade, activated ERK translocates to the nucleus.35 Interestingly, this scenario is completely reshaped when β2ARs are coactivated with the α1AR on Epi stimulation. Coactivation of the α1 and β2ARs leads to sequestration of phospho-ERK within the cytosol. Under Epi stimulation, it was possible that two pools of ERK existed; a transient pool activated by the β2AR and a prolonged pool activated by the α1AR. The first pool becomes dominant simply because β2ARs are more prominent in cardiac tissues than α1ARs. This explanation is unlikely for several reasons. First, α1AR antagonist ...
Upon ligand binding, the Gs-coupled GPCR receptor activates adenylyl cyclase that in turn produces cAMP, governing important cellular responses. Gi-coupled GPCR receptors, however, inhibit adenylyl cyclase and cAMP production. The phosphatidylinositol pathway, on the other hand, is triggered by the Gq-coupled receptors. In Gq-coupled signaling, DAG and intracellular calcium act as second messengers, ultimately influencing cell functions." ...
Upon ligand binding, the Gs-coupled GPCR receptor activates adenylyl cyclase that in turn produces cAMP, governing important cellular responses. Gi-coupled GPCR receptors, however, inhibit adenylyl cyclase and cAMP production. The phosphatidylinositol pathway, on the other hand, is triggered by the Gq-coupled receptors. In Gq-coupled signaling, DAG and intracellular calcium act as second messengers, ultimately influencing cell functions." ...
A 15-residue peptide corresponding to the C-terminal domain of the Gq protein alpha subunit (Gaq-Ct peptide) was synthesized and characterized using NMR spectroscopic studies ...
In two papers in this issue (see Falkenburger et al. [Kinetics of M1 muscarinic receptor…] and Falkenburger et al. [Kinetics of PIP2 metabolism…]), the authors used all of the above-listed advances and performed a systematic analysis of the signal transmission process starting with M1 muscarinic receptors and mediated via Gq proteins to activation of PLCβ1 yielding to PtdIns(4,5)P2 hydrolysis and altered KCNQ channel activity. In a previous paper (Jensen et al., 2009), the authors measured the kinetic parameters of M1R activation, Gq conformational transition, PLC activation, PtdIns(4,5)P2 hydrolysis, and M current suppression after the application of 10 µM of the muscarinic agonist, oxotremorin, using the FRET approach for the individual steps outlined above. These studies measured activation and recovery rates (after removal of the stimulus) for each of the steps in this series of reactions and concluded that the rate-limiting step was the hydrolysis of PtdIns(4,5)P2 in the membrane. ...
Total synthesis and structure-activity relationship studies of cyclic depsipeptide YM-254890, as selective inhibitors of Gq proteins
The current studies provide evidence that TrpC4α, but not the closely related TrpC4β, is involved in pathways downstream of PLCβ1b and contributes to cellular hypertrophic responses. PLCβ1b is an immediate effector of signaling responses downstream of Gq-coupled receptors and is required for Gq-initiated cardiomyocyte hypertrophy (Filtz et al., 2009). PLCβ1b expression and activity are elevated in diseased myocardium from humans, rats, mice, and sheep, and, furthermore, activity increases with disease progression (Woodcock et al., 2009). Thus, PLCβ1b and its downstream effectors, including TrpC4α, may contribute to disease. TrpC4α differs from the other splice variant, TrpC4β, only in the inclusion of an 84-amino-acid sequence located close to, but not at, the extreme C-terminal end of the protein (Fig. 2A). Despite the apparently small sequence difference between the two splice variants, we found that TrpC4α, but not TrpC4β, associated with both PLCβ1b and Shank3 (Fig. 2) and ...
β-Arrestins are ubiquitously expressed and function in the activation of GPCRs, desensitization of most 7-transmembrane receptors, and regulation of other signaling molecules such as protein kinases. For GPCRs, ligand-induced β-arrestin recruitment activates signaling cascades independent of G-protein signaling to provide a non-amplified signal which is ideal for antagonist mode screening, studying ligand pharmacologies, and deorphanizing GPCRs. With decades of experience and hundreds of customer publications, DiscoverX provides a complete set of tools to analyze β-arrestin biology. The PathHunter β-arrestin assays and reagents offer a powerful and universal screening and profiling platform that can be used for virtually any Gi-, Gs-, or Gq-coupled receptor ...
The KiSS1-derived peptide receptor (also known as GPR54 or the Kisspeptin receptor) is a Gq-coupled receptor which binds the peptide hormone kisspeptin (metastin).
We are interested in learning how small molecules in the blood stream can cause cells to react in specific ways, such as growing, dividing or migrating. While there are many agents that can stimulate or inhibit cell behavior, we are most interested in the ability of certain hormones and neurotransmitters to activate a family of proteins called "G Proteins". G proteins can simulate an enzyme called phospholipase Cbeta (PLCbeta). Activation of PLCbeta raises the level of calcium in the cell, which changes the activity of many other proteins. Additionally, PLCbeta can also affect the ability of a cell to control the transcription of specific genes into proteins by changing the stability of their messenger RNA. ...
Genomes and Genes, Scientific Experts, Publications, Species, Research Topics, Research Grants about gq g11 gtp binding protein alpha subunits
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Previously we used mass spectrometry to show that the yeast G protein alpha subunit Gpa1 is ubiquitinated at Lys-165, located within a subdomain not present in other G alpha proteins (Marotti, L. A., Jr., Newitt, R., Wang, Y., Aebersold, R., and Dohlman, H. G. (2002) Biochemistry 41, 5067-5074). Here we describe the functional role of Gpa1 ubiquitination. We find that Gpa1 expression is elevated in mutants deficient in either proteasomal or vacuolar protease function. Vacuolar protease pep4 mutants accumulate monoubiquitinated Gpa1, and much of the protein is localized within the vacuolar compartment. In contrast, proteasome-defective rpt6/cim3 mutants accumulate polyubiquitinated Gpa1, and in this case the protein exhibits cytoplasmic localization. Cells that lack Ubp12 ubiquitin-processing protease activity accumulate both mono- and polyubiquitinated forms of Gpa1. In this case, Gpa1 accumulates in both the cytoplasm and vacuole. Finally, a Gpa1 mutant that lacks the ubiquitinated subdomain remains
G protein alpha S兔多克隆抗体(ab97629)可与人样本反应并经WB实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
There are no specific protocols for Recombinant Rat G protein alpha (mutated Q212 L + D280 N) (ab90410). Please download our general protocols booklet
PAR1 agonist-induced Gq but not Gi signaling is impaired in NCI-H28 cells.A, thrombin-induced intracellular Ca2+ mobilization in HMEC-1, Met-5A, and NCI-H28 cel
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alpha(1B)-Adrenergic receptors mediate many of the actions of the natural catecholamines, adrenaline and noradrenaline. They belong to the seven transmembrane domains G protein-coupled receptor superfamily and exert their actions mainly through activation of Gq proteins and phosphoinositide turnover/calcium signaling. Many hormones and neurotransmitters are capable of inducing alpha(1B)-adrenergic receptor phosphorylation and desensitization; among them: adrenaline and noradrenaline, phorbol esters, endothelin-I, bradykinin, lysophosphatidic acid, insulin, EGF, PDGF, IGF-I, TGF-beta, and estrogens. Key protein kinases for these effects are G protein coupled receptor kinases and protein kinase C. The lipid/protein kinase, phosphoinositide-3 kinase also appears to play a key role, acting upstream of protein kinase C. In addition to the agents employed for cells stimulation, we observed that paracrine/autocrine mediators also participate; these processes include EGF transactivation and ...
Bee stings or other allergens can cause anaphylactic shock in severely allergic individuals by triggering mast cell activation and the release of anaphylactic mediators like histamine and platelet activating factor (PAF). At high enough levels, these mediators cause blood pressure to drop precipitously and vessels to leak, eventually leading to shock. Although much is known about causes and consequences of anaphylaxis, the precise pathogenic pathways remain murky. Here, investigators find that shock was sidestepped in mice whose endothelia lacked the G protein go-betweens Gq/G11.. Many anaphylactic mediators act through G protein-coupled receptors, which link to downstream signaling molecules via G proteins, including Gq/G11, G12/G13, and Gi. Here, Gq/G11 turned out to be vital for opening the endothelial barrier and activating endothelial cells during an allergic reaction. Without Gq/G11, there was no phosphorylation of myosin light chain, which allows endothelial cells to retract from one ...
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Regulator of G protein signaling (RGS) proteins accelerate GTP hydrolysis by Gα subunits and thus facilitate termination of signaling initiated by G protein-coupled receptors (GPCRs). RGS proteins hold great promise as disease intervention points, given their signature role as negative regulators of GPCRs-receptors to which the largest fraction of approved medications are currently directed. RGS proteins share a hallmark RGS domain that interacts most avidly with Gα when in its transition state for GTP hydrolysis; by binding and stabilizing switch regions I and II of Gα, RGS domain binding consequently accelerates Gα-mediated GTP hydrolysis. The human genome encodes more than three dozen RGS domain-containing proteins with varied Gα substrate specificities. To facilitate their exploitation as drug-discovery targets, we have taken a systematic structural biology approach toward cataloging the structural diversity present among RGS domains and identifying molecular determinants of their ...
Neurotensin receptors respond to the endogenous tridecapeptide neurotensin. There are two different Neurotensin Receptors, NTSR1 and NTSR2
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Heart failure (HF) has been described as the inability of the myocardium to deliver oxygen and nutrients to a degree commensurate with the metabolic requirements of the body.1 Myocardial dysfunction induces compensatory neurohumoral mechanisms, including the sympathetic nervous system (SNS), as an attempt to preserve contractile performance. Mediators of the SNS consist predominantly of 2 catecholamines, namely epinephrine and norepinephrine (NE), released by cardiac sympathetic nerve terminals or secreted directly into the circulation by the adrenal medulla. Effects of these neurotransmitters are mediated through cell surface adrenergic receptors (ARs), members of the G protein-coupled receptor superfamily. Stimulation of the β-AR promotes a conformational change to activate the heterotrimeric G protein Gα and Gβγ subunits, promoting positive inotropic and chronotropic effects culminating in improved myocardial function.2. Article, see p 1116. This functionally beneficial pathway refers ...
Regulator of G protein signaling (RGS) family members are regulatory molecules that act as GTPase activating proteins (GAPs) for G alpha subunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Gi alpha, Go alpha and Gq alpha subtypes. They drive G proteins into their inactive GDP-bound forms. Regulator of G protein signaling 4 belongs to this family. All RGS proteins share a conserved 120-amino acid sequence termed the RGS domain. Regulator of G protein signaling 4 protein is 37% identical to RGS1 and 97% identical to rat Rgs4. This protein negatively regulate signaling upstream or at the level of the heterotrimeric G protein and is localized in the cytoplasm. Alternatively spliced transcript variants have been found for this gene ...
G protein G(alpha)o is essential for vomeronasal function and aggressive behavior in mice.s profile, publications, research topics, and co-authors
C. elegans strains are listed in the order in which they appear in the figures first and then in tables. The following strains were used: Figures: RJP133 (Is[tph-1prom::gfp]; RJP1325 dpy-18(ok162); Is[tph-1prom::gfp]); RJP1472 (phy-2(ok802); Is[tph-1prom::gfp]); RJP154 (phy-3(ok199); Is[tph-1prom::gfp]); RJP1473 (phy-4(tm3539); Is[tph-1prom::gfp]); RJP1272 (dpy-18(ok162); Is[sra-6prom::gfp]); RJP1231 (dpy-18(ok162); Is[odr-2prom::CFP::sra-6prom::DsRed2]); RJP1476 (dpy-18(ok162); Is[flp-1prom::gfp]); RJP882 (rpEx442 Ex[dpy-18prom::gfp]); RJP6 (rpEx1 Ex[WRM0614bC10]; dpy-18(ok162); Is[tph-1prom::gfp]); RJP7 (rpEx2 Ex[WRM0614bC10]; dpy-18(ok162); Is[tph-1prom::gfp]); RJP8 (rpEx3 Ex[WRM0614bC10]; dpy-18(ok162); Is[tph-1prom::gfp]); RJP217 (rpEx59 Ex[dpy-7prom::dpy-18 cDNA]; dpy-18(ok162); Is[tph-1prom::gfp]); RJP218 (rpEx60 Ex[dpy-7prom::dpy-18 cDNA]; dpy-18(ok162); Is[tph-1prom::gfp]); RJP433 (rpEx188 Ex[dpy-7prom::dpy-18 cDNA]; dpy-18(ok162); Is[tph-1prom::gfp]); RJP442 (rpEx193 ...
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Summary is not available for the mouse gene. This summary is for the human ortholog.] Regulator of G protein signaling (RGS) family members are regulatory molecules that act as GTPase activating proteins (GAPs) for G alpha subunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Gi alpha, Go alpha and Gq alpha subtypes. They drive G proteins into their inactive GDP-bound forms. Regulator of G protein signaling 4 belongs to this family. All RGS proteins share a conserved 120-amino acid sequence termed the RGS domain. Regulator of G protein signaling 4 protein is 37% identical to RGS1 and 97% identical to rat Rgs4. This protein negatively regulate signaling upstream or at the level of the heterotrimeric G protein and is localized in the cytoplasm. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2008 ...
Ric-8A and Ric-8B are positive regulators of heterotrimeric G protein a subunit function. We have recently defined the cellular action of Ric-8 proteins towards...
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