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anti-Mouse (Murine) GNAI1 Anticorps:
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Human Polyclonal GNAI1 Primary Antibody pour IHC, IHC (p) - ABIN441599
Matsumura, Kojidani, Kamioka, Uchida, Haraguchi, Kimura, Toyoshima: Interphase adhesion geometry is transmitted to an internal regulator for spindle orientation via caveolin-1. dans Nature communications 2016
Human Polyclonal GNAI1 Primary Antibody pour WB - ABIN4890045
Hurst, Henkel, Brown, Hooks: Endogenous RGS proteins attenuate Galpha(i)-mediated lysophosphatidic acid signaling pathways in ovarian cancer cells. dans Cellular signalling 2008
Human Polyclonal GNAI1 Primary Antibody pour ELISA, WB - ABIN561067
Sasaki, Yamasaki, Omotuyi, Mishina, Ueda: Age-dependent dystonia in striatal G?7 deficient mice is reversed by the dopamine D2 receptor agonist pramipexole. dans Journal of neurochemistry 2013
Human Polyclonal GNAI1 Primary Antibody pour IHC, IHC (p) - ABIN4312948
Ye, Vattai, Ditsch, Kuhn, Rahmeh, Mahner, Ripphahn, Immler, Sperandio, Jeschke, von Schönfeldt: Prostaglandin E2 receptor 3 signaling is induced in placentas with unexplained recurrent pregnancy losses. dans Endocrine connections 2018
This study presents an unexpected proinflammatory switch from Galphas to GalphaI glp1r signaling in burn monocytes which promotes ERK1/2 and NF-kappaB activation
Gnai1 function is impaired in the spinal cord of Ews/Ewsr1 KO mice
LGN and Galphai participate in a long-inferred signal that originates outside the bundle to model its staircase-like architecture, a property that is essential for direction sensitivity to mechanical deflection and hearing.
stimulation of GPR17 by the small molecule agonist MDL29,951 (2-carboxy-4,6-dichloro-1H-indole-3-propionic acid) decreases myelin basic protein expression levels mainly by triggering the Galphai/o signaling pathway.
Gnai1 missense mutation is responsible of hyperpigmentation in mouse model.
acidosis in inflamed tissues may be a decisive factor to regulate switching of PKA and PKCepsilon dependence via proton-sensing G-protein-coupled receptors.
Data show that guanine nucleotide-binding protein G(i) subunit alpha-1 and alpha-3 (Galphai1/3) can interact with CD14 antigen/Grb2-associated binding protein Gab1, which modulates macrophage polarization in vitro and in vivo.
By using mice deficient in individual Galphai/o G-protein subunits, authors demonstrate that Galphai1 and Galphai3 are the critical in vivo targets of ADP-ribosylation underlying vasoactive amine sensitization elicited by pertussis toxin exposure.
leucine can directly facilitate insulin signaling through a Galphai protein-dependent intracellular signaling pathway
Inactive Galpha(i1)-GDP enhances the affinity of RGS14 for H-Ras-GTP in live cells, resulting in a ternary signaling complex that is further regulated by G protein-coupled receptors.
Mice with mutations of Gnai1 or Gnai2 have neither fusions of ribs nor lumbar vertebrae, but loss of both Gnai3 and one of the other two genes increases the number and severity of rib fusions without affecting the lumbar fusions.
Results suggest a model in which the Gbetagamma dimer that is released as a result of the dissociation from Galpha(o) upon activation of mGluR6 closes the TRPM1 channel, perhaps via a direct interaction.
RGS14 can form complexes with GPCRs in cells that are dependent on Galpha(i/o) and these RGS14.Galpha(i1).GPCR complexes may be substrates for other signaling partners such as Ric-8A
The decrease in beta(2)-AR may account for additional relaxation impairment, given that there is no enhancement over nontransgenic after pertussis toxin, despite AC5 overexpression.
in osteoblasts CB2 targets a Gi protein-cyclin D1 mitogenic axis
Data show that mice lacking G(o2)alpha, but not those lacking alpha subunits of either G(o1) or any G(i) proteins, handle glucose loads more efficiently than wild-type (WT) mice.
Activation of the Rsg14-Galphai1-GDP signaling complex is regulated by Ric8.
analysis of a novel Gi, P2Y-independent signaling pathway mediating Akt phosphorylation in response to thrombin receptors
CKbeta8- and CKbeta8-1-induced activation of ERK1/2 is mediated by the G(i)/G(o) protein, PLC, and PKCdelta.
Gi-mediated signaling pathways are activated by G12/G13 and are sufficient to induce integrin alpha(IIb)beta3 activation
Interplay between negative and positive design elements in Galpha helical domains of G proteins determines interaction specificity toward RGS2.
Galphai1 mRNA and protein expression were significantly upregulated in human glioma tissues and correlates with Akt hyperactivation and microRNA-200a downregulation. Galphai1 is the primary target of microRNA-200a in mediating its anti-glioma cell activity.
using cryo-electron microscopy, it is shown that the major interactions between activated rhodopsin and Gi are mediated by the C-terminal helix of the Gi alpha-subunit, which is wedged into the cytoplasmic cavity of the transmembrane helix bundle and directly contacts the amino terminus of helix 8 of rhodopsin
3.5 A resolution cryo-electron microscopy structure of the mu-opioid receptor (muOR) bound to the agonist peptide DAMGO and nucleotide-free Gi; these results shed light on the structural features that contribute to the Gi protein-coupling specificity of the microOR
HL-60 neutrophil-like cells expressing Rap1a(G12V) or Radil have an elongated phenotype because of enhanced uropod adhesion as they attempt to migrate on fibronectin. This elongated phenotype driven by Rap1a(G12V) or Radil is reversed by Galphai1(Q204L), but not by WT Galphai1 expression, suggesting that Galphai-GTP also regulates adhesion in immune cells at the level of, or downstream of, Radil.
complex between M2R and holo-Gi1 is an octamer comprising four copies of each, and that activation is accompanied by a decrease in the oligomeric size of Gi1
GIV is a bifunctional modulator of G proteins; it serves as a guanine nucleotide dissociation inhibitor (GDI) for Galphas using the same motif that allows it to serve as a guanine-nucleotide exchange factor for Galphai
The authors demonstrate that Glu53, Glu60, and Glu118 of human Ngb are crucial for both the neuroprotective activity and interaction with Gi. Moreover, they show that Lys46, Lys70, Arg208, Lys209, and Lys210 residues of Gi are important for binding to human Ngb.
GTP analogs leads to a rigid and closed arrangement of the Galphai1, whereas the apo and GDP-bound forms are considerably more open and dynamic.
The results show ZIP9 is a specific Gi coupled-membrane AR mediating testosterone-induced MAP kinase and zinc signaling in PC3-ZIP9 cells.
These data indicate that, unlike in taste cells, TAS2Rs couple to the prevalent G proteins, Galphai1, Galphai2, and Galphai3, with no evidence for functional coupling to Galphagust.
testosterone rapidly increased whole-cell HCAEC SKCa and BKCa currents via a surface androgen receptor, Gi/o protein, and protein kinase A
These findings suggest that Gi1 interacts only with active GPCRs and that the well known high speed of GPCR signal transduction does not require preassembly between G proteins and GPCRs.
Silencing of Galphai1 expression blocked the inhibitory effects of G-1 on prostate cancer cell growth
CGRP family of receptors displays both ligand- and RAMP-dependent signaling bias among the Galphas, Galphai, and Galphaq/11 pathways.
biochemical and computational data indicate that the interactions between alpha5, alpha1, and beta2-beta3 are not only vital for GDP release during G protein activation, but they are also necessary for proper GTP binding (or GDP rebinding).
In activation cluster I, helices alpha1 and alpha5 pack against strands beta1-beta3 to stabilize the nucleotide-bound states.
The loss-of-function mutations of GNAI loci are rare or nonexistent in familial pituitary adenomas.
Employed time-resolved FTIR difference spectroscopy to investigate the molecular reaction mechanisms of Galphai1. Mutants of the intrinsic arginine finger (Galphai1-R178S) affected exclusively the hydrolysis reaction.
Data indicate that hydroxyurea (HU) induces SAR1 protein expression, which in turn activates gamma-globin expression, predominantly through the Gialpha/JNK/Jun pathway.
Guanine nucleotide binding proteins are heterotrimeric signal-transducing molecules consisting of alpha, beta, and gamma subunits. The alpha subunit binds guanine nucleotide, can hydrolyze GTP, and can interact with other proteins. The protein encoded by this gene represents the alpha subunit of an inhibitory complex. The encoded protein is part of a complex that responds to beta-adrenergic signals by inhibiting adenylate cyclase. Two transcript variants encoding different isoforms have been found for this gene.
adenylate cyclase-inhibiting G alpha protein
, guanine nucleotide binding protein, alpha inhibiting 1
, guanine nucleotide-binding protein G(i) subunit alpha-1
, Gi1 protein alpha-subunit
, alpha-subunit of G-protein, type G-alpha-i-1
, guanine nucleotide-binding protein G(i), alpha-1 subunit
, Gi1 protein alpha subunit
, Gi-alpha-1 protein
, guanine nucleotide binding protein (G protein), alpha inhibiting 1
, Galpha i1a