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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
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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
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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.
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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
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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
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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.
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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.
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The results show ZIP9 is a specific Gi coupled-membrane AR mediating testosterone-induced MAP kinase and zinc signaling in PC3-ZIP9 cells.
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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.
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testosterone rapidly increased whole-cell HCAEC SKCa and BKCa currents via a surface androgen receptor, Gi/o protein, and protein kinase A
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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.
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Silencing of Galphai1 expression blocked the inhibitory effects of G-1 on prostate cancer cell growth
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CGRP family of receptors displays both ligand- and RAMP-dependent signaling bias among the Galphas, Galphai, and Galphaq/11 pathways.
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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).
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In activation cluster I, helices alpha1 and alpha5 pack against strands beta1-beta3 to stabilize the nucleotide-bound states.
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The loss-of-function mutations of GNAI loci are rare or nonexistent in familial pituitary adenomas.
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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.
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Data indicate that hydroxyurea (HU) induces SAR1 protein expression, which in turn activates gamma-globin expression, predominantly through the Gialpha/JNK/Jun pathway.
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We observed increased expression of Galphai1/3 in wounded human skin and keloid skin tissues, suggesting the possible involvement of Galphai1/3 in wound healing and keloid formation.
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Gi alpha subunit was found to be a key modulator of GABAB-receptors signaling in analgesia.
