ライフサイエンスコーパス: Gi protein

1 tory guanine nucleotide regulatory proteins (Gi-proteins).

2 ls that is consistent with the activation of Gi protein.

3 oxin, a known method for the inactivation of Gi protein.

4 or state is a form of receptor precoupled to Gi protein.

5 gnificantly reduce dissociation rates of the Gi protein.

6 icient posttranslational modification of the gI protein.

7 1, via a mechanism requiring a PTX-sensitive Gi protein.

8 gh the adenylyl cyclase-inhibitory family of Gi protein.

9 that the SMC MCP-1 receptor is coupled to a Gi-protein.

10 on and Ca2+ responses only partially through Gi proteins.

11 eptors are coupled to three MAPK cascades by Gi proteins.

12 beta-adrenergic receptors can also couple to Gi proteins.

13 by seven transmembrane receptors coupled to Gi proteins.

14 hway and is required by PT to ADP-ribosylate Gi proteins.

15 mably through G beta gamma released from the Gi proteins.

16 catalytically to stimulate GTP hydrolysis by Gi proteins.

17 in G-protein coupling for 5-HT2AR from Gq to Gi proteins.

18 A G protein-coupled receptors that couple to Gi proteins.

19 riants uses inhibition of cAMP synthesis via Gi proteins.

20 athway is activated by Galpha(i2)-containing Gi proteins.

21 The beta2-AR couples to Gs and Gi proteins.

22 quires activated alpha subunits (Galphai) of Gi proteins.

23 ctivating proteins for heterotrimeric Gq and Gi proteins.

24 on signal transduction via a heterotrimeric Gi protein acting upstream of a common cell spreading pa

25 tering on the plasma membrane independent of Gi protein activation.

26 odium fluoride (NaF; range, 0.1-4 mmol/L), a Gi protein activator, were determined in a cumulative ma

27 lated but also agonist-independent ("basal") Gi-protein activity, suggesting that the FPR is constitu

28 PT abrogated in vitro ADP-ribosylation of Gi protein alpha subunit(s) indicating near-total decrea

29 Thus, the Gi protein and beta-arrestin2 compete for the same bindi

30 er replacing the nanobody with the activated Gi protein and from the 3.5- angstrom cryo-EM structure

31 t involves a pertussis toxin (PTX)-sensitive Gi protein and is abolished by inhibition of serine and

32 n kappaOR complexed with both heterotrimeric Gi protein and MP1104 agonist.

33 xoenzyme, suggesting requirements for both a Gi protein and Rho GTPase.

34 mediated by A1AR coupled to a PTX-sensitive Gi protein and subsequent activation of phospholipase C,

35 reversible (or very slow) and independent of Gi protein and that neither receptor state is a form of

36 human SMO complexed with the heterotrimeric Gi protein and two sterol ligands, equilibrated at 310 K

37 s that predominantly activate heterotrimeric Gi proteins and are involved in immune cell migration.

38 necessary for ligand-mediated activation of Gi proteins and MAPK cascades.

39 the full or partial activation of the three Gi proteins and the two Go isoforms.

40 Moreover, SDF-1-mediated signaling by both Gi proteins and ZAP-70 was required for RasGRP1 mobiliza

41 inhibited by pertussis toxin (inactivator of Gi proteins) and by DPCPX (A1-selective antagonist), but

42 itory guanine nucleotide-binding regulatory (Gi) proteins, and is associated with increased cell surf

43 t rather to an activation of beta2AR-coupled Gi proteins; and (3) spontaneous beta2AR activation may

44 Neither GRKs nor Gi proteins appear to contribute to the age-associated r

45 ave shown previously that the BHV-1.1 gE and gI proteins are capable of complementing the virulence f

46 tructural versatility of APJR in coupling to Gi proteins as a monomer or dimer, the dynamic regulatio

47 In addition, ethanol directly activated a Gi-protein, because pertussis toxin (PTx)-catalyzed, ade

48 erminal fragment that inhibited signaling by Gi protein beta gamma subunits in these cells had no eff

49 re, generated altered versions of individual Gid proteins by deleting or mutating these domains and p

50 an inhibitory guanine nucleotide regulatory (Gi) protein can result in endothelium-dependent relaxati

51 rograde spread, we identified the PRV US9/gE/gI protein complex as a viral factor facilitating the pr

52 e we report cryo-EM structures of human FPR1-Gi protein complex bound to S. aureus-derived peptide fM

53 ed at defining the trafficking of the VZV gE:gI protein complex.

54 tor of HA binding (Pep-1) and independent of Gi protein coupled or EGF-R signaling, both targets of c

55 sion of NPY receptors, a group of inhibitory Gi protein coupled receptors in the PVH, and with the ov

56 ciated with increased muscarinic M2-receptor/Gi protein-coupled expression and function.

57 invasive and migratory responses elicited by Gi protein-coupled LPA receptors via the Gbetagamma subu

58 invasive and migratory responses elicited by Gi protein-coupled LPA receptors via the GBy subunit com

59 ives are naturally occurring agonists of the Gi protein-coupled P2Y14 receptor, which occurs in the i

60 cell line, we found that a stably expressed Gi protein-coupled receptor (the delta-opioid receptor (

61 Here we show that activation of the Gi protein-coupled receptor CXCR4 is critical for the gr

62 Experimental evidence suggests that CXCR4, a Gi protein-coupled receptor for the ligand CXCL12/stroma

63 The Gi protein-coupled receptor GPR84, which is activated by

64 the chemokine receptor CCR7 but sensitive to Gi protein-coupled receptor inhibitors.

65 Blocking Gi protein-coupled receptor signaling by pertussis toxin

66 nduced motor impairment most likely involved Gi protein-coupled receptor(s) (such as adenosine recept

67 Our results implicate GALR1, a Gi protein-coupled receptor, as a tumor suppressor gene

68 of nicotinic acid are mediated by GPR109A, a Gi protein-coupled receptor, expressed primarily on adip

69 ceptor, whereas hS100A15 functions through a Gi protein-coupled receptor.

70 Microglial Gi protein-coupled receptors (Gi-GPCRs) play a critical

71 t time that the activation of SHP-2 by these Gi protein-coupled receptors requires Fyn kinase and tha

72 mediated by a putative n-3 FA receptor via a Gi protein-coupled signal transduction pathway that decr

73 aises the intriguing question of whether the Gi-protein-coupled EP3 receptor may counteract the EP2 a

74 repeated administration of an agonist at the Gi-protein-coupled MOR to the peripheral terminal of the

75 ed whether lactate and the lactate receptor, Gi-protein-coupled receptor 81 (GPR81), regulate TLR ind

76 irudin, suggesting a possible involvement of Gi-protein-coupled receptor activation.

77 hat the pharmacologically selective designer Gi-protein-coupled receptor hM4D is a presynaptic silenc

78 mediated its effects by the activation of a Gi-protein-coupled receptor leading to decreased intrace

79 nd pertussis toxin, a selective inhibitor of Gi-protein-coupled signaling pathways, reduced LPA-stimu

80 The Gi protein couples to SMO at seven strong anchor points

81 anism and functional consequences of dual Gs/Gi protein coupling of the beta3-adrenergic receptor (be

82 P) but is not required for apelin binding or Gi protein coupling.

83 r internalization that is not dependent upon Gi-protein coupling, calcium transients, or protein kina

84 ranscription is clock-controlled, consequent GI protein cycling confers a post-translational rhythm o

85 sustains rhythms in the dark by stabilizing GI protein, dependent on the F-box protein ZEITLUPE, and

86 Whereas the Gs/Gi-protein-dependent tuning of striatal neurons is fairl

87 Whereas the Gs/Gi-protein-dependent tuning of striatal neurons is fairl

88 Lastly, TgI4.4 recognizes the gI protein directly since completely deglycosylated form

89 s) of the adenosine A(1) receptor (A(1)R) in Gi protein dissociation and supported simulation finding

90 The mechanism appears to be a Gi protein down-regulation.

91 n immunoblot analysis demonstrated that: (a) Gi protein expression was significantly enhanced in memb

92 marked decrease in gI phosphorylation while gI protein expression was unaffected.

93 pendent pathway partly reflects the enhanced Gi-protein expression in PHT vessels.

94 ompared with sham concomitant with increased Gi-protein expression in PHT vessels.

95 Gi-protein expression was determined by Western blotting

96 We demonstrate that FKF1 and GI proteins form a complex in a blue-light-dependent man

97 t that CD47, its beta3 integrin partner, and Gi proteins form a stable, detergent-soluble complex tha

98 effects of pertussis toxin, an uncoupler of Gi protein from adenylate cyclase, and luzindole, a comp

99 subunit(s) indicating near-total decrease in Gi protein function.

100 on of the animals tested, the BHV-1.1 gE and gI proteins functioned autonomously to promote spread of

101 ng from this report is that the BHV-1 gE and gI proteins functioned together to complement the virule

102 The Gi protein Galpha(i2) mediates platelet activation in vi

103 We have explored whether PKA-inhibiting Gi-proteins (GiPs) may also be involved in the regulatio

104 These data suggest that inactive Gi proteins impair CCX-CKR signaling most likely by hind

105 -1 and enhanced expression and activation of Gi protein in the RV-infected ASM.

106 hrough the Gbetagamma subunits of endogenous Gi proteins in COS-7 cells were tested because both PLC

107 es allowed for light-dependent activation of Gi proteins in different experimental systems.

108 inhibit the ability of PT to ADP-ribosylate Gi proteins in intact CHO cells also inhibited the prefe

109 lar tool to specifically address the role of Gi proteins in normal and dysfunctional myocardium.

110 regulation of the expression and activity of Gi-proteins in HCC.

111 ls may partly reflect enhanced expression of Gi-proteins in PHT vessels and may, thus, represent an i

112 -protein-mediated receptor up-regulation and Gi-protein-independent receptor affinity conversion.

113 not a consequence of the down-regulation of Gi proteins induced by NECA treatment and was not associ

114 n, we tested the hypothesis that exaggerated Gi-protein induced relaxation via a nitric oxide (NO)-de

115 e data suggest that the enhanced endothelial Gi-protein-induced relaxation in PHT vessels may partly

116 effect that was completely blocked following Gi-protein inhibition (PTx; 100 ng/mL).

117 process was abrogated by pertussis toxin, a Gi protein inhibitor, and W peptide, another potent mFPR

118 d neurotrophins simultaneously, but with the Gi protein inhibitor, inhibition is blocked.

119 l-1,3-dipropylxanthine (DPCPX, 300 nM), or a Gi protein inhibitor, pertussis toxin (PTX, 200 ng/ml).

120 e in cAMP level could be blocked by both the Gi-protein inhibitor, pertussis toxin, and the thrombin

121 sensitive to pertussis toxin, thus excluding Gi-protein involvement.

122 While the gI protein is incapable of endocytosis on its own, it ca

123 mast cells through CysLT1R and EP3 involving Gi, protein kinase G, and Erk and contributing to vascul

124 ered that this synergism is mediated through Gi, protein kinase G, and Erk signaling.

125 Pertussis toxin, which ADP-ribosylates the Gi proteins known to couple to the C5a receptor, produce

126 at the amino-side IL3 also may interact with Gi proteins leading to inhibition of adenylate cyclase.

127 uscarinic receptors are usually coupled to a Gi protein, leading to inhibition of adenylyl cyclase an

128 that loss of UBP12 and UBP13 reduces ZTL and GI protein levels through a post-transcriptional mechani

129 e mutant also exhibits compromised GIGANTEA (GI) protein levels, crucial for CO stabilization during

130 lecules are ligands for seven-transmembrane, Gi protein-linked receptors that induce a signaling casc

131 Strikingly, Gi protein makes identical strong bonds with these same

132 -fold greater than those required to produce Gi protein mediated responses.

133 of HIV-1 replication by cathepsin G requires Gi protein-mediated signal transduction.

134 Results suggest Gi-protein-mediated receptor up-regulation and Gi-protei

135 The contribution of SDF-1/CXCR4- or Gi-protein-mediated signals to BM homing became apparent

136 Using the FKF1 and GIGANTEA (GI) proteins of Arabidopsis thaliana, we have generated

137 ent, yet blocked by inhibitors that uncouple Gi proteins or sequester intracellular Ca2+.

138 i requires both muscarinic receptor-mediated Gi protein/phosphatidylinositol 3-kinase/Akt signaling a

139 22, or chelerythrine chloride, inhibitors of Gi-protein, phospholipase C, and protein kinase C, respe

140 Interestingly, each Gid protein possesses several remarkable motifs (e.g. SP

141 amma5 subunit isoform associated with Go and Gi proteins purified from bovine brain.

142 initiates a signaling cascade through which Gi-protein reduces cAMP levels and attenuates protein ki

143 s coupled to pertussis toxin (PTX)-sensitive Gi proteins regulate T lymphocyte cytokine secretion, pr

144 KELCH REPEAT, F-BOX 1 (FKF1), and GIGANTEA (GI) proteins regulate CO transcription in Arabidopsis.

145 resentative of those GPCRs coupled to Gq and Gi proteins, respectively, can readily activate an epito

146 ing D1R and D3R homodimers coupled to Gs and Gi proteins, respectively.

147 usively to one protomer that is coupled with Gi proteins, revealing a distinct ligand-binding behavio

148 nd 48/80-induced secretion in mast cells via Gi protein(s), phospholipase C, calcium, and protein kin

149 dicate that constitutive beta3AR coupling to Gi proteins serves both to restrain Gs-mediated activati

150 These data demonstrate that endogenous Gi protein signaling has a primary role in the regulatio

151 e is known about the molecular mechanisms of Gi protein signaling in mammalian lymphocytes.

152 We explored the role of Gi protein signaling in the regulation of interleukin (I

153 , and in this capacity they may inhibit GPCR/Gi protein signaling in vivo.

154 se-independent pathway for ERK activation by Gi protein signaling that is distinct from ERK activatio

155 ce with pertussis toxin (PT), which inhibits Gi protein signaling, enhanced the capacity of splenocyt

156 r receptor-mediated activation of inhibitory Gi-protein signaling during a defined postnatal time win

157 ation in part by altering the redox tone and Gi-protein signaling of cells.

158 HETE-induced JNK activation, suggesting that Gi-protein signaling participates in 12-HETE-induced eff

159 ered through pertussis toxin (Ptx)-sensitive Gi-protein signaling.

160 In summary, we show that Gi protein signals are required for BM homing and, as su

161 itory trimeric guanidine nucleotide binding (Gi) protein signals.

162 t chronic ethanol treatment further enhanced Gi-protein-stimulated MAPK activity in hepatic tumorigen

163 y autologously upregulated expression of the Gi protein subtype, Gialpha3, in the ASM.

164 with an agonistic antibody, with or without Gi proteins, suggest that G protein coupling may promote

165 ruction of revertants, measurement of gE and gI protein synthesis in the Us9 null mutants, and mixed-

166 Coupling of the Gi protein to these receptors is demonstrated by failure

167 ly activated in RBL-2H3 cells by subunits of Gi proteins to induce cellular responses.

168 alpha subtypes, and was not able to activate Gi proteins to inhibit adenylate cyclase.

169 Ts, the cys-LT type 1 receptor (CysLT1), and Gi proteins to promote MC proliferation.

170 ) couples to pertussis toxin (PTX)-sensitive Gi-proteins to activate chemotaxis and exocytosis in neu

171 ation of the 125I-labeled 3LP complexed with Gi protein using anti-Gialpha antibody.

172 In contrast, activation of Gi-proteins using M7 failed to alter cellular mitogenesi

173 ling between the receptor and heterotrimeric Gi protein was assayed by high affinity, guanine nucleot

174 This effect to activate Gi proteins was abolished by a selective beta2AR blocker

175 Receptor signaling through Gi proteins was required.

176 active mastoparan analog known to stimulate Gi proteins, was found to stimulate the GTPase activity

177 ation of the pseudorabies virus (PRV) gE and gI proteins, we constructed viral mutants encoding speci

178 on largely through pertussis toxin-sensitive Gi proteins, whereas Edg4 requires both Gi and Gq.

179 g is required because MAG/myelin activates a Gi protein, which blocks increases in cAMP.

180 h WEB-2086, and inactivation of PAFR-coupled Gi protein with pertussis toxin all effectively attenuat

181 and metaMD we discovered interactions to the Gi protein with strong anchors to two intracellular loop