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 icient posttranslational modification of the gI protein.

6 1, via a mechanism requiring a PTX-sensitive Gi protein.

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

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

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

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

11 by seven transmembrane receptors coupled to Gi proteins.

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

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

14 catalytically to stimulate GTP hydrolysis by Gi proteins.

15 riants uses inhibition of cAMP synthesis via Gi proteins.

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

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

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

19 ctivating proteins for heterotrimeric Gq and Gi proteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 Blocking Gi protein-coupled receptor signaling by pertussis toxin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Gi-protein expression was determined by Western blotting

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

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

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

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

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

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

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

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

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

90 -1 and enhanced expression and activation of Gi protein in the RV-infected ASM.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 22, or chelerythrine chloride, inhibitors of Gi-protein, phospholipase C, and protein kinase C, respe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 Receptor signaling through Gi proteins was required.

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

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

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

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

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