ライフサイエンスコーパス: G-alpha

1 R-1/2 is largely interdependent and requires G alpha.

2 ss closely related G alpha(s) and G alpha(q)/G alpha(11) families.

3 both form stable complexes with G alpha(q), G alpha(11), G alpha(14), G alpha(12), and G alpha(13).

4 Activating G alpha 12 (QL point mutation or stimulating endogenous

5 G alpha 12 activation led to decreased phosphorylation o

6 MDCK cell 3D-tubulogenesis assay, activated G alpha 12 inhibited tubulogenesis and led to the format

7 Herein, we demonstrate that G alpha 12 inhibits interaction of MDCK cells with colla

8 (QL point mutation or stimulating endogenous G alpha 12 with thrombin) inhibited focal adhesions and

9 ase completely restored normal attachment in G alpha 12-activated cells, and there was partial recove

10 r, these studies provide direct evidence for G alpha 12-integrin regulation of epithelial cell spread

11 Consistent with G alpha 12-regulated attachment to collagen-I, G alpha 1

12 alpha 12-regulated attachment to collagen-I, G alpha 12-silenced MDCK cells revealed a more adherent

13 Furthermore, G alpha 12-silenced MDCK cells were resistant to thrombi

14 s with G alpha(q), G alpha(11), G alpha(14), G alpha(12), and G alpha(13).

15 are likely coupled to GTP hydrolysis in the G alpha(12/13) class of heterotrimeric G proteins.

16 Furthermore, S1P5 appears to engage the G alpha(12/13) protein coupled Rho/ROCK signaling pathwa

17 sly, structural analyses of fully functional G alpha(12/13) subunits have been hindered by insufficie

18 btypes including G alpha(q), G alpha(i), and G alpha(12/13).

19 eric G-protein-coupled receptors (G-protein) G alpha 13 subunit leading to activation of RhoA, and Rh

20 G alpha(13) activity in cell migration is retained in a

21 Thus, G alpha(13) appears to be a critical signal transducer f

22 This broader role of G alpha(13) in cell migration initiated by two types of

23 for the vascular system defects exhibited by G alpha(13) knockout mice.

24 ere we show that a heterotrimeric G protein, G alpha(13), is essential for RTK-induced migration of m

25 main, p115RhoGEF also functions as a GAP for G alpha(13).

26 , G alpha(11), G alpha(14), G alpha(12), and G alpha(13).

27 able complexes with G alpha(q), G alpha(11), G alpha(14), G alpha(12), and G alpha(13).

28 ressing mGluR7 and the promiscuous G protein G alpha(15).

29 rhodopsin and the heterotrimeric transducin (G alpha beta gamma) in an all-atom DOPC (1,2-dioleoylsn-

30 s but did not perturb interaction with other G alpha-binding partners, i.e. G betagamma, AGS3 (a guan

31 Anti-G alpha common totally blocked the effects of NE on memb

32 raised against alpha and beta subunits (anti-G alpha common, anti-G beta, anti-G alpha i1/2/3, and an

33 Thus G alpha-directed GAP activity, the first biochemical fun

34 These results suggest that a complex of G alpha/GPR-1/2/LIN-5 is asymmetrically localized in res

35 al transduction by affecting the kinetics of G alpha-GTP binding.

36 Genetic ablation of either G alpha-gustducin or TrpM5, essential elements of the T2

37 eceptor (GPCR) Moody, the G protein subunits G alpha i and G alpha o, and the regulator of G protein

38 ith a cortical Partner of Inscuteable (Pins)-G alpha i crescent to divide asymmetrically, but the lin

39 LT receptor 1 antagonist CP 105,696, and the G alpha i inhibitor pertussis toxin.

40 dy was undertaken to test whether one of the G alpha i proteins, G alpha i3, signals in the same path

41 t GIV/Girdin serves as a nonreceptor GEF for G alpha i through an evolutionarily conserved motif that

42 tion signals mediated by CCR7 and additional G alpha i-coupled receptors.

43 ing the functional disruption of this unique G alpha i-GIV interface a promising target for therapy a

44 pha i1 complex as a template, we modeled the G alpha i-GIV interface and identified the key residues

45 pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress comp

46 or (GPCR) that coimmunoprecipitates with the G alpha i-subunit of heterotrimeric G-proteins from huma

47 and efficiency of the GEF activity of GIV on G alpha(i) and that represents an attractive target site

48 reduction of Ric-8A expression, or decreased G alpha(i) expression similarly affected metaphase cells

49 sis-toxin insensitive, indicating that other G alpha(i) family members are not involved in this proce

50 We show here that Ric-8A and G alpha(i) function to orient the metaphase mitotic spin

51 ylyl cyclase (AC) 2 and 4, and/or inactivate G alpha(i) inhibitory function, thereby transiently enha

52 a(i/o) protein family, but whether these two G alpha(i) proteins have distinguishable roles guiding T

53 gs reveal for the first time an interplay of G alpha(i) proteins in transmitting G protein-coupled re

54 timulation of cells coexpressing a wild-type G alpha(i) subunit and the dopamine D2 receptor with the

55 We identified Trp-258 in the G alpha(i) subunit as a novel structural determinant for

56 leotide exchange factor (GEF) that activates G alpha(i) subunits.

57 GDP x AlF4(-)- and GTPgammaS-bound states of G alpha(i) subunits.

58 his is the site of effector interactions for G alpha(i) subunits.

59 discovered a novel structural determinant on G alpha(i) that plays a key role in defining the selecti

60 Elevated AGS3 binds to G alpha(i) to prevent its inhibition on AC activation.

61 ric G-protein subtypes including G alpha(q), G alpha(i), and G alpha(12/13).

62 es since it blocked the binding of Ric-8A to G alpha(i), thus preventing its GEF activity for G alpha

63 n activation of opioid receptors, AGS3 binds G alpha(i)-GDP to promote free G betagamma stimulation o

64 for designing small molecules to disrupt the G alpha(i)-GIV interface for therapeutic purposes.

65 G alpha(i)-independent neutrophil recruitment into the i

66 efore parturition, whereas expression of the G alpha(i)-linked receptor Htr1d increased at the end of

67 5-initiated signaling is not mediated by the G alpha(i)-protein coupled pathway.

68 This signaling is independent of G alpha(i)-protein-coupled receptors, results in slow ro

69 pha(i), thus preventing its GEF activity for G alpha(i).

70 CXCR4-induced G alpha(i)/G betagamma activities were suppressed after

71 alpha13 generated soluble chimeric subunits (G alpha(i/12) and G alpha(i/13)) that could be purified

72 Crystal structures of the G alpha(i/12) x GDP x AlF4(-) and G alpha(i/13) x GDP co

73 ld-type counterparts, G alpha(i/13), but not G alpha(i/12), stimulated the activity of p115RhoGEF.

74 res of the G alpha(i/12) x GDP x AlF4(-) and G alpha(i/13) x GDP complexes were determined using diff

75 soluble chimeric subunits (G alpha(i/12) and G alpha(i/13)) that could be purified in sufficient amou

76 Like their wild-type counterparts, G alpha(i/13), but not G alpha(i/12), stimulated the act

77 lpha(i2) and G alpha(i3), two members of the G alpha(i/o) protein family, but whether these two G alp

78 of pertussis toxin, a broad inhibitor of the G alpha(i/o) protein family.

79 ation of PKC by kainate receptors - requires G alpha(i/o) proteins.

80 n of seven proteins (C5a receptor; G-beta-2; G-alpha,i-2,3; regulator of G-protein signaling-10; G-pr

81 ase-activating protein for the G-alpha-q and G-alpha-i subunits of heterotrimeric G-proteins that tur

82 sing the available structure of the KB-752 x G alpha i1 complex as a template, we modeled the G alpha

83 Individually, anti-G alpha i1/2/3 and anti-G alpha o only partially inhibit

84 nits (anti-G alpha common, anti-G beta, anti-G alpha i1/2/3, and anti-G alpha o) were used.

85 h guanosine 5'-O-(3-thio)triphosphate-loaded G alpha(i1) and isolated using an automated robotic colo

86 that substitution of the N-terminal helix of G alpha(i1) for the corresponding region of G alpha12 or

87 The crystal structure of KB-1753 bound to G alpha(i1) x GDP x AlF4(-) reveals binding to a conserv

88 s found to be nearly identical to wild-type, G alpha(i1)(G202A) x GDP assumed a divergent conformatio

89 hat PAR1 but not PAR2 coupled to G alpha(o), G alpha(i1), and G alpha(i2).

90 vely inactive, G(203)A, mutant nor wild-type G alpha(i1).

91 a (germ-free), or active for immune colitis (G alpha i2-/- CD3+ transferred into Rag-/- recipients) w

92 s, CXCL9, CXCL10, and CXCL11, as the lack of G alpha(i2) abolished CXCR3-stimulated migration and gua

93 G alpha(i3)-mediated blockade of G alpha(i2) activation did not result from G alpha(i3) a

94 A mutation in this domain abrogated not only G alpha(i2) activation induced by a CXCR3 agonist but al

95 This study details distinct G alpha(i2) and G alpha(i3) effects on chemokine recepto

96 T lymphocytes express G alpha(i2) and G alpha(i3), two members of the G alpha(

97 We explore the role of RGS proteins and G alpha(i2) in the physiologic regulation of body weight

98 lted from competition or steric hindrance of G alpha(i2) interaction with the CXCR3 receptor via the

99 ults with GiCT indicate that upregulation of G alpha(i2) is an adaptive protective response after isc

100 uroepithelium, consistently coexpress either G alpha(i2) or G alpha(o), and lack other chemoreceptors

101 RGS proteins and G alpha(i2) signaling play important roles in the contro

102 ly causes a "functional knockout" of cardiac G alpha(i2) signaling.

103 tor peptide, GiCT, composed of the region of G alpha(i2) that interacts specifically with G protein-c

104 Our data showed that G alpha(i2) was indispensable for T cell responses to th

105 c "knock-in" mice expressing RGS-insensitive G alpha(i2) with a G184S mutation that blocks RGS protei

106 Homozygous G alpha(i2)(G184S) knock-in mice show slightly reduced a

107 On a high-fat diet, male G alpha(i2)(G184S) mice are resistant to weight gain, ha

108 Both male and female G alpha(i2)(G184S) mice on a high-fat diet also exhibit

109 PAR2 coupled to G alpha(o), G alpha(i1), and G alpha(i2).

110 uanine nucleotide (G) protein alpha subunit, G alpha(i2).

111 dy work with the additional information that G alpha i3 and G alpha o1 were not involved.

112 B6/NCrl) to study the effects of the loss of G alpha i3 or Oa1 function.

113 Furthermore, they suggest a common Oa1-G alpha i3 signaling pathway that ultimately affects axo

114 Although G alpha i3(-/-) and Oa1(-/-) mice had normal results on

115 In addition, the RPE cells of G alpha i3(-/-) and Oa1(-/-) mice showed abnormal melano

116 Adult G alpha i3(-/-) and Oa1(-/-) mice were compared with the

117 Although G alpha i3(-/-) and Oa1(-/-) photoreceptors were compara

118 These results indicate that G alpha i3, like Oa1, plays an important role in melanos

119 test whether one of the G alpha i proteins, G alpha i3, signals in the same pathway as OA1 to regula

120 sting of BLT1, its primary coupled G protein G alpha i3, Src kinase, and Fc gamma RI within LRs.

121 in-linked receptors were generated by fusing G alpha(i3) (PAFR-G alpha(i3)) or G alpha(q) (PAFR-G alp

122 on to PAF by all the receptors but only PAFR-G alpha(i3) activation cross-inhibited the response of C

123 f G alpha(i2) activation did not result from G alpha(i3) activation, but instead resulted from compet

124 ial for biological functions associated with G alpha(i3) activation.

125 PAFR-G alpha(i3) and PAFR-G alpha(q) mediated greater GTPase

126 Thus activation of G alpha(i3) by GIV is essential for biological functions

127 Activation of G alpha(i3) by GIV was also dramatically reduced when Tr

128 This study details distinct G alpha(i2) and G alpha(i3) effects on chemokine receptor CXCR3-mediated

129 in vitro pulldown assays we demonstrate that G alpha(i3) is a better substrate for GIV than the highl

130 In sharp contrast, T cells isolated from G alpha(i3) knock-out mice displayed a significant incre

131 investigated the structural determinants in G alpha(i3) necessary for its regulation by GIV/girdin,

132 eased GTPgammaS incorporation was blocked by G alpha(i3) protein in a dose-dependent manner.

133 a CXCR3 agonist but also the interaction of G alpha(i3) to the CXCR3 receptor.

134 Moreover, when mutant G alpha(i3) W258F was expressed in HeLa cells they faile

135 s were generated by fusing G alpha(i3) (PAFR-G alpha(i3)) or G alpha(q) (PAFR-G alpha(q)) at the C te

136 PAFR and PAFR-G alpha(i3), but not PAFR-G alpha(q), mediated chemotaxi

137 -2H3) stably expressing wild-type PAFR, PAFR-G alpha(i3), or PAFR-G alpha(q) was generated and charac

138 T lymphocytes express G alpha(i2) and G alpha(i3), two members of the G alpha(i/o) protein fam

139 G alpha(i3)-mediated blockade of G alpha(i2) activation

140 for GIV binding by comparing GIV binding to G alpha(i3)/G alpha(o) chimeras.

141 t was found to act as a sensor for activated G alpha in vitro.

142 Further, LIN-5 immunoprecipitates with G alpha in vivo, and this association is GPR-1/2 depende

143 ling, we discovered a selective induction of G alpha inhibiting subunit 1 (Gi alpha1) expression in t

144 ese data suggest that selective induction of G alpha inhibiting subunit 1 expression and activity is

145 d raft disruptor beta-methyl cyclodextrin or G alpha inhibitor pertussis toxin blocked resveratrol- a

146 lo by using the interaction of Drd3 with the G-alpha interacting protein (GAIP) C terminus 1 (GIPC1)

147 onounsaturated fatty acid; MUFA), MUFA + 3.5 g alpha-linolenic acid (ALA; MUFA + ALA) from high-ALA c

148 Signal deactivation is achieved by G alpha-mediated GTP hydrolysis (GTPase activity) which

149 Individually, anti-G alpha i1/2/3 and anti-G alpha o only partially inhibited the action of NE on K

150 , anti-G beta, anti-G alpha i1/2/3, and anti-G alpha o) were used.

151 Moody, the G protein subunits G alpha i and G alpha o, and the regulator of G protein signaling Loco

152 he basal layer express the G-protein subunit G alpha(o) and members of the V2R superfamily of vomeron

153 ding by comparing GIV binding to G alpha(i3)/G alpha(o) chimeras.

154 ation of Trp-258 to the corresponding Phe in G alpha(o) decreased GIV binding in vitro and in culture

155 n for m2 muscarinic receptors, PTX-sensitive G alpha(o) G-proteins, and Kir3.2c channels.

156 S11 has little effect on the deactivation of G alpha(o) in dark-adapted cells or during adaptation to

157 consistently coexpress either G alpha(i2) or G alpha(o), and lack other chemoreceptors examined.

158 an cells can be blocked by overexpression of G alpha(o), and this inhibition is relieved by activatio

159 All ON cone bipolar cells express mGluR6 and G alpha(o), but only a subset expresses Ret-PCP2.

160 These channels, as well as the G-protein G alpha(o), function in neuroendocrine cells to promote

161 surprising that PAR1 but not PAR2 coupled to G alpha(o), G alpha(i1), and G alpha(i2).

162 lar dendrites (labeled by antibodies against G alpha(o), G gamma 13, or mGluR6).

163 strong interactor with the G-protein subunit G alpha(o), localizes to retinal ON bipolar cells.

164 substrate for GIV than the highly homologous G alpha(o).

165 G alpha(o/i) also activates the Src-Stat3 pathway.

166 h a signaling network involving antagonistic G alpha(o/i) and G alpha(s) pathways and gap-junctional

167 Overall, this study demonstrated that G alpha(o/i)-coupled CB1R triggers neurite outgrowth in

168 e additional information that G alpha i3 and G alpha o1 were not involved.

169 stem, GFP (green fluorescent protein)-tagged G alpha(oA) subunits remained mobile after cross-linking

170 ive agent of chestnut blight, contains three G alpha, one G beta, one G gamma subunits and phosducin-

171 A sensory G-alpha protein mutation affects temporal filtering in A

172 action, resulting in NO production through a G alpha-protein-coupled mechanism.

173 ivo and in vitro in myocytes after increased G alpha q activity, the trigger for pressure-overload hy

174 NTS1 monomers activate G alpha q beta(1)gamma(2), whereas receptor dimers catal

175 In contrast, G alpha q expression levels were significantly lower in

176 indings suggest that compensatory changes in G alpha q expression occur in mice with persistently alt

177 expression of mRNA and protein encoding the G alpha q subunit of G-protein that couples to 5-HT2A/2C

178 ellet was implanted subcutaneously into male G alpha q transgenic (Gq) mice.

179 caused by cardiac-specific overexpression of G alpha q, i.p. ITPP increased exercise capacity, with a

180 lectively expressing a constitutively active G alpha(q) (mutation of Q209L) in osteoblasts.

181 by fusing G alpha(i3) (PAFR-G alpha(i3)) or G alpha(q) (PAFR-G alpha(q)) at the C terminus of PAFR.

182 We have measured complex formation between G alpha(q) and PLC beta1 in vitro and in living PC12 and

183 ppear to physically overlap with the site on G alpha(q) bound by regulator of G-protein signaling (RG

184 ession of a mini-gene that inhibits receptor-G alpha(q) coupling blunted stretch-induced hypertrophy

185 orts the hypothesis that GRK2 is a bona fide G alpha(q) effector.

186 roteins bind to the effector-binding site of G alpha(q) in a manner that does not appear to physicall

187 Continuous signaling via G alpha(q) in mouse osteoblastic MC3T3-E1 cells impaired

188 cent crystallographic studies have shown how G alpha(q) interacts with two activation-dependent targe

189 Signal transduction through G alpha(q) involves stimulation of phospholipase C beta

190 is of fluorescent-tagged proteins shows that G alpha(q) is localized almost entirely to the plasma me

191 imum) of FRET is surprising considering that G alpha(q) is more highly expressed than PLC beta1 and t

192 PAFR-G alpha(i3) and PAFR-G alpha(q) mediated greater GTPase activity in isolated

193 We propose that the GAR-3(mAChR)/G alpha(q) pathway sensitizes the spicule neurons and mu

194 xotremorine M), we identified a GAR-3(mAChR)-G alpha(q) pathway that promotes protractor muscle contr

195 s functionally distinct from the presynaptic G alpha(q) pathway with which it interacts.

196 We propose that continuous activation of the G alpha(q) signal in osteoblasts plays a crucial, previo

197 ice that expressed the constitutively active G alpha(q) transgene in cells of the osteoblast lineage

198 ng wild-type PAFR, PAFR-G alpha(i3), or PAFR-G alpha(q) was generated and characterized.

199 osine 5'-3-O-(thio)triphosphate) and also to G alpha(q)(GDP), and the latter association has a differ

200 easurements show that PLC beta1 will bind to G alpha(q)(guanosine 5'-3-O-(thio)triphosphate) and also

201 a(i3) (PAFR-G alpha(i3)) or G alpha(q) (PAFR-G alpha(q)) at the C terminus of PAFR.

202 AR1 and PAR2 both form stable complexes with G alpha(q), G alpha(11), G alpha(14), G alpha(12), and G

203 heterotrimeric G-protein subtypes including G alpha(q), G alpha(i), and G alpha(12/13).

204 PAFR and PAFR-G alpha(i3), but not PAFR-G alpha(q), mediated chemotaxis to PAF.

205 eta activation in epithelial cells via LPA2, G alpha(q), RhoA, and Rho kinase, and that this pathway

206 al stretch is mediated primarily through the G alpha(q)-coupled angiotensin II AT(1) receptor leading

207 Substance P-mediated activation of the G alpha(q)-coupled human neurokinin 1 (hNK-1) receptor c

208 We demonstrate that a G alpha(q)-coupled muscarinic acetylcholine receptor (mA

209 Transmembrane signaling through G alpha(q)-coupled receptors is linked to physiological

210 Herein we confirm the formation of RGS-G alpha(q)-GRK2/p63RhoGEF ternary complexes using flow c

211 Expression of the G alpha(q)-linked serotonin receptor 5-hydroxytryptamine

212 cible, whereas Nix expression was induced by G alpha(q)-mediated hypertrophic stimuli.

213 We explored the role of G alpha(q)-mediated signaling on skeletal homeostasis by

214 Luciferase activity increased in G alpha(q)-NixP hearts 3.2 +/- 0.4-fold and in TAC heart

215 s, possibly involving PKC activation via the G alpha(q)-PLC (phospholipase C) signaling pathway commo

216 G alpha(q)-PLC beta1 complexes are observed in both sing

217 ted via the LPA2 receptor, which signals via G alpha(q).

218 t to the less closely related G alpha(s) and G alpha(q)/G alpha(11) families.

219 ivation mechanisms but appeared to depend on G alpha(q)/phosphatidylinositol 3-kinase gamma activity

220 ylation of G alpha(q/11) with an increase in G alpha(q/11) activity.

221 the activation of membrane-bound G proteins G alpha(q/11) also mediate flow-induced responses.

222 ochemistry, we observed a co-localization of G alpha(q/11) and PECAM-1 at the cell-cell junction in t

223 action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 ca

224 In Chinese hamster ovary cells, the loss of G alpha(q/11) binding did not affect the ability of the

225 TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation.

226 vation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidyli

227 Here, we investigated whether PECAM-1 and G alpha(q/11) could act in unison to rapidly respond to

228 hin 30 s and a partial relocalization of the G alpha(q/11) staining to perinuclear areas within 150 m

229 issociation of OTRs and G beta subunits from G alpha(q/11) subunits shown by coimmunoprecipitation an

230 In contrast, G alpha(q/11) was absent from junctions in atheroprone a

231 utely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity

232 Thus, we further examined G alpha(q/11)-associated signaling pathways in OT-evoked

233 Co-transfection of neurons with either a non-G alpha(q/11)-binding (D110A) GRK2 mutant or the catalyt

234 ve complex and its localization suggests the G alpha(q/11)-PECAM-1 complex is a critical mediator of

235 ar stress led to a rapid dissociation of the G alpha(q/11)-PECAM-1 complex within 30 s and a partial

236 on eliminated temporal gradient flow-induced G alpha(q/11)-PECAM-1 dissociation.

237 These results allow us to conclude that G alpha(q/11)-PECAM-1 forms a mechanosensitive complex a

238 inding of the RGS homology domain of GRK2 to G alpha(q/11).

239 carinic receptors are typically coupled with G-alpha(q)/11, we investigated whether other receptors k

240 GS18) is a GTPase-activating protein for the G-alpha-q and G-alpha-i subunits of heterotrimeric G-pro

241 nteractions with GPCRs and effectors such as G alpha-regulated RhoGEFs, but also novel conformational

242 a prompted intriguing speculations on the IP/G alpha s coupling which mediates vasodilatation and inh

243 s (Q384-L394 in the protein sequence) of the G alpha s protein (G alpha s-Ct), were determined by 2D

244 of the human prostacyclin receptor (IP) and G alpha s protein have been identified.

245 P1 domain and the C-terminal residues of the G alpha s protein in the receptor/G protein coupling.

246 The N-terminal domain (Q384-Q390 in the G alpha s protein) of the peptide adopted an alpha-helic

247 e of the C-terminal domain (Q390-E392 in the G alpha s protein) of the peptide was destabilized upon

248 elationship of the iLP1 in coupling with the G alpha s protein, the solution structures of a constrai

249 hand, the solution structural models of the G alpha s-Ct peptide in the absence and presence of the

250 Arg45 was observed upon the addition of the G alpha s-Ct peptide.

251 protein sequence) of the G alpha s protein (G alpha s-Ct), were determined by 2D 1H NMR spectroscopy

252 The G alpha(s) activates protein kinase A, which is required

253 proteins but not to the less closely related G alpha(s) and G alpha(q)/G alpha(11) families.

254 etic analysis shows that UNC-31 and neuronal G alpha(s) are different parts of the same pathway and t

255 promoters, we show that both UNC-31 and the G alpha(s) pathway function in cholinergic motor neurons

256 arts of the same pathway and that the UNC-31/G alpha(s) pathway is functionally distinct from the pre

257 ractivation of one or more components of the G alpha(s) pathway.

258 work involving antagonistic G alpha(o/i) and G alpha(s) pathways and gap-junctional communication wit

259 analysis suggests that PDE-4 regulates both G alpha(s)-dependent and G alpha(s)-independent cAMP poo

260 DE-4 regulates both G alpha(s)-dependent and G alpha(s)-independent cAMP pools in the neurons control

261 nstead, adenosine A2A receptor activation of G alpha(s/olf) seems to initiate cAMP superactivation an

262 on may thus provide a simple explanation for G alpha-specific activation of GIRK channels and other G

263 rs, composed of a guanine nucleotide-binding G alpha subunit and an obligate G betagamma dimer, regul

264 of G beta1 and have little overlap with the G alpha subunit binding interface.

265 nse to an external signal depends largely on G alpha subunit function or G protein-independent signal

266 To test the contribution of G alpha subunit functional specificity, the chimeric G a

267 bunit Gs, which signals via cAMP, or via the G alpha subunit Go, which we show signals via Phospholip

268 When placed within Saccharomyces cerevisiae G alpha subunit Gpa1, the fast-hydrolysis mutation resto

269 Reducing signaling in LN(v)s via the G alpha subunit Gs, which signals via cAMP, or via the G

270 is not limited to receptor coupling and that G alpha subunit sequences outside of the carboxyl termin

271 These results indicate that Dictyostelium G alpha subunit specificity is not limited to receptor c

272 generate a unique type of dominant-negative G alpha subunit that can effectively block signaling by

273 cholinesterase 8 (Ric-8), a G protein alpha (G alpha) subunit guanine nucleotide exchange factor (GEF

274 le of activating as well as sequestering the G alpha-subunit, thereby enhancing Akt signaling via the

275 strains expressing a mutationally activated G alpha-subunit, which activates adenylate cyclase.

276 In Caenorhabditis elegans embryos, G alpha subunits act with the positive regulators GPR-1/

277 , no in vivo evidence exists that any of the G alpha subunits are cardioprotective.

278 Dictyostelium discoideum expresses multiple G alpha subunits but only a single G beta and G gamma su

279 y to identify a series of peptides that bind G alpha subunits in a nucleotide-dependent manner.

280 5'-O-(3-[(35)S]thio)triphosphate binding to G alpha subunits, and the subsequent increase in intrace

281 erminus of G alpha12, but not those of other G alpha subunits, contains a predicted mitochondrial tar

282 subunit functional specificity, the chimeric G alpha subunits, G alpha2/4 and G alpha5/4, were create

283 Here, we validated and exploited a G alpha switch-region point mutation, known to engender

284 een observed that diverse set of proteins (e.g alpha-synuclein, insulin, TATA-box binding protein, Su

285 ated transgenic mice that expressed a mutant G alpha(t) lacking N-terminal acylation sequence (G alph

286 ents containing G alpha(t)G2A at 5-6% of the G alpha(t) levels in wild-type rods showed only a sixfol

287 s of transgenic rods, indicating the role of G alpha(t) membrane tethering for its efficient inactiva

288 erstood G-protein alpha-subunit, transducin (G alpha(t)), we generated transgenic mice that expressed

289 In contrast to native G alpha(t), which resides in the outer segments of dark-

290 enic rods with the outer segments containing G alpha(t)G2A at 5-6% of the G alpha(t) levels in wild-t

291 tant and quantitative expression analysis of G alpha(t)G2A rods.

292 Rods expressing G alpha(t)G2A showed a severe defect in transducin cellu

293 in the outer segments of dark-adapted rods, G alpha(t)G2A was found predominantly in the inner compa

294 ha(t) lacking N-terminal acylation sequence (G alpha(t)G2A).

295 nt activation of cGMP phosphodiesterase 6 by G alpha(t)G2A; alternatively, nonlinear relationships be

296 to pertussis toxin, to siRNA against either G alpha t2 or p38 alpha, and to the p38 inhibitor SB2035

297 ignaling events downstream of the Frizzled-2/G alpha t2/PDE6 triad activated in response to Wnt5a, we

298 KB-1753 blocks interaction of G alpha(transducin) with its effector, cGMP phosphodiest

299 pha(z) impacts are intact in beta-cells, and G alpha(z) activation inhibits both cAMP production and

300 Furthermore, signaling pathways upon which G alpha(z) impacts are intact in beta-cells, and G alpha