ライフサイエンスコーパス: IP3 receptor

1 ated by the inositol trisphosphate receptor (IP3 receptor).

2 3) and spike-evoked Ca2+ entry acting on the IP3 receptor.

3 ells, and lipid vesicles containing purified IP3 receptor.

4 did not increase the phosphorylation of the IP3 receptor.

5 h as caveolin, phospholipase C, Src, and the IP3 receptor.

6 TP; and (4) inhibitors of phospholipase C or IP3 receptors.

7 ate to alterations in expression of cellular IP3 receptors.

8 anism that does not involve interaction with IP3 receptors.

9 release via ryanodine receptors but not via IP3 receptors.

10 + increase, indicating a role for functional IP3 receptors.

11 on as well as for ubiquitin association with IP3 receptors.

12 tion appears to result from a drug effect on IP3 receptors.

13 on is consistent with the down-regulation of IP3 receptors.

14 inhibits RNF170 expression and signaling via IP3 receptors.

15 eggs contain a greater number of functional IP3 receptors.

16 ng the diffusive environment for Ca(2+) near IP3 receptors.

17 canonical EL channels but, surprisingly, by IP3 receptors.

18 lumen where it diffuses and is released via IP3 receptors.

19 identical ubiquitin ligase activities toward IP3 receptors.

20 dine receptors and abolished by blocking the IP3 receptors.

21 iated by TRP channels without involvement of IP3 receptors.

22 channels by a direct mechanism not involving IP3 receptors.

23 rged by thapsigargin, which does not involve IP3 receptors.

24 ryanodine and inositol-1,4,5-trisphosphate (IP3) receptors.

25 t inhibitor of inositol 1,4,5-trisphosphate (IP3) receptors.

26 Finally, increased expression of IP3 receptor 1 and BDNF after neuronal exposure to BDNF

27 it interacts with the phosphorylated form of IP3 receptor-1, influencing the activity of this channel

28 lations in intracellular Ca(2+), mediated by IP3 receptor activation, which condition asymmetrical st

29 re is an increase in the number of available IP3 receptors after maturation and whether there is a re

30 Bcl-2 with the inositol 1,4,5-trisphosphate (IP3) receptor, an IP3-gated Ca(2+) channel on the endopl

31 ely through a direct interaction between the IP3 receptor and a Trp subunit of the Ca2+ entry channel

32 to the regulatory and coupling domain of the IP3 receptor and inhibits IP3-dependent channel opening,

33 cells may be generated by cooperation of the IP3 receptor and RYR1.

34 z, which would be expected to interfere with IP3 receptor and/or calmodulin binding, had no effect on

35 low frequency (2 Hz) caused inactivation of IP3 receptors and abolished IP3 facilitation of single A

36 xydiphenylborane (2-APB) is an antagonist at IP3 receptors and an inhibitor of canonical transient re

37 investigating the structure and function of IP3 receptors and Ca2+ signaling in neuronal and nonneur

38 sma membrane of DT40 cells lacking all three IP3 receptors and forms functional ion channels.

39 Secretagogues rapidly down-regulate IP3 receptors and other proteins involved in intracellul

40 Initial demonstration of the presence of IP3 receptors and ryanodine receptors in the NG108-15 va

41 bnormal localization of ryanodine receptors, IP3 receptors and SERCA in heart, and of IP3 receptors i

42 ith tetrameric inositol 1,4,5-trisphosphate (IP3) receptor and the existence of heterotetrameric IP3

43 nts that block inositol 1,4,5-trisphosphate (IP3) receptors and mitochondrial Ca2+ uptake were tested

44 of phospholipase C, inositol trisphosphate (IP3) receptors and ryanodine receptors inhibited the act

45 peroxidation, activation of phospholipase C, IP3 receptors, and release of Ca(2+) from the intracellu

46 n of activated inositol 1,4,5-trisphosphate (IP3) receptors, and also, when point mutated (arginine t

47 d by removing extracellular Ca(2+) and by an IP3 receptor antagonist (2-APB).

48 that the in vivo NR2B tyr-P is blocked by an IP3 receptor antagonist 2-aminoethoxydiphenylborate (2AP

49 , thapsigargin, or ryanodine, but not by the IP3 receptor antagonist xestospongin C.

50 ls, because they were blocked by heparin, an IP3 receptor antagonist, and reproduced by photolytic ap

51 In contrast, xestospongin C, an IP3 receptor antagonist, had no effect on Ca2+ signals b

52 -73122 and the inositol 1,4,5-trisphosphate (IP3) receptor antagonist xestospongin C blocked the cann

53 fected by TTX (1 microM) but were blocked by IP3 receptor antagonists xestospongin-C (Xe-C; 2 microM)

54 holipase C (PLC) and inositol trisphosphate (IP3) receptor antagonists U73122 and xestospongin C, dem

55 phosphate (IP3) inhibitor heparin or an anti-IP3 receptor antibody and were unchanged when the endopl

56 l approaches to studying the kinetics of the IP3 receptor are now beginning to give some insight into

57 xes via PMCA, SERCA, ER leakage, and Type II IP3 receptors are also represented.

58 ecific Ca2+-mobilising pathways, whereas the IP3 receptors are generally required for Ca2+ signals.

59 We conclude that IP3 receptors are in vivo substrates for Akt kinase and

60 To determine whether IP3 receptors are one of these loci, we measured IP3 rec

61 We conclude that type 3 IP3 receptors are the predominant subtype in the develop

62 of TRPC3 has been shown to interact with the IP3 receptor as well as calmodulin (calmodulin/IP3 recep

63 involves calcium release from stores through IP3 receptors as well as calcium influx through TRP chan

64 IP3 receptor binding thus acts as an eligibility trace t

65 protein IRBIT (inositol-1,4,5-trisphosphate [IP3] receptors binding protein released with IP3), a pre

66 3 receptor as well as calmodulin (calmodulin/IP3 receptor-binding (CIRB) region).

67 this study, we report the identification of IP3 receptor-binding protein released with IP3 (IRBIT) a

68 IP3 receptor blockade did not inhibit the Ca2+ release e

69 nt a new class of potent, membrane permeable IP3 receptor blockers exhibiting a high selectivity over

70 aired by intracellular application of PLC or IP3 receptor blockers, and it was absent in mice lacking

71 lar Ca(2+) store depletion and inhibition of IP3 receptors blocks both 8-pCPT-AM-mediated CaMKII phos

72 etagogues rapidly down-regulated acinar cell IP3 receptors both in vitro and in vivo.

73 tetrameric chromogranin and heterotetrameric IP3 receptor but also appears to reflect their important

74 ibited cAMP-dependent phosphorylation of the IP3 receptor but did not inhibit nuclear localization of

75 phenomenon reflecting the regulation of the IP3 receptor by [Ca2+]i.

76 are driven by the biphasic regulation of the IP3 receptor by Ca(2+), and, unlike hormone-dependent re

77 itive and negative regulation of the hepatic IP3 receptor by cytosolic calcium and by IP3, which may

78 Block of IP3 receptors by carbacyclin-stimulated elevations in cA

79 receptors by either NAADP or cADPR, and the IP3 receptors by IP3.

80 activation of inositol 1,4,5-trisphosphate (IP3) receptors by photolysis of caged IP3 The rate of Ca

81 dy-state process wherein Ca2+ efflux via the IP3 receptor Ca2+ channel is regulated by [Ca2+]s, appar

82 e supported by local calcium control between IP3 receptor Ca2+ channels (IP3R) and mitochondria, but

83 e cell models to date is the assumption that IP3 receptor Ca2+ channels (IP3Rs) are globally coupled

84 ol 1,4,5-trisphosphate (IP3) and Ca2+ on the IP3 receptor Ca2+ release channel (IP3R) is a fundamenta

85 inetics of the inositol 1,4,5-trisphosphate (IP3) receptor Ca2+ channel.

86 interacts with inositol 1,4,5-trisphosphate (IP3) receptor Ca2+ channels on the ER, regulating their

87 These responses require phospholipase C, IP3 receptors, Ca2+ stores, and Ca2+ influx, suggesting

88 ER) as determined by inositol trisphosphate (IP3) receptor/Ca2+ channels and sarcoendoplasmic reticul

89 of the model include stochastic behavior of IP3 receptor calcium channels and comparisons of channel

90 In both models, inhibitors of SERCA or IP3 receptor calcium-release channels blocked calcium tr

91 Blockade of IP3 receptors can not prevent BDNF-induced potentiation,

92 ntracellular Ca2+ stores was used to monitor IP3 receptor channel (IP3R) function and to demonstrate

93 alcium from intracellular stores through the IP3 receptor channel.

94 ryanodine and inositol 1,4,5-trisphosphate (IP3) receptor channels which contribute to cell-wide inc

95 receptors are one of these loci, we measured IP3 receptor concentration, distribution, and modificati

96 amples of cells or pancreata were probed for IP3 receptor content and distribution as well as for ubi

97 The IP3 receptor controls these periodic muscle contractions

98 -phosphonobutyric acid)], mGluR agonists, an IP3 receptor (D-IP3) agonist, and a PKC (PMA) activator,

99 NGFCs through muscarinic receptor-mediated, IP3 receptor-dependent elevations of intracellular calci

100 nts in the presence of beta-estradiol, in an IP3 receptor-dependent manner.

101 perates via an inositol 1,4,5-trisphosphate (IP3) receptor-dependent mechanism to augment drive poten

102 Furthermore, because its own activity of the IP3 receptor depends partly on cytoplasmic calcium, the

103 however, proteasome inhibitors did not block IP3 receptor down-regulation, and phospholipase Cbeta1 a

104 s systems model employed kinetics describing IP3-receptor, DTS-plasmalemma puncta formation, SOCE via

105 The switch in isoforms of the IP3 receptor during development from the type 3 with low

106 al stores, and no homologues of ryanodine or IP3 receptors exist in the genome.

107 ed significantly higher levels of the type 3 IP3 receptor expression in neonatal, compared with devel

108 tina are represented by the isoform 2 of the IP3 receptor family and the isoform 2 of the ryanodine r

109 TPR1 encodes one of the three members of the IP3-receptors family that form Ca(2+) release channels l

110 -fold increase in immunoreactive mass of the IP3 receptor following oocyte maturation.

111 nsistent with the requirement for functional IP3 receptors for voltage control of Ca2+ release from i

112 calcium from voltage-sensitive channels and IP3 receptor-gated stores.

113 y triggers internal store Ca(2)+ release via IP3 receptors, generating repetitive Ca(2)+ oscillations

114 pling with the inositol 1,4,5-trisphosphate (IP3) receptor has been suggested as a possible mechanism

115 ial relationship between phospholipase C and IP3 receptors, impairing phospholipase C-dependent calci

116 In contrast, expression of the type 1 IP3 receptor in neonates was lower compared with develop

117 Western blot analysis of the IP3 receptor in oocytes and eggs demonstrated a 1.8-fold

118 ceptor and the existence of heterotetrameric IP3 receptor in the cell, the heterotetramer formation b

119 Since the IP3 receptor in Xenopus oocytes is nearly identical to t

120 nd Homer cooperate to induce accumulation of IP3 receptors in dendritic spines and formation of putat

121 e intracellular stores via the activation of IP3 receptors in LLC-PK1 cells.

122 Immunolocalization of the type 3 IP3 receptors in neonatal tissues revealed that staining

123 rs, IP3 receptors and SERCA in heart, and of IP3 receptors in the thymus of ankyrin-B (-/-) mice.

124 ulation of the inositol 1,4,5-trisphosphate (IP3) receptor in liver was analyzed using a novel superf

125 for functional inositol 1,4,5-trisphosphate (IP3) receptors in Ca2+ release induced by membrane depol

126 results suggest that the number of cortical IP3 receptors increases during mouse oocyte maturation a

127 ly, through the inositol-1,4,5-triphosphate (IP3) receptor, indicating a communication between these

128 The larger CaTs were due to enhanced IP3 receptor-induced Ca(2+) release (IICR) and reduced m

129 agonist, a PKC inhibitor (chelerythrine), an IP3 receptor inhibitor (2-aminoethoxydiphenylborate), an

130 ly, correction of the calcium overload by an IP3 receptor inhibitor, but not by a store-operated calc

131 An IP3 receptor inhibitor, mitochondrial inhibitors, low ex

132 duced [Ca](i) release that was blocked by an IP3 receptor inhibitor.

133 An inositol 1,4,5-triphosphate (IP3) receptor inhibitor prevented the induction of primi

134 noncompetitive inositol 1,4,5-trisphosphate (IP3)-receptor inhibitor 2-aminoethoxydiphenyl borane (2-

135 A peptide inhibitor of Bcl-2-IP3 receptor interaction prevents these BH4-mediated eff

136 inhibition of inositol-1,4,5-trisphosphate (IP3) receptors, intracellular Ca(2+) ([Ca(2+)](i)) or th

137 ne (2-APB) has been widely used to probe for IP3-receptor involvement in calcium signaling pathways.

138 )-induced release of Ca(2+) from ER via the IP3 receptor (IP3 R).

139 inositol(1,4,5)-trisphosphate (Ins(1,4,5)P3 [IP3]) receptors (IP3-R) to disease progression in mouse

140 ER stores via Galphaq signaling, leading to IP3 receptor (IP3R) activation at the growth cone of dif

141 n studies, Ang1 inhibited the association of IP3 receptor (IP3R) and TRPC1, consistent with the coupl

142 inhibitor, phospholipase C (PLC) inhibitor, IP3 receptor (IP3R) antagonist, or Ca2+ chelators.

143 tudied the interaction and effect of several IP3 receptor (IP3R) constructs on the gating of the stor

144 itol 1,4,5-triphosphate (IP3) binding to the IP3 receptor (IP3R) is particularly important for the ac

145 al microscopy, we have found a high level of IP3 receptor (IP3R) staining in satellite cells, which h

146 (ITPR1), 2 (ITPR2), and 3 (ITPR3) encode the IP3 receptor (IP3R), a key player in intracellular calci

147 IP3 activates the IP3 receptor (IP3R), an intracellular calcium release ch

148 hosphate (IP3) generation, activation of the IP3 receptor (IP3R), and postsynaptic endocannabinoid re

149 forms a complex with phospholipase C gamma1, IP3 receptor (IP3R), and the Golgi Ca2+-ATPase, secretor

150 hat overexpression of PC2, as well as type I IP3 receptor (IP3R), significantly prolonged the half-de

151 We show here that in IP3 receptor (IP3R)-deficient photoreceptors, both light

152 lated, and mTORC2 at MAM interacted with the IP3 receptor (IP3R)-Grp75-voltage-dependent anion-select

153 have characterized effects of nucleotides on IP3 receptor (IP3R)-mediated calcium (Ca2+) flux in puri

154 ociation of ankyrin B 220 (ANK 220) from the IP3 receptor (IP3R-3), releasing it from inhibition.

155 use Ca2+-dependent local interactions among IP3 receptors (IP3R) and other Ca2+ channels leading to

156 (2+)]c) signaling, but the exact role of the IP3 receptors (IP3R) in this process remains unclear.

157 pressed by the inositol-1,4,5-trisphosphate (IP3) receptor (IP3R) blocker 2-aminoethoxydiphenyl borat

158 interact with inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) Ca(2+) release channels resulting i

159 The inositol 1,4,5 trisphosphate (IP3) receptor (IP3R) is a Ca2+ release channel that resp

160 l of all three inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) isoforms.

161 e activation of inositol 1,4,5-triphosphate (IP3) receptor (IP3R) via CHOP-induced ERO1-alpha (ER oxi

162 d the roles of inositol 1,4,5-trisphosphate (IP3) receptors (IP3R) in calcium signaling using DT40 B

163 ee subtypes of inositol 1,4,5-trisphosphate (IP3) receptors (IP3R1, -2, and -3).

164 cium-activated potassium channels (IKCa) and IP3 receptors (IP3Rs) in the MPs.

165 3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors (IP3Rs) located on the endoplasmic reticul

166 More specifically, antagonists of ER IP3 receptors (IP3Rs) rapidly and completely blocked Ca(

167 IP3 receptors (IP3Rs) release Ca(2+) from the ER when th

168 a2+ from the sarcoplasmic reticulum (SR) via IP3 receptors (IP3Rs).

169 Thus, the IP3 receptor is an essential component of the timekeeper

170 concentrations, suggesting that the hepatic IP3 receptor is regulated by [Ca2+] at two sites, a high

171 propose that the closed conformation of the IP3 receptor is very stable and therefore minimally susc

172 hat concomitant activation of PI3 kinase and IP3 receptors is both necessary and sufficient to mediat

173 In order to better understand the roles of IP3 receptor isoforms in brain function, a first step is

174 fraction indicated that both PLC-gamma1 and IP3 receptors (isoforms 2 and 3, IP3R2 and IP3R3) were c

175 ied the type 1 inositol-1,4,5-trisphosphate (IP3) receptor (ITPR1), an IP3-gated, endoplasmic reticul

176 n requires two SR calcium channels (RYRs and IP3 Receptors), JPH-1/Junctophilin, a PDZ (PSD95, Dlg1,

177 IP3 receptor labeling was observed within cell bodies, d

178 Moreover, IP3 receptor levels are not different in cortical homoge

179 aired, whereas neither Ca(2+) store content, IP3 receptor levels, nor IP3 production were altered, in

180 IP3 receptors--ligand-gated channels that release Ca2+ f

181 ed, indicative of a functional defect at the IP3 receptor locus, which may be the cause of neurodegen

182 ts downstream signaling molecules (PLC, PKC, IP3 receptors) markedly attenuated SKF38393-induced ERK1

183 icity may allow cooperation among sequential IP3 receptor-mediated [Ca2+] transients in the control o

184 Elementary IP3 receptor-mediated Ca(2+) release events (Ca(2+) puff

185 eactivation kinetics of the uniporter during IP3 receptor-mediated Ca2+ mobilization, we established

186 ly modulate these signals by regulating only IP3 receptor-mediated release; neither mitochondrial loc

187 Inhibition of inositol 1,4,5-trisphosphate (IP3) receptor-mediated Ca2+ release by cGMP was examined

188 elationship of inositol 1,4,5-trisphosphate (IP3) receptor-mediated signal transduction and cellular

189 tein kinase A (PKA)-induced sensitization of IP3 receptors mediates this upregulation of mGluR action

190 try of the Ca(2+) diffusive environment near IP3 receptor microdomains to limit IP3 -mediated Ca(2+)

191 Cessation of calcium release via the IP3 receptor might accelerate this fall and thus explain

192 3), which, via endoplasmic reticulum-located IP3 receptors, mobilizes intracellular Ca2+ stores.

193 gonist-stimulated Ca(2+) signaling involving IP3 receptors modulates ER export rates through activati

194 n the absence of PLC activity indicates that IP3 receptor modulation by PKC regulates Ca(2+) release

195 ine receptors, inositol 1,4,5-trisphosphate (IP3) receptors) monitor a simultaneous increase of cAMP

196 ugates known to become attached to activated IP3 receptors (monoubiquitin and Lys(48)- and Lys(63)-li

197 , adaptive response resulting in a decreased IP3 receptor number.

198 hed, at least in part, by down-regulation of IP3 receptor number.

199 ase, phospholipase C-gamma or the downstream IP3 receptors of phospholipase C-gamma, but not by inhib

200 emonstrated increased phosphorylation of the IP3 receptor on the PKG site, although the selective cAM

201 -80% inhibition of the binding of [3H]IP3 to IP3 receptors on macrophage membranes isolated from CsA-

202 e of Ca2+ from inositol 1,4,5-trisphosphate (IP3) receptor-operated stores, uptake of Ca2+ into mitoc

203 Overexpressing IP3 receptor or glucose transporter mitigates the S1RE10

204 ot involve changes in the sensitivity of the IP3 receptor or size of internal Ca(2+) stores.

205 rative action of Ca release channels such as IP3 receptors or ryanodine receptors arranged in cluster

206 m storage capacity, impaired function of the IP3 receptor, or diminished phospholipase C activity.

207 fective as M1 receptors when PIP2 synthesis, IP3 receptors, or the activity of neuronal Ca2+ sensor-1

208 cotinic receptor activation of a Galphaq and IP3 receptor pathway.

209 c agent paclitaxel triggers CIPN by altering IP3 receptor phosphorylation and intracellular calcium f

210 suggesting that PKG mediates the increase in IP3 receptor phosphorylation by both cyclic nucleotides

211 o)-cGMP (8-CPT-cGMP), demonstrated increased IP3 receptor phosphorylation in situ, which was both tim

212 h sodium nitroprusside and forskolin-induced IP3 receptor phosphorylation more potently than the sele

213 m regulation within striatal cells while the IP3 receptor plays a specialized role within spiny neuro

214 to inhibit store-operated Ca2+ channels and IP3 receptors, produces robust activation of recombinant

215 the total amount of inositol trisphosphate (IP3) receptor protein was decreased in Q212L-alpha 16 ce

216 3R)-mediated calcium (Ca2+) flux in purified IP3 receptors reconstituted in lipid vesicles (IP3RV) an

217 d predominantly via A1 receptors, stimulated IP3 receptor-regulated calcium release from intracellula

218 ol (1,4,5) triphosphate (IP3) binding to the IP3 receptor, respectively.

219 Immunolocalization of the IP3 receptor revealed that receptors were present in lar

220 Recent studies have shown that ryanodine and IP3 receptor (RyR/IP3R)-mediated cytosolic Ca2+ signals

221 s are inducible by osmotic stress through an IP3 receptor signaling-dependent pathway, indicating act

222 ion and whether there is a redistribution of IP3 receptors similar to the redistribution of the ER th

223 Mutations in the IP3 receptor slow down or eliminate the cycle, while ove

224 Mutations in the IP3 receptor slow or eliminate these calcium oscillation

225 d GSK5498A did not reduce Ca(2+) release via IP3 receptors stimulated with IP3 released from caged-IP

226 on and distribution of the type 1 and type 3 IP3 receptor subtypes in developing rat vascular smooth

227 discoveries of inositol 1,4,5-trisphosphate (IP3) receptor subtypes with different affinities for IP3

228 ibitor of the 1,4, 5-inositol trisphosphate (IP3) receptor, suggesting that Ca2+ influx is secondary

229 While the IP3 receptor system is considered as the main regulator

230 The nuclear envelope contains ryanodine and IP3 receptors that can be activated separately and indep

231 feine-sensitive inositol 1,4,5-triphosphate (IP3) receptor that releases calcium from the endoplasmic

232 Immunohistochemical staining of type III IP3 receptors, the endoplasmic reticulum-specific protei

233 , which suggested localization of the type 3 IP3 receptor throughout the sarcoplasmic reticulum netwo

234 Immunocytochemistry showed type I IP3 receptor to be abundant in red-sensitive and green-s

235 and Rinzel to include the desensitization of IP3 receptors to IP3.

236 naling Na/K-ATPase may tether PLC-gamma1 and IP3 receptors together to form a Ca(2+)-regulatory compl

237 By immunofluorescence, the IP3 receptor type 1 (IP3R-1) was distributed over the en

238 Inositol 1,4,5-trisphosphate (IP3) receptor type 1 (ITPR1), 2 (ITPR2), and 3 (ITPR3) e

239 mphoblasts is apparently not due to aberrant IP3 receptor ubiquitination.

240 hilic migration, and calcium release through IP3 receptors was found to stimulate migration.

241 lation of the inositol 1,4, 5-trisphosphate (IP3) receptor were examined in intact rat aorta using th

242 PB is incapable of significant inhibition of IP3 receptors when applied to intact cells.

243 -induced Ca2+ release via both ryanodine and IP3 receptors, which are activated independently by Ca2+

244 the cerebellar inositol-1,4,5-trisphosphate (IP3) receptor, whose activation is required for LTD indu

245 olipase C inhibitor U-73122, by blocking the IP3 receptor with pentosan polysulfate or heparin, and b

246 nodine or 5 microm thapsigargin, by blocking IP3 receptors with 2 microm 2-APB or 10 microm xestospon

247 exogenous agonist following sensitization of IP3 receptors with thimerosal.

248 Inhibiting inositol trisphosphate (IP3) receptors with a high concentration of caffeine blo