ライフサイエンスコーパス: trisphosphate

1 cytoplasmic concentration of inositol 1,4,5-trisphosphate.

2 the PI3K pathway, phosphatidylinositol (3-5)-trisphosphate.

3 messengers diacylglycerol and 1,4,5-inositol trisphosphate.

4 d accumulation of phosphatidylinositol 3,4,5-trisphosphate.

5 o bind membrane phosphatidylinositol (3,4,5)-trisphosphate.

6 -3 kinase (PI3K), phosphatidylinositol-3.4,5-trisphosphate.

7 ble to generate phosphatidylinositol (3,4,5)-trisphosphate.

8 e Ca(2+)-releasing second messenger inositol trisphosphate.

9 Inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A) is a molecule enriched

10 Here, we identify Inositol-trisphosphate 3-kinase B (Itpkb) as an essential regulat

11 Here we show that inositol-trisphosphate 3-kinase B (Itpkb) via its enzymatic produ

12 hoinositide 3-kinase (PI3K), and by inositol-trisphosphate 3-kinase B (Itpkb).

13 in human platelets identified inositol 1,4,5-trisphosphate 3-kinase isoform B (IP3KB) as a binding pa

14 In particular, inhibitors of p38, inositol trisphosphate 3-kinase, and Aurora A kinase potently enh

15 cted by increased phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1 and interferon-gamma recep

16 f ILT3, BCRs, and phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1 into inhibitory clusters a

17 The enzyme inositol 1,3,4-trisphosphate 5/6-kinase (ITPK1) catalyzes the rate-limi

18 Including phosphatidylinositol 3,4,5-trisphosphate, a downstream effector for the phosphoinos

19 We used inositol 1,4,5-trisphosphate accumulation and radioligand binding exper

20 h regulation of phosphatidylinositol [3,4,5]-trisphosphate activity.

21 endent memory in part through inositol 1,4,5-trisphosphate and brain-derived neurotrophic factor.

22 Increases in inositol 1,4,5-trisphosphate and cytoplasmic Ca(2+) levels in response

23 athways through production of inositol 1,4,5-trisphosphate and diacylglycerol (DAG).

24 enerate the second messengers inositol 1,4,5-trisphosphate and diacylglycerol, PLC, unlike the other

25 hate to the second messengers inositol 1,4,5-trisphosphate and diacylglycerol.

26 tion of the second messengers inositol 1,4,5-trisphosphate and diacylglycerol.

27 50-75% and diminished activation of inositol trisphosphate and ERK1/2 by 60-80%.

28 he head group of phosphatidyl inositol 3,4,5-trisphosphate and N-terminally truncated Arf6-GTP reveal

29 tide binds both phosphatidylinositol (3,4,5)-trisphosphate and phosphatidylinositol (4,5)-bisphosphat

30 lipid messengers phosphatidylinositol-3,4,5-trisphosphate and phosphatidylinositol-3,4-bisphosphate

31 creased levels of phosphatidylinositol 3,4,5-trisphosphate and phosphorylated AKT protein and were pr

32 e induction of the second messenger inositol trisphosphate and the mobilization of calcium are clearl

33 4-phosphate, diacylglycerol, inositol 1,4,5-trisphosphate, and Ca(2+) upon muscarinic stimulation in

34 -bisphosphate and phosphatidylinositol 3,4,5-trisphosphate, and increases their levels in the plasma

35 epletes PIP2 without changing inositol 1,4,5-trisphosphate, and monitored NBCe1-mediated currents wit

36 Thus, inositol trisphosphate, and not calcium, diffused interendothelia

37 via the second messenger myo-inositol 1,4,5-trisphosphate, and phosphoinositides comprises a huge fi

38 ,5-biphosphate or phosphatidylinositol 3,4,5-trisphosphate application compared with channels lacking

39 ream targets of Plc-generated inositol 1,4,5-trisphosphate are poorly described.

40 phosphoinositide phosphatidylinositol 3,4,5-trisphosphate at the plasma membrane and mediate protein

41 of inositol trisphosphate (IP(3)), adenosine trisphosphate (ATP), and intracellular calcium (Ca(2+)).

42 P4BP)) as a major phosphatidylinositol 3,4,5-trisphosphate-binding protein in human platelets and a k

43 idylinositol 4,5-bisphosphate/inositol 1,4,5-trisphosphate biosensor GFP-PLCdelta1-PH was reduced by

44 lving M1/M3 receptor-mediated inositol 1,4,5-trisphosphate/Ca(+2) signalling and downstream inhibitio

45 lving M1/M3 receptor-mediated inositol 1,4,5-trisphosphate/Ca(+2) signalling and downstream inhibitio

46 ocytes by activation of D-myo-inositol 1,4,5-trisphosphate/Ca(2+) /calmodulin-dependent protein kinas

47 whereas hydrolysis of PIP2 to inositol 1,4,5-trisphosphate/Ca(2+) can stimulate the transporter.

48 tact oocyte primarily through inositol 1,4,5-trisphosphate/Ca(2+).

49 Instead, S1PR2 stimulated inositol 1,4,5-trisphosphate-dependent Ca(++) release and Elk-1 phospho

50 n of P2Y receptors evoked prominent inositol trisphosphate-dependent Ca(2+) release.

51 ) channels and, on the other, inositol 1,4,5-trisphosphate-dependent Ca(2+) release.

52 iii) persistent activation of inositol 1,4,5-trisphosphate-dependent cell signaling causes Bok degrad

53 5-bisphosphate hydrolysis and inositol 1,4,5-trisphosphate-dependent intra-acrosomal calcium release.

54 ow is mediated by SHP-2 in an inositol-1,4,5-trisphosphate-dependent manner.

55 ed signalling cascade involving the inositol trisphosphate-dependent mobilization of intracellular ca

56 ta reveal the existence of an inositol 1,4,5-trisphosphate-dependent nuclear Ca(2+) toolkit located i

57 d-type and mutant phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2 (PREX2) us

58 identified PREX2 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2)--a PTEN-i

59 ly, we identified phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 1 (P-Rex1) as the

60 y investigating phosphatidylinositol (3,4,5)-trisphosphate-dependent Rac exchanger 1 (P-Rex1), one of

61 interaction with phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 2 (P-REX2).

62 Stimulation of endothelial inositol 1,4,5-trisphosphate-dependent signaling with substance P cause

63 ses apoptosis, triggered by phosphoinositide trisphosphate depletion and decreased Akt phosphorylatio

64 which are dependent on the P2R/PLC/inositol trisphosphate/ER pathway.

65 channels in the plasma membrane and inositol trisphosphate-gated channels in the endoplasmic reticulu

66 Inositol 1,4,5-trisphosphate-generating agonist evoked cytosolic Ca(2+)

67 r these conditions depends on inositol-1,4,5-trisphosphate generation from phospholipase C (PLC)-depe

68 mental cues that promote IP3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors (IP3Rs) located

69 )-dependent local phosphatidylinositol 1,4,5-trisphosphate gradient, which guides the focal movement

70 epends on phospholipase C (PLC) --> inositol trisphosphate --> Ca(2+) --> calcineurin signaling and i

71 gly, in plants, phosphatidylinositol (3,4,5)-trisphosphate has not been detected, and the enzymes tha

72 s have implicated phosphatidylinositol-3,4,5-trisphosphate in cell migration, it remains unknown whet

73 blocking phospholipase C and inositol 1,4,5-trisphosphate-induced Ca(2+) release, indicating that ac

74 stigated the contribution of inositol(1,4,5)-trisphosphate (Ins(1,4,5)P3 [IP3]) receptors (IP3-R) to

75 ellular signaling through its inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) 3-kinase and phosphatidylin

76 the Ca(2+) transient induced by an inositol-trisphosphate (InsP(3))-linked plasma membrane agonist.

77 as well as upon formation of inositol 1,4,5,-trisphosphate (InsP3) in the nucleus, whereas insulin's

78 we found that specific infusion of inositol trisphosphate (InsP3) into either distal or proximal ast

79 n of phospholipase C and opening of inositol trisphosphate (InsP3) receptors.

80 airway contraction evoked by inositol-1,4,5-trisphosphate (InsP3) uncaging in airway SMCs.

81 tact oocyte primarily through inositol 1,4,5-trisphosphate (InsP3)/Ca(2+).

82 SWAP-70, a phosphatidylinositol 3,4,5-trisphosphate-interacting, F-actin-binding protein, part

83 2, which converts phosphatidylinositol 3,4,5-trisphosphate into phosphatidylinositol 4,5-bisphosphate

84 4,5-bisphosphate (PIP(2)) to inositol 1,4,5-trisphosphate (IP(3)) and diacylglycerol (DAG).

85 Inositol 1,4,5-trisphosphate (IP(3)) is a crucial second messenger that

86 ma2) accounts for LPS-induced inositol 1,4,5-trisphosphate (IP(3)) production and subsequent calcium

87 easing the sensitivity of the inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R) to IP(3).

88 The inositol 1,4,5-trisphosphate (IP(3)) receptor is a Ca(2+) channel locat

89 g NHE3 regulatory factors (NHERFs), inositol trisphosphate (IP(3)) receptor-binding protein released

90 786 functions upstream of the inositol 1,4,5-trisphosphate (IP(3)) receptor.

91 depending on the concentrations of inositol trisphosphate (IP(3)), adenosine trisphosphate (ATP), an

92 Although inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release from the e

93 tiated by Ca(2+) release from inositol 1,4,5-trisphosphate (IP(3))-sensitive intracellular stores.

94 release of diacylglycerol and inositol 1,4,5-trisphosphate (IP(3)).

95 Ca(2+) puffs and waves mediated by inositol trisphosphate (IP(3)).

96 cyclase, Epac-1 protein, and inositol 1,4,5-trisphosphate (IP(3))/IP(3) receptor, were next demonstr

97 e C, the intercellular diffusion of inositol trisphosphate (IP(3), and to a lesser extent Ca(2+)), IP

98 Hormone-induced inositol 1,4,5 trisphosphate (IP3 ) accumulation and phospholipase C (P

99 the level of hormone-induced inositol 1,4,5 trisphosphate (IP3 ) production and does not involve cha

100 itol 4,5-bisphosphate (IP2 ), inositol 1,4,5-trisphosphate (IP3 ), and inositol hexakisphosphate (IP6

101 se in [Ca(2+) ]i triggered by inositol 1,4,5-trisphosphate (IP3 )-induced release of Ca(2+) from ER v

102 atiotemporally complex, propagating inositol trisphosphate (IP3 )-mediated Ca(2+) waves that originat

103 tion is probably initiated by inositol 1,4,5-trisphosphate (IP3 )-mobilized Ca(2+) : 8-pCPT-AM fails

104 ownstream Ca(2+) release from inositol 1,4,5-trisphosphate (IP3 )-triggered Ca(2+) -store release, or

105 ed by TGFbeta-induced inhibition of inositol trisphosphate (IP3) production, leading to a decrease in

106 resenilins (PS) interact with inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) Ca(2+) release chann

107 ion, we identified the type 1 inositol-1,4,5-trisphosphate (IP3) receptor (ITPR1), an IP3-gated, endo

108 lished by phospholipase C (PLC) and inositol trisphosphate (IP3) receptor antagonists U73122 and xest

109 es code for three subtypes of inositol 1,4,5-trisphosphate (IP3) receptors (IP3R1, -2, and -3).

110 s, or by direct activation of inositol 1,4,5-trisphosphate (IP3) receptors by photolysis of caged IP3

111 e ubiquitination of activated inositol 1,4,5-trisphosphate (IP3) receptors, and also, when point muta

112 2 (ip3k2), thereby affecting inositol 1,4,5-trisphosphate (IP3) signaling and calcium levels during

113 a (PLC-gamma) which increases inositol 1,4,5-trisphosphate (IP3) to release intracellular calcium ([C

114 ctivators cause a transient rise in inositol trisphosphate (IP3) to trigger calcium mobilization from

115 Genetically blocking inositol 1,4,5-trisphosphate (IP3)-dependent Ca(2+) increases in astroc

116 les and strengthens the efficacy of inositol trisphosphate (IP3)-induced Ca(2+) transfer from the ER

117 We previously reported decreased inositol trisphosphate (IP3)-mediated Ca(2+) release from the end

118 tdIns(3,4,5)P3 (phosphatidylinositol (3,4,5)-trisphosphate) is potentially involved in metabolic regu

119 autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (ip3k2), thereby affecting inosit

120 IPMK homologue, Arg82, is the sole inositol-trisphosphate kinase.

121 se and tensin homologue/phosphatidylinositol trisphosphate kinase/Akt/mammalian target of rapamycin p

122 Inositol trisphosphate kinases (IP3Ks) and inositol hexakisphosph

123 rmation of diacylglycerol and inositol 1,4,5-trisphosphate, leading to the release of Ca(2+) from int

124 lates growth cone phosphatidylinositol 3,4,5-trisphosphate levels and mediates chemorepulsion, wherea

125 ent depression of phosphatidylinositol 3,4,5-trisphosphate levels in the growth cone induced by the r

126 despite unaltered phosphatidylinositol 3,4,5-trisphosphate levels.

127 nd to involve phospholipase C/inositol 1,4,5-trisphosphate-mediated Ca(2+) mobilization from intracel

128 sitizing receptors evoked prolonged inositol-trisphosphate-mediated Ca(2+) release, which led to acce

129 differentiation by modulating inositol 1,4,5-trisphosphate-mediated calcium oscillations and the up-r

130 ncrease was abrogated by inhibiting inositol trisphosphate-mediated calcium release with Xestospongin

131 n plasma membrane phosphatidylinositol 3,4,5-trisphosphate, moderate Akt activation, and substantial

132 C to generate the second messenger inositol trisphosphate often evokes repetitive oscillations in cy

133 me that the POCKET containing inositol 1,4,5-trisphosphate on crystal structure (the "POCKET" Lys-63,

134 ell membrane without producing DAG, inositol trisphosphate, or calcium signals.

135 PTEN [phosphatidylinositol (3,4,5)-trisphosphate phosphatase and tensin homolog deleted fro

136 e distribution of phosphatidylinositol 3,4,5-trisphosphate, phosphatidylinositol 3-phosphate, and pho

137 nteracting with phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P(3)).

138 omes enriched for phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) and phosphatidylinositol 3,4

139 he 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PI(3,4,5)P3) and play important roles in

140 phosphate from phosphatidylinositol (3,4,5)-trisphosphate (PI(3,4,5)P3) to form phosphatidylinositol

141 domain (PHD) and phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

142 domain (PHD) and phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

143 egatively charged phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3).

144 tidylinositol bisphosphate (PI[4,5]P(2)) and trisphosphate (PI[3,4,5]P(3)) are two major phosphoinosi

145 oinositide lipid phosphatidylinositol (3,4,5)trisphosphate [PI(3,4,5)P3, or PIP3] by class I phosphoi

146 osphoinositide bisphosphate/phosphoinositide trisphosphate (PIP(2)/PIP(3)).

147 hate (PIP(2)) and phosphatidylinositol-3,4,5-trisphosphate (PIP(3)) activated TRPC1/C5 channel activi

148 (EGF)-stimulated phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) generation and concomitant activa

149 role of the lipid phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) has been particularly controversi

150 rane phospholipid phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) to the Pleckstrin Homology (PH) d

151 he PI3K reaction, phosphatidylinositol 3,4,5-trisphosphate (PIP(3)), in the nucleus.

152 degradation of phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)).

153 ing imaging for phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and active Rac1 and Cdc42 in primar

154 the increase in phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and the translocation of TRPC6 to t

155 of small-molecule phosphatidylinositol-3,4,5-trisphosphate (PIP3) antagonists (PITs) that block pleck

156 e signaling lipid phosphatidylinositol-3,4,5-trisphosphate (PIP3) by the lipid kinase phosphoinositid

157 iled to elevate phosphatidylinositol (3,4,5)-trisphosphate (PIP3) in mutant-expressing cells.

158 ion by generating phosphatidylinositol 3,4,5-trisphosphate (PIP3) in the inner leaflet of the plasma

159 annular accumulation of phosphatidylinositol trisphosphate (PIP3) in the synaptic membrane.

160 signaling lipid phosphatidylinositol (3,4,5)-trisphosphate (PIP3) is a key regulator of cell prolifer

161 or accumulating phosphatidylinositol (3,4,5)-trisphosphate (PIP3) on B cell receptor-containing early

162 etically driven phosphatidylinositol (3,4,5)-trisphosphate (PIP3) production results in only transien

163 central role in phosphatidylinositol (3,4,5)-trisphosphate (PIP3) signaling and converts PIP3 to phos

164 tes tumorigenic phosphatidylinositol (3,4,5)-trisphosphate (PIP3) signaling, is a commonly mutated tu

165 s such as Ras and phosphatidylinositol 3,4,5-trisphosphate (PIP3) to form protrusions.

166 Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), an IPMK product, restores ALY reco

167 ignaling molecule phosphatidylinositol 3,4,5-trisphosphate (PIP3), and inappropriate activation of th

168 e production of phosphatidylinositol (3,4,5)-trisphosphate (PIP3), and the activity of the serine/thr

169 total Akt, and phosphatidylinositol (3,4,5)-trisphosphate (PIP3), from mouse embryonic fibroblasts w

170 g phospholipid, phosphatidylinositol (3,4,5)-trisphosphate (PIP3), in the membrane.

171 ends on ciliary phosphatidylinositol (3,4,5)-trisphosphate (PIP3), not stimulatory G protein (Galphas

172 lular infusion of phosphatidylinositol 3,4,5-trisphosphate (PIP3), the second messenger produced by P

173 d accumulation of phosphatidylinositol 3,4,5-trisphosphate (PIP3), which promotes the formation of ac

174 ing pathways by a phosphatidylinositol-3,4,5-trisphosphate (PIP3)-dependent mechanism.

175 stimulation, the phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent Rac exchange factor (PREX

176 Phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent Rac exchanger 2 (PREX2) i

177 The P-Rex (phosphatidylinositol (3,4,5)-trisphosphate (PIP3)-dependent Rac exchanger) family (P-

178 e signaling lipid phosphatidylinositol-3,4,5-trisphosphate (PIP3).

179 the production of phosphatidylinositol 3,4,5-trisphosphate (PIP3).

180 ced generation of phosphatidylinositol-3,4,5-trisphosphate (PIP3).

181 Inositol trisphosphate production and release of calcium from int

182 spholipase C, which catalyses inositol-1,4,5-trisphosphate production and thereby induces release of

183 tidylinositol 4,5-biphosphate inositol 1,4,5-trisphosphate production, nuclear Ca(2+) release, and ac

184 phorylation and inhibition of inositol 1,4,5-trisphosphate production.

185 beta2 and the stimulation of inositol 1,4,5-trisphosphate production.

186 e production of phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) by mTORC1 in CTLs.

187 zation of PIP3 (Phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3, leading to the inhibitio

188 preferentially to phosphatidylinositol 3,4,5-trisphosphate (PtdInsP(3)).

189 The inositol trisphosphate receptor ([Formula: see text]) is one of t

190 e Atx2 specifically binds the inositol 1,4,5-trisphosphate receptor (InsP(3)R) and increases its sens

191 um release through the type 2 inositol 1,4,5-trisphosphate receptor (InsP(3)R2) in cardiac myocytes r

192 Bcl-2 interacts with the inositol 1,4,5-trisphosphate receptor (InsP3R) and thus prevents InsP3-

193 ium sensor 1 (NCS-1), and the inositol 1,4,5-trisphosphate receptor (InsP3R) to prevent treatment-ind

194 r Ca(2+) channels such as the inositol 1,4,5-trisphosphate receptor (InsP3R), is necessary to maintai

195 Htt protein binds to type 1 inositol (1,4,5)-trisphosphate receptor (InsP3R1) and increases its sensi

196 Genetic reduction of the type 1 inositol trisphosphate receptor (InsP3R1) by 50% normalized exagg

197 PR2, which encodes the type 2 inositol 1,4,5-trisphosphate receptor (InsP3R2), that was present in al

198 The type III isoform of the inositol 1,4,5-trisphosphate receptor (InsP3R3) is apically localized a

199 Functional coupling between inositol (1,4,5)-trisphosphate receptor (IP(3)R) and ryanodine receptor (

200 domain that are critical for inositol 1,4,5-trisphosphate receptor (IP(3)R) channel function.

201 cs of a single, nonconducting inositol 1,4,5-trisphosphate receptor (IP(3)R) channel, using an exact

202 hrough ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3 R) channels is supported by

203 adation of the Ca(2+) channel inositol 1,4,5-trisphosphate receptor (IP3R) affects progression to car

204 Inositol 1,4,5-trisphosphate receptor (IP3R) antagonists (xestospongin

205 Furthermore, inositol 1,4,5-trisphosphate receptor (IP3R) but not ryanodine receptor

206 A canonical example is the inositol 1,4,5-trisphosphate receptor (IP3R) channel, whose regulation

207 hrough ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3R) channels is supported by a

208 The inositol 1,4,5-trisphosphate receptor (IP3R) is a ubiquitously expresse

209 The inositol 1,4,5 trisphosphate receptor (IP3R) is an intracellular Ca(2+)

210 ) pools that are gated by the inositol 1,4,5-trisphosphate receptor (IP3R) types 2 and 3.

211 Inositol 1, 4, 5-trisphosphate receptor (IP3R)-mediated Ca(2+) release fr

212 ylates, and stabilizes type 3 inositol-1,4,5-trisphosphate receptor (IP3R3), modulating calcium (Ca(2

213 on expression of the type II inositol 1,4,5-trisphosphate receptor (ITPR2), the principle calcium re

214 The type 3 isoform of the inositol 1,4,5-trisphosphate receptor (ITPR3) is the most abundant intr

215 ei acidocalcisomes possess an inositol 1,4,5-trisphosphate receptor (TbIP(3)R) for Ca(2+) release.

216 tion of the ER Ca(2+) channel inositol 1,4,5-trisphosphate receptor 1 (IP3R1) in CNG channel-deficien

217 ted by a C terminus "calmodulin and inositol trisphosphate receptor binding" (CIRB) domain.

218 y internal store depletion or inositol 1,4,5-trisphosphate receptor blockade.

219 differential distribution of inositol 1,4,5-trisphosphate receptor channel isoforms in the nucleopla

220 f calcium through clusters of inositol 1,4,5-trisphosphate receptor channels constitute elementary si

221 s) are due to upregulation of inositol-1,4,5-trisphosphate receptor induced Ca(2+) release (IICR) and

222 Inositol 1,4,5-trisphosphate receptor isoforms are a family of ubiquito

223 e is conserved in all RyR and inositol 1,4,5-trisphosphate receptor isoforms.

224 ic P2Y receptors and stimulated the inositol trisphosphate receptor to provoke transient release of c

225 659T>G [p.Phe2553Leu]) in the inositol 1,4,5-trisphosphate receptor type 1 gene (ITPR1).

226 tion is absent in conditional inositol 1,4,5 trisphosphate receptor type 2 KO mice, which lack astroc

227 dine receptor type 2, but not inositol 1,4,5-trisphosphate receptor type 2, were required for the gen

228 alcium uniporter) and TcIP3R (inositol 1,4,5-trisphosphate receptor).

229 tation assay, we found ITPR1 (inositol 1,4,5-trisphosphate receptor, type 1) as a direct novel target

230 A variant (rs718314) in the inositol 1,4,5-trisphosphate receptor, type 2 gene (ITPR2) was found to

231 ry tumors, include C17orf104, inositol 1,4,5-trisphosphate receptor, type 3 (ITPR3), and discoidin do

232 pply our formalism to models of the inositol trisphosphate receptor, which plays a key role in genera

233 ed low-frequency (~2 min(-1)) inositol 1,4,5-trisphosphate receptor-based Ca(2+) events.

234 bfamily 4 channels via type 2 inositol 1,4,5-trisphosphate receptor-mediated Ca(2+) release in subsar

235 tial Ca(2+) rise in PSCs was due to inositol trisphosphate receptor-mediated release from internal st

236 alternative molecular models of the inositol trisphosphate receptor.

237 rs of the phospholipase C and inositol 1,4,5-trisphosphate receptor.

238 um levels via signaling through the inositol trisphosphate receptor.

239 certed opening of tightly clustered inositol trisphosphate receptor/channels (IP(3)R).

240 and global Ca2+ signals mediated by inositol trisphosphate receptor/channels (IP3R) in human neurobla

241 They arise from clustered inositol 1,4,5-trisphosphate receptor/channels (IP3Rs), whose openings

242 A-mediated phosphorylation of inositol-1,4,5-trisphosphate receptors (InsP(3)Rs), which associate wit

243 ative [Ca(2+)](i) feedback on inositol 1,4,5-trisphosphate receptors (InsP(3)Rs).

244 Inositol-1,4,5-trisphosphate receptors (InsP3Rs) are ubiquitous ion cha

245 al Ca(2+) channels, including inositol 1,4,5-trisphosphate receptors (InsP3Rs).

246 , a Markov model for types I and II inositol trisphosphate receptors (IP(3)R) is developed.

247 most potent agonist of d-myo-inositol 1,4,5-trisphosphate receptors (IP(3)R), is thought to mimic IP

248 ic reticulum Ca(2+) channels, inositol 1,4,5-trisphosphate receptors (IP(3)Rs) and ryanodine receptor

249 tamate receptors (mGluRs) and inositol 1,4,5-trisphosphate receptors (IP(3)Rs), supported by higher l

250 gh the ryanodine receptors or inositol 1,4,5-trisphosphate receptors (IP3 R) and upon depletion of sa

251 Inositol 1,4,5-trisphosphate receptors (IP3 Rs) are a family of ubiquit

252 yanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3 Rs) are calcium (Ca(2+) ) r

253 Inositol 1,4,5-trisphosphate receptors (IP3 Rs) are expressed in nearly

254 Inositol-1,4,5-trisphosphate receptors (IP3 Rs) modulate pacemaking in

255 The ability of inositol 1,4,5-trisphosphate receptors (IP3R) to precisely initiate and

256 receptors (RyR2s) and type 2 inositol 1,4,5-trisphosphate receptors (IP3R2s).

257 1,4,5-Inositol trisphosphate receptors (IP3Rs) and ryanodine receptors

258 doplasmic reticulum-localized inositol 1,4,5-trisphosphate receptors (IP3Rs) and the voltage-dependen

259 Tightly clustered inositol trisphosphate receptors (IP3Rs) control localized Ca(2+)

260 s known about the function of inositol 1,4,5-trisphosphate receptors (IP3Rs) in the adult heart exper

261 trongly and constitutively to inositol 1,4,5-trisphosphate receptors (IP3Rs), proteins that form tetr

262 t Bok interacts strongly with inositol 1,4,5-trisphosphate receptors (IP3Rs), suggesting that it may

263 Ca(2+)-induced Ca(2+) release from inositol trisphosphate receptors (IP3Rs).

264 disulfide bond formation in inositol 1, 4, 5-trisphosphate receptors (IP3Rs).

265 e occurs through a cluster of inositol 1,4,5-trisphosphate receptors (IP3Rs).

266 Ca2+ oscillation mediated by inositol 1,4,5-trisphosphate receptors 2 and 3 (ITPR2 and ITPR3) in the

267 the endoplasmic reticulum via inositol 1,4,5-trisphosphate receptors and by Ca(2+) entry via P/Q-type

268 results from potentiation of inositol 1,4,5-trisphosphate receptors and/or phospholipase C.

269 Thus, we have identified inositol trisphosphate receptors as unique effectors of K-Ras4B t

270 ernal stores or inhibition of inositol 1,4,5-trisphosphate receptors but not by inhibition of ryanodi

271 hat sensitization of type 1 inositol (1,4,5)-trisphosphate receptors by mHtt, which depletes endoplas

272 eract with both ryanodine and inositol 1,4,5-trisphosphate receptors during agonist stimulation.

273 channels in the plasma membrane and inositol trisphosphate receptors in the endoplasmic reticulum, le

274 sphorylated K-Ras4B associates with inositol trisphosphate receptors on the ER in a Bcl-xL-dependent

275 either ryanodine receptors or inositol 1,4,5-trisphosphate receptors reduced [Ca(2+)](rest).

276 k mGluR5, and knockout of the inositol 1,4,5-trisphosphate receptors that release Ca(2+) from stores

277 -dependent phosphorylation of inositol 1,4,5-trisphosphate receptors was decreased, reducing cytoplas

278 also blunted by inhibition of inositol 1,4,5-trisphosphate receptors with 2-aminoethoxydiphenyl borat

279 tors, increased expression of inositol-1,4,5-trisphosphate receptors, and differential orientation am

280 c proteins involved in EDH, such as inositol trisphosphate receptors, small and intermediate conducta

281 reticulum Ca(2+) release via inositol 1,4,5-trisphosphate receptors.

282 annels, the ryanodine and the inositol-1,4,5-trisphosphate receptors.

283 henyl borate, an inhibitor of store inositol trisphosphate receptors.

284 certed opening of tightly clustered inositol trisphosphate receptors/channels (IP3Rs).

285 activated by spot-uncaging of inositol 1,4,5-trisphosphate) remain unaffected by GPR55 agonists.

286 ling between SP signaling and inositol 1,4,5-trisphosphate sensitive Ca(2+) stores, together with the

287 is largely uncoupled from the inositol 1,4,5-trisphosphate sensitive Ca(2+) stores.

288 enerative Ca(2+) release from inositol 1,4,5-trisphosphate-sensitive stores followed by Ca(2+) entry

289 due to initial Ca(2+) release from inositol trisphosphate-sensitive stores followed by Ca(2+) entry

290 Disruption of inositol trisphosphate signaling, but not extracellular-regulated

291 eased levels of phosphatidylinositol (3,4,5)-trisphosphate, stimulation of glucose and lipid metaboli

292 with its PIP3 (phosphatidylinositol (3,4,5)-trisphosphate) substrate.

293 IPMK phosphorylates inositol 1,4,5-trisphosphate to inositol tetrakisphosphate and subseque

294 beta to generate diacylglycerol and inositol trisphosphate, two known activators of the PKC pathway.

295 the anchor lipid phosphatidylinositol-3,4,5-trisphosphate unchanged.

296 -bisphosphate and phosphatidylinositol-3,4,5-trisphosphate were below detection limits, phosphatidyli

297 zed production of phosphatidylinositol 3,4,5-trisphosphate, whereas MAPK and Ca(2+) signaling are dis

298 itol phosphates including myo-inositol 1,4,5-trisphosphate, which is a secondary messenger in transme

299 rmation of diacylglycerol and inositol 1,4,5-trisphosphate, which results in the release of intracell

300 nd inhibitable by phosphatidylinositol 3,4,5-trisphosphate, with hours of dofetilide exposure in huma