ライフサイエンスコーパス: trisphosphate

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

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

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

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

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

6 -bisphosphate and phosphatidylinositol 3,4,5-trisphosphate.

7 essengers, diacylglycerol and inositol-1,4,5-trisphosphate.

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

9 intracellular messenger d-myo-inositol 1,4,5-trisphosphate [1, Ins(1,4,5)P(3)] are important syntheti

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

11 d kinome RNAi screen, we identified inositol-trisphosphate 3-kinase B (ITPKB) as a critical enzyme th

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

13 In turn, inositol 1,4,5-trisphosphate 3-kinase B (Itpkb) phosphorylates IP3 to n

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

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

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

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

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 ted hydrolysis of PIP(2) into inositol 1,4,5-trisphosphate and diacylglycerol, which are well known t

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

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

28 osstalk between phosphatidylinositol-(3,4,5)-trisphosphate and inhibitory G-protein-coupled receptor

29 iomers, methyl alpha-d-glucopyranoside 2,3,6-trisphosphate and methyl alpha-d-glucopyranoside 2,4,6-t

30 igands, methyl alpha-l-glucopyranoside 2,3,6-trisphosphate and methyl alpha-l-glucopyranoside 2,4,6-t

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

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

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

34 4-phosphate, diacylglycerol, inositol 1,4,5-trisphosphate, and Ca(2+) upon muscarinic stimulation in

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

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

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

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

39 ,5-biphosphate or phosphatidylinositol 3,4,5-trisphosphate application compared with channels lacking

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

41 ate and methyl alpha-l-glucopyranoside 2,4,6-trisphosphate, are also active, while their correspondin

42 ate and methyl alpha-d-glucopyranoside 2,4,6-trisphosphate, are inactive.

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

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

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

46 ion of the production of IP3 (inositol-1,4,5-trisphosphate) by phospholipase-C and accordingly were n

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

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

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

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

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

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

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

54 5-bisphosphate hydrolysis and inositol 1,4,5-trisphosphate-dependent intra-acrosomal calcium release.

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

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

57 ha) interact with phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchange factor 1 (P-REX1),

58 amma signaling to phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchange factor 1 (P-REX1),

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

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

61 ted against the phosphatidylinositol (3,4,5) trisphosphate-dependent Rac exchanger 1 (P-Rex1) pleckst

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

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

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

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

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

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

68 Here we show that phosphatidylinositol-3,4,5-trisphosphate generation and activated Akt are instead l

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

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

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

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

75 intracellular messenger d-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)].

76 uced by selectively buffering inositol 1,4,5-trisphosphate (InsP(3)) within the nucleus.

77 of phytate and production of inositol-1,4,5-trisphosphate (InsP(3)).

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

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

80 a(2+) ](cyt) oscillation; and inositol 1,4,5-trisphosphate (InsP3) production.

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

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

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

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

85 2, which converts phosphatidylinositol 3,4,5-trisphosphate into phosphatidylinositol 4,5-bisphosphate

86 We propose that inositol 1,4,5-trisphosphate (IP(3) )-dependent Ca(2+) signalling gives

87 It is widely assumed that inositol trisphosphate (IP(3)) and ryanodine (Ry) receptors share

88 dea and indicate that receptors for inositol trisphosphate (IP(3)) and ryanodine may be located in tw

89 Inositol 1, 4, 5-trisphosphate (IP(3)) binding at the N-terminus (NT) of

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

91 pp5a overexpression decreases inositol 1,4,5-trisphosphate (IP(3)) levels and ameliorates Purkinje ce

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

93 The inositol 1,4,5-trisphosphate (IP(3)) receptors (IP(3)Rs), which form te

94 Upon inositol trisphosphate (IP(3)) stimulation of non-excitable cells

95 The 'building-block' model of inositol trisphosphate (IP(3))-mediated Ca(2+) liberation posits

96 However, local inositol trisphosphate (IP(3))-mediated Ca(2+) signaling predomin

97 ilization of Ca(2+) from both inositol 1,4,5-trisphosphate (IP(3))-sensitive stores and caffeine/ryan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 2 (ip3k2), thereby affecting inositol 1,4,5-trisphosphate (IP3) signaling and calcium levels during

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

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

116 T-cell activation releases inositol 1,4,5-trisphosphate (IP3), inducing cytoplasmic calcium (Ca2+)

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

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

119 ospholipase C gamma 2 (PLCG2)/inositol 1,4,5-trisphosphate (IP3)/Ca(2+)/protein kinase C (PKC) pathwa

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

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

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

123 Inositol trisphosphate kinases (IP3Ks) and inositol hexakisphosph

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

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

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

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

128 rmation, distinct phosphatidylinositol 3,4,5-trisphosphate lipid (PI(3,4,5)P3) production and F-actin

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

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

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

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

133 ular Ca(2+), and that the PLC-inositol 1,4,5-trisphosphate pathway, which controls the release of cal

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

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

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

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

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

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

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

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

142 IP5Pase substrate phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P3], and catalytic mutation of P

143 ial generation of phosphatidylinositol-3,4,5-trisphosphate (PI3,4,5P(3)).

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

145 ts, we identify a phosphatidylinositol (3-5)-trisphosphate (PIP(3)) sensing mechanism that achieves s

146 econd messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP(3)) to the axon tip, thus contributin

147 Phosphatidylinositol (3,4,5)-trisphosphate (PIP(3))-dependent Rac exchanger 1 (P-Rex1

148 Phosphatidylinositol (3,4,5) trisphosphate (PIP(3))-dependent Rac exchanger 1 (P-Rex1

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

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

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

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

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

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

155 P2) and reduced phosphatidylinositol (3,4,5)-trisphosphate (PIP3) levels, whereas strong TCR signals

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 n that recognizes phosphatidylinositol 3,4,5-trisphosphate (PIP3).

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

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

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

176 , a decrease of phosphatidylinositol (3,4,5)-trisphosphate pools and AKT activity occurred in MPS-tre

177 Inositol trisphosphate production and release of calcium from int

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

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

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

181 ns that require phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) for their activation.

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

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

184 smic reticulum (ER)-localized inositol 1,4,5-trisphosphate receptor (InsP(3)R) Ca(2+)-release channel

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

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

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

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

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

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

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

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

193 approach, we identify type 1 inositol 1,4,5-trisphosphate receptor (IP(3)R1) as a specific synaptic

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

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

196 PLC/inositol trisphosphate receptor (IP3R) and estrogen receptor co-r

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

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

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

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

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

202 with the Ca2+ channel Orai1 and the inositol trisphosphate receptor (IP3R), thereby linking the endo-

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

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

205 g the neuronal isoform of the inositol 1,4,5-trisphosphate receptor (ITPR1) and genes involved in ino

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

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

208 The type 3 inositol 1,4,5-trisphosphate receptor (ITPR3) is the principal intracel

209 pression and function of the type 3 inositol trisphosphate receptor (ITPR3), because this is the main

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

211 organelles through a channel, inositol 1,4,5-trisphosphate receptor (TbIP(3)R), which is essential fo

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

213 dent Ca(2+) channels, and the inositol 1,4,5-trisphosphate receptor as well as the N-methyl-d-asparta

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

215 Pase, ryanodine receptor, and inositol 1,4,5-trisphosphate receptor channel in various kidney disease

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

217 , ER Ca(2+) release channels, inositol 1,4,5-trisphosphate receptor channel, ryanodine receptor, and

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

219 nd express IP3R3, which is an inositol-1,4,5-trisphosphate receptor constitutively expressed in stem

220 (ITPR1) and genes involved in inositol 1,4,5-trisphosphate receptor degradation (ERLIN1, ERLIN2) are

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 endoplasmic reticulum protein inositol 1,4,5-trisphosphate receptor type 1 (IP3R1), which triggers pr

226 659T>G [p.Phe2553Leu]) in the inositol 1,4,5-trisphosphate receptor type 1 gene (ITPR1).

227 IP(3)R (Inositol-trisphosphate receptor) stimulation produced larger [Ca(

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 lting in reduced phosphorylation of inositol trisphosphate receptor, which mediates endoplasmic retic

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

234 wed that HAX-1 interacts with inositol 1,4,5-trisphosphate receptor-1 (InsP3R1) in the liver, and its

235 d membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kinase subst

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

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

238 um levels via signaling through the inositol trisphosphate receptor.

239 alternative molecular models of the inositol trisphosphate receptor.

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 Inositol 1,4,5-trisphosphate receptors (InsP3Rs) are endoplasmic reticu

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

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

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

246 stimulates Ca(2+) release via inositol 1,4,5-trisphosphate receptors (IP(3)Rs), engaging hypertrophic

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

248 lular calcium release through inositol 1,4,5-trisphosphate receptors (IP(3)Rs).

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

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

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

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

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

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

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

256 1,4,5-Inositol trisphosphate receptors (IP3Rs) and ryanodine receptors

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

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

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

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

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

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

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

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

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

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

267 Activated inositol 1,4,5-trisphosphate receptors are then rapidly degraded by the

268 etermined the distribution of inositol-1,4,5-trisphosphate receptors at MAMs by operating as a scaffo

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

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

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

272 se gene RNF170, which targets inositol 1,4,5-trisphosphate receptors for degradation, are the likely

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

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

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

278 rane (ryanodine receptors and inositol 1,4,5-trisphosphate receptors) of isolated cardiomyocytes to b

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 lease from stores most probably via inositol trisphosphate receptors.

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

283 he nucleoplasmic reticulum by inositol 1,4,5-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 due to initial Ca(2+) release from inositol trisphosphate-sensitive stores followed by Ca(2+) entry

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

288 Our findings highlight inositol 1,4,5-trisphosphate signaling as a candidate key pathway for h

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

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

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

292 m is controlled by binding of inositol 1,4,5-trisphosphate to its receptor.

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

294 ults support the concept that inositol-1,4,5-trisphosphate type 3 receptor signaling in HBCs, togethe

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 interaction of phosphatidylinositol (3,4,5)-trisphosphate with AKT facilitates its interaction with

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