ライフサイエンスコーパス: inositol trisphosphate

1 s were emptied by thrombin, thapsigargin, or inositol trisphosphate.

2 e second messengers diacylglycerol and 1,4,5-inositol trisphosphate.

3 ed sensitive to thapsigargin, ionomycin, and inositol trisphosphate.

4 cellular Ca(2+) stores with thapsigargin, or inositol trisphosphate.

5 acologically distinct from that activated by inositol trisphosphate.

6 totally independent of cyclic ADP-ribose or inositol trisphosphate.

7 tol bisphosphate yielding diacylglycerol and inositol trisphosphate.

8 ol monophosphate, inositol bisphosphate, and inositol trisphosphate.

9 rce of the Ca(2+)-releasing second messenger inositol trisphosphate.

10 e did not cause an increase in either of the inositol trisphosphates.

11 of calcium from intracellular stores through inositol trisphosphates.

12 activate phospholipase C (PLC) and generate inositol trisphosphate (1,4,5).

13 Inositol trisphosphate 3-kinase A (ITPKA) terminates Ins

14 Inositol trisphosphate 3-kinase B (InsP3KB) belongs to a

15 In particular, inhibitors of p38, inositol trisphosphate 3-kinase, and Aurora A kinase pot

16 The overall structure of Ipk2 is related to inositol trisphosphate 3-kinase.

17 sm-related kinome RNAi screen, we identified inositol-trisphosphate 3-kinase B (ITPKB) as a critical

18 Here, we identify Inositol-trisphosphate 3-kinase B (Itpkb) as an essentia

19 Here we show that inositol-trisphosphate 3-kinase B (Itpkb) via its enzyma

20 or, phosphoinositide 3-kinase (PI3K), and by inositol-trisphosphate 3-kinase B (Itpkb).

21 LIGRL (an agonist peptide for PAR-2) promote inositol trisphosphate accumulation, stimulate mitogen-a

22 domain sequence (SFLLRN) and which promotes inositol trisphosphate accumulation, stimulates extracel

23 products of this enzyme, diacylglycerol and inositol trisphosphate, activate the conventional and no

24 In addition, neither di-C4-PI(4,5)P2 nor inositol trisphosphate-activated PTEN.

25 cases and for all concentrations tested, the inositol trisphosphate analogues induced biphasic transi

26 investigation of the effects of a number of inositol trisphosphate analogues on the transient kineti

27 Both [3H]inositol trisphosphate and [3H]inositol hexakisphosphate

28 spholipase C, resulting in the liberation of inositol trisphosphate and Ca2+ release from intracellul

29 , light increases the intracellular level of inositol trisphosphate and causes the dispersion of mela

30 physiological experiments indicate that both inositol trisphosphate and cyclic nucleotides function i

31 e hydrolysis, resulting in the production of inositol trisphosphate and diacylglycerol (DAG).

32 activates phospholipase C with production of inositol trisphosphate and diacylglycerol in part by for

33 ch hydrolyze inositol phospholipids to yield inositol trisphosphate and diacylglycerol, are regulated

34 In addition to being the precursor of inositol trisphosphate and diacylglycerol, it complexes

35 hat PIP2, in addition to being the source of inositol trisphosphate and diacylglycerol, two messenger

36 beta2, which produces the second messengers inositol trisphosphate and diacylglycerol.

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

38 described Ca2+ stores that are sensitive to inositol trisphosphate and from mitochondrial Ca2+ store

39 glioma cells reduced intracellular levels of inositol trisphosphate and inhibited extracellular Ca2+

40 ereas the inhibitors of PLC (U73122) and the inositol trisphosphate and ryanodine receptors (xestospo

41 Simultaneous blockade of inositol trisphosphate and ryanodine receptors abolished

42 n as inositol polyphosphate multikinase), an inositol trisphosphate and tetrakisphosphate 6/5/3-kinas

43 hand, the induction of the second messenger inositol trisphosphate and the mobilization of calcium a

44 ylcarboxamidodoadenosine (IB-MECA) stimulate inositol trisphosphates and calcium accumulation in HEK-

45 Inositol-trisphosphate and inositol-hexaphosphate also p

46 increases in PEt and diacylglycerol, but not inositol trisphosphate, and by reduction of GnRH-induced

47 Thus, inositol trisphosphate, and not calcium, diffused intere

48 he two phases appeared to be similar for all inositol trisphosphates (approximately 45% for the fast

49 the second messenger systems cyclic AMP and inositol trisphosphate are important in transducing bitt

50 The method can detect channels activated by inositol trisphosphate, as well as other types of intrac

51 Inositol trisphosphate binds to the type III inositol tr

52 e occurrence of neuronal domains seems to be inositol trisphosphate but not calcium.

53 We have shown previously that inositol trisphosphate, Ca2+/calmodulin-dependent protei

54 These data show that the inositol trisphosphate/calcium arm of the phospholipase

55 lular Ca by intracellular messengers such as inositol trisphosphate, cellular ion pumps and membrane

56 aring the rate constants for Ca2+ release at inositol trisphosphate concentrations for the analogues

57 Ca signaling involves the interaction of inositol trisphosphate, cyclic ADP ribose, and nicotinic

58 hich is based on time-course measurements of inositol trisphosphate, cytosolic calcium, and diacylgly

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

60 coupled AT1A receptors via activation of the inositol trisphosphate-dependent intracellular Ca2+ rele

61 e C-coupled signalling cascade involving the inositol trisphosphate-dependent mobilization of intrace

62 The rate constants for all other inositol trisphosphates did not appear to exceed 0.4 s-1

63 llations, which are dependent on the P2R/PLC/inositol trisphosphate/ER pathway.

64 by more transient Ca2+ signals generated by inositol trisphosphate-evoked release of endoplasmic ret

65 t significantly inhibit carbachol-stimulated inositol trisphosphate formation and did not alter the i

66 on carbachol-stimulated aminopyrine uptake, inositol trisphosphate formation, and intracellular Ca2+

67 anism that does not involve major changes in inositol trisphosphate formation.

68 ted CRAC channels in the plasma membrane and inositol trisphosphate-gated channels in the endoplasmic

69 ted that Edg2 and Edg4 mobilize Ca2+ through inositol trisphosphate generated by phospholipase C acti

70 duced subsequent U46619-induced increases in inositol trisphosphate generation by both receptors; how

71 In contrast, TxA2-induced inositol trisphosphate generation by the mutant receptor

72 n, as assayed by either Ca2+ mobilization or inositol trisphosphate generation, was greatly reduced i

73 tgrowth depends on phospholipase C (PLC) --> inositol trisphosphate --> Ca(2+) --> calcineurin signal

74 Inositol trisphosphate has been joined by two other Ca-r

75 Inositol trisphosphates identified in Arabidopsis includ

76 4-AP also increased the second messenger inositol trisphosphate in both neurons and astrocytes.

77 ycerol (decrease in ERK phosphorylation) and inositol trisphosphate (increase in [Ca(2+)](i) and flui

78 n induce intracellular calcium release in an inositol trisphosphate-independent manner and has been h

79 at fertilization of mammalian eggs requires inositol trisphosphate, indicating that an enzyme of the

80 do not release Ca2+, nor do they potentiate inositol trisphosphate-induced Ca2+ entry across the pla

81 Ca2+ channels by angiotensin is mediated by inositol trisphosphate-induced intracellular Ca2+ releas

82 Along with the inositol trisphosphate-induced release of stored Ca(2+),

83 yphosphate kinases rIPK2, a dual specificity inositol trisphosphate/inositol tetrakisphosphate kinase

84 phosphatidylinositol bisphosphate, producing inositol trisphosphate (InsP(3)) and diacylglycerol (DAG

85 The inositol trisphosphate (InsP(3)) receptor (InsP(3)R) is

86 ssembly of Na/Ca exchanger, Na/K ATPase, and inositol trisphosphate (InsP(3)) receptor at transverse-

87 excitation-contraction coupling, whereas the inositol trisphosphate (InsP(3)) receptors are separatel

88 centrations of Taxol leads to a reduction in inositol trisphosphate (InsP(3))-mediated Ca(2+) signali

89 seline of the Ca(2+) transient induced by an inositol-trisphosphate (InsP(3))-linked plasma membrane

90 In cerebellum, inositol trisphosphate- (InsP(3)-) gated Ca channels pla

91 Inositol trisphosphate (InsP3) and cyclic adenosine 5'-d

92 Purkinje neurons contain both inositol trisphosphate (InsP3) and ryanodine (Ry) recept

93 Photolysis of caged inositol trisphosphate (InsP3) close to the plasma membr

94 Inositol trisphosphate (InsP3) had no effect on the same

95 gs, where we found that specific infusion of inositol trisphosphate (InsP3) into either distal or pro

96 cillations are not affected by inhibition of inositol trisphosphate (InsP3) production or blockade of

97 sitive and a negative feedback signal on the inositol trisphosphate (InsP3) receptor.

98 The quantal behaviour of inositol trisphosphate (InsP3) receptors allows rapid gr

99 activation of phospholipase C and opening of inositol trisphosphate (InsP3) receptors.

100 excitation-contraction coupling, and smaller inositol trisphosphate (InsP3)-activated Ca2+ channels.

101 l cycle calcium signals are generated by the inositol trisphosphate (InsP3)-mediated release of calci

102 intracellular calcium (Ca2+i) transients by inositol trisphosphate (InsP3)-mediated release of intra

103 In addition to inositol trisphosphate, intracellular messengers include

104 It is widely assumed that inositol trisphosphate (IP(3)) and ryanodine (Ry) recept

105 ge this idea and indicate that receptors for inositol trisphosphate (IP(3)) and ryanodine may be loca

106 cellular Ca(2+) stores via the production of inositol trisphosphate (IP(3)) and the consequent activa

107 n of PhLP had no effect on Ang II-stimulated inositol trisphosphate (IP(3)) formation, whereas furthe

108 f known elementary Ca(2+) signalling events, inositol trisphosphate (IP(3)) receptor mediated blips,

109 including NHE3 regulatory factors (NHERFs), inositol trisphosphate (IP(3)) receptor-binding protein

110 ze Ca(2+) from the endoplasmic reticulum via inositol trisphosphate (IP(3)) receptors, but how a sing

111 Upon inositol trisphosphate (IP(3)) stimulation of non-excita

112 ulum Ca(2+) stores as a result of binding of inositol trisphosphate (IP(3)) to IP(3) receptors, follo

113 of IP(3)R depending on the concentrations of inositol trisphosphate (IP(3)), adenosine trisphosphate

114 adation of PI 4,5-bisphosphate to form [(3)H]inositol trisphosphate (IP(3)), CaR stimulated the accum

115 phospholipase Cgamma-mediated production of inositol trisphosphate (IP(3)), indicating that a tyrosi

116 Instead, we observed spontaneous and inositol trisphosphate (IP(3))-evoked Ca(2+) signals wit

117 The 'building-block' model of inositol trisphosphate (IP(3))-mediated Ca(2+) liberatio

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

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

120 spholipase C, the intercellular diffusion of inositol trisphosphate (IP(3), and to a lesser extent Ca

121 tagamma-, phospholipase Cbeta (PLCbeta)- and inositol trisphosphate (IP) receptor-dependent manner, w

122 ggered spatiotemporally complex, propagating inositol trisphosphate (IP3 )-mediated Ca(2+) waves that

123 r cells where intracellular infusion of both inositol trisphosphate (IP3) and cADPR evoke repetitive

124 NAADP, inositol trisphosphate (IP3) and cyclic ADP-ribose (cADP

125 ied metabolite of NADP+ that is as potent as inositol trisphosphate (IP3) and cyclic ADP-ribose (cADP

126 gamma), which produces the second messengers inositol trisphosphate (IP3) and diacylglycerol, we used

127 the subsequent quest led to the discovery of inositol trisphosphate (IP3) and its role in calcium sig

128 s were elicited by intracellular infusion of inositol trisphosphate (IP3) but not of calcium, indicat

129 Ang II-stimulated inositol trisphosphate (IP3) formation measured at 15 s,

130 Although inositol trisphosphate (IP3) functions in releasing Ca2+

131 e and a number of agents including sperm and inositol trisphosphate (IP3) generate Ca2+ transients.

132 relevance of this observation, intracellular inositol trisphosphate (IP3) generation and calcium rele

133 ependent Btk activation led to enhanced peak inositol trisphosphate (IP3) generation and depletion of

134 3 blocked the denatonium-induced increase of inositol trisphosphate (IP3) in taste tissue.

135 id not alter basal Ca2+ or the intracellular inositol trisphosphate (IP3) pool after 6 h butyrate cot

136 Whereas much attention has been devoted to inositol trisphosphate (IP3) production and intracellula

137 rt mediated by TGFbeta-induced inhibition of inositol trisphosphate (IP3) production, leading to a de

138 osphorylation of PLC gamma 1, and subsequent inositol trisphosphate (IP3) production, which preceded

139 were abolished by phospholipase C (PLC) and inositol trisphosphate (IP3) receptor antagonists U73122

140 Accordingly, the total amount of inositol trisphosphate (IP3) receptor protein was decrea

141 parin, a competitive inhibitor of the 1,4, 5-inositol trisphosphate (IP3) receptor, suggesting that C

142 endoplasmic reticulum (ER) as determined by inositol trisphosphate (IP3) receptor/Ca2+ channels and

143 Antagonists of phospholipase C, inositol trisphosphate (IP3) receptors and ryanodine rec

144 Inhibiting inositol trisphosphate (IP3) receptors with a high conce

145 mbosis, activators cause a transient rise in inositol trisphosphate (IP3) to trigger calcium mobiliza

146 eported that synthetic receptor 1 recognizes inositol trisphosphate (IP3) with a binding constant of

147 osolic free calcium [Ca2+]i, accumulation of inositol trisphosphate (IP3), and redistribution of Ca2+

148 racellular messengers, cyclic AMP (cAMP) and inositol trisphosphate (IP3), are thought to mediate thi

149 an submandibular gland cells with carbachol, inositol trisphosphate (IP3), thapsigargin, or tert-buty

150 ropagation, both of which involve release of inositol trisphosphate (IP3)- sensitive intracellular ca

151 The large Ca(2+) wave in aroused mice was inositol trisphosphate (IP3)-dependent, evoked by the lo

152 o organelles and strengthens the efficacy of inositol trisphosphate (IP3)-induced Ca(2+) transfer fro

153 We previously reported decreased inositol trisphosphate (IP3)-mediated Ca(2+) release fro

154 These properties were first demonstrated for inositol trisphosphate (IP3)-sensitive channels and used

155 l astrocytes was dependent on intracellular (inositol trisphosphate [IP3]) and extracellular voltage-

156 est that both the generation and response to inositol trisphosphate is highly compartmentalized withi

157 D-Inositol trisphosphate is less potent at inhibiting E54K

158 When the level of the channel activator inositol trisphosphate is low, the wave undergoes fragme

159 Moreover, an inositol trisphosphate kinase negatively regulates this

160 sregulated genes in the AD portrait were the inositol trisphosphate kinase, ITPKB (upregulated), the

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

162 Inositol trisphosphate kinases (IP3Ks) and inositol hexa

163 ases canine mastocytoma cell cAMP, Ca2+, and inositol trisphosphate levels; these responses are antag

164 Using diacylglycerol-stimulated TRPC6 and inositol trisphosphate-mediated Ca(2+) transients as cel

165 ise from muscarinic receptor stimulation and inositol trisphosphate-mediated Ca2+ release.

166 es potassium-calcium counterion exchange for inositol trisphosphate-mediated calcium ion release.

167 This increase was abrogated by inhibiting inositol trisphosphate-mediated calcium release with Xes

168 te potassium-calcium counterion exchange for inositol trisphosphate-mediated calcium release.

169 eggs, the Ca(2+) rise occurs as a result of inositol trisphosphate-mediated release of Ca(2+) from t

170 non-desensitizing receptors evoked prolonged inositol-trisphosphate-mediated Ca(2+) release, which le

171 served as a basis for stochastic modeling of inositol-trisphosphate-mediated calcium responses.

172 Inositol trisphosphate mobilizes intracellular stores of

173 pholipase C to generate the second messenger inositol trisphosphate often evokes repetitive oscillati

174 ger, with that of the prototypical messenger inositol trisphosphate on cytosolic Ca2+ levels and diff

175 s show that brief elevation of intracellular inositol trisphosphate or Ca2+ is sufficient to gate TRP

176 bsolute requirement for a gradient in either inositol trisphosphate or cyclic ADP-ribose, respectivel

177 Ca(2+) waves mediated by inositol trisphosphate or ryanodine receptors propagate

178 in the cell membrane without producing DAG, inositol trisphosphate, or calcium signals.

179 vidence for involvement of protein kinase C, inositol trisphosphate, or intracellular calcium.

180 otein kinase C (PKC) in this regulation, the inositol trisphosphate pathway was bypassed by direct ac

181 protein, phospholipase C, diacylglycerol and inositol trisphosphate pathway, to increase the expressi

182 release mediated by the phospholipase C and inositol trisphosphate pathways.

183 votal role in mediating opioid modulation of inositol trisphosphate production and cytosolic calcium

184 ulation in CD45- cells, despite much reduced inositol trisphosphate production and lack of calcium mo

185 Inositol trisphosphate production and release of calcium

186 llular calcium concentration ([Ca(2+)]i) and inositol trisphosphate production and, subsequently, to

187 This stimulated inositol trisphosphate production, activated an nuclear

188 e of intracellular calcium concentration and inositol trisphosphate production, and, subsequently, th

189 -/- cells, but intermediate events including inositol trisphosphate production, calcium mobilization,

190 phosphorylation, Ca2+ mobilization, and only inositol trisphosphate production, which were not of a s

191 uced store depletion may be due to increased inositol trisphosphate production.

192 amma (PLCgamma) tyrosine phosphorylation and inositol trisphosphate production.

193 The inositol trisphosphate receptor ([Formula: see text]) is

194 Antiapoptotic Bcl-x(L) binds to the inositol trisphosphate receptor (InsP(3)R) Ca(2+) releas

195 bition or knockdown of the expression of the inositol trisphosphate receptor (InsP(3)R) Ca(2+) releas

196 In DT40 chicken B lymphocytes, the permeant inositol trisphosphate receptor (InsP(3)R) modifier, 2-a

197 tabotropic glutamate receptor (DmGluRA), the inositol trisphosphate receptor (InsP(3)R), or inositol

198 A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-ami

199 Genetic reduction of the type 1 inositol trisphosphate receptor (InsP3R1) by 50% normali

200 ctional properties and spatial clustering of inositol trisphosphate receptor (IP(3)R) Ca(2+) release

201 e regulated by a reversible interaction with inositol trisphosphate receptor (IP(3)R) in the endoplas

202 hat altered regulation of the Ca(2+) channel inositol trisphosphate receptor (IP(3)R) was an adipocyt

203 ease of endoplasmic reticulum Ca(2+) via the inositol trisphosphate receptor (IP(3)R), increased mito

204 release through ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3 R) channels is supp

205 by periodic calcium release mediated by the inositol trisphosphate receptor (IP3 receptor).

206 PLC/inositol trisphosphate receptor (IP3R) and estrogen rece

207 release through ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3R) channels is suppo

208 y it to examine the clustered arrangement of inositol trisphosphate receptor (IP3R) channels underlyi

209 we demonstrate that Ca(+2) released via the inositol trisphosphate receptor (IP3R) increases nuclear

210 topology, processing, and oligomerization of inositol trisphosphate receptor (IP3R) isoforms, we have

211 GTP-binding protein, induces association of inositol trisphosphate receptor (IP3R) with transient re

212 ructures with the Ca2+ channel Orai1 and the inositol trisphosphate receptor (IP3R), thereby linking

213 One is the inositol trisphosphate receptor (ITPR), a channel that m

214 xin on expression and function of the type 3 inositol trisphosphate receptor (ITPR3), because this is

215 rotein 12.6 (FKBP12.6) were reduced, whereas inositol trisphosphate receptor (type 2) and Ca/calmodul

216 tyrosine kinase activity, was independent of inositol trisphosphate receptor activation, and required

217 The inositol trisphosphate receptor activator, inositol 2,4,

218 3O-C12 also appears to directly activate the inositol trisphosphate receptor and release Ca(2+) from

219 intracellular calcium signals via opening of inositol trisphosphate receptor and ryanodine receptor (

220 +), mediated by a C terminus "calmodulin and inositol trisphosphate receptor binding" (CIRB) domain.

221 inated by phospholipase Cbeta inhibition and inositol trisphosphate receptor blockade.

222 and the endoplasmic reticulum (ER)-localized inositol trisphosphate receptor Ca(2+) release channel (

223 We show that an inositol trisphosphate receptor can act as a RAS-indepen

224 eceptors, heterotrimeric G proteins, and the inositol trisphosphate receptor have all been shown to b

225 restoration of abnormal localization of the inositol trisphosphate receptor in the sarcoplasmic reti

226 -InsP(3) binding studies indicated that this inositol trisphosphate receptor inhibitor (IRI) could co

227 ulum Ca(2+) pump inhibitor thapsigargin, the inositol trisphosphate receptor inhibitor xestospongin D

228 ells in the same tissue containing different inositol trisphosphate receptor isoforms.Within pA, four

229 Inhibition of Gi, phospholipase C, or inositol trisphosphate receptor prevented the S1P-activa

230 h as CXCR4 and agonists mediating Ca2+ flux (inositol trisphosphate receptor subtype 2) are induced b

231 purinergic P2Y receptors and stimulated the inositol trisphosphate receptor to provoke transient rel

232 is predicted to differentially impact local inositol trisphosphate receptor transport.

233 -permeable, hyperphosphorylated state of the inositol trisphosphate receptor type 1 (IP3R-1).

234 ntigen; PCNA) or calcium channel expression (inositol trisphosphate receptor type 1; IP(3)R1) using i

235 nd intracellular Ca2+ release channels (e.g. inositol trisphosphate receptor) in neurons, which poten

236 in airway epithelial cells by activating the inositol trisphosphate receptor, thus lowering [Ca(2+)]

237 Inositol trisphosphate binds to the type III inositol trisphosphate receptor, which causes the releas

238 ies, resulting in reduced phosphorylation of inositol trisphosphate receptor, which mediates endoplas

239 We apply our formalism to models of the inositol trisphosphate receptor, which plays a key role

240 restricted membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kin

241 The initial Ca(2+) rise in PSCs was due to inositol trisphosphate receptor-mediated release from in

242 lar calcium levels via signaling through the inositol trisphosphate receptor.

243 between alternative molecular models of the inositol trisphosphate receptor.

244 bilization by the ryanodine receptor and the inositol trisphosphate receptor.

245 paired protein trafficking downstream of the inositol trisphosphate receptor.

246 rough concerted opening of tightly clustered inositol trisphosphate receptor/channels (IP(3)R).

247 on local and global Ca2+ signals mediated by inositol trisphosphate receptor/channels (IP3R) in human

248 n membrane protein, MrcA, interacts with the inositol-trisphosphate receptor (IP(3)R), an ER cationic

249 cid, calcineurin-Bcl-2 and calcineurin-1,4,5-inositol-trisphosphate receptor (IP3-R) interactions inc

250 proteins, Ca(2+) pump type 2 (SERCA 2), and inositol-trisphosphate receptor type 1 (IP(3)R-1).

251 IP(3)R (Inositol-trisphosphate receptor) stimulation produced la

252 ontent, by imaging Ca(2+) liberation through inositol trisphosphate receptors (IP(3)R) in Xenopus ooc

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

254 ent on external calcium entry acting on both inositol trisphosphate receptors (IP(3)Rs) and ryanodine

255 nvolved in regulating neuronal [Ca(2+)](i) : inositol trisphosphate receptors (IP(3)Rs) and sarcoplas

256 channels like ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP(3)Rs) mediate large

257 e application of adenophostin, an agonist of inositol trisphosphate receptors (IP(3)Rs) that evokes C

258 at Trp3 can be regulated by interacting with inositol trisphosphate receptors (IP(3)Rs), reminiscent

259 he ER through ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP(3)Rs), respectively

260 Heparin inhibition of endogenous inositol trisphosphate receptors (IP3R) had little effec

261 ed Ca2+ entry in this cell type depends upon inositol trisphosphate receptors (IP3R).

262 rm a physical tether linking mGluRs with the inositol trisphosphate receptors (IP3R).

263 1,4,5-Inositol trisphosphate receptors (IP3Rs) and ryanodine r

264 Tightly clustered inositol trisphosphate receptors (IP3Rs) control localiz

265 agated by Ca(2+)-induced Ca(2+) release from inositol trisphosphate receptors (IP3Rs).

266 resynaptic ER ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs).

267 ropic glutamate receptors with intracellular inositol trisphosphate receptors and is modified by neur

268 al inhibitor of PLC-gamma1, or inhibitors of inositol trisphosphate receptors and PKC, increased thei

269 In human airway goblet cells, inositol trisphosphate receptors are found in rough endo

270 cular myocytes and also that CaMKIIdelta and inositol trisphosphate receptors are upregulated in HF.

271 Thus, we have identified inositol trisphosphate receptors as unique effectors of

272 (TRPV4) channels in the plasma membrane and inositol trisphosphate receptors in the endoplasmic reti

273 ound, phosphorylated K-Ras4B associates with inositol trisphosphate receptors on the ER in a Bcl-xL-d

274 that chronic upregulation and activation of inositol trisphosphate receptors, CaMKII, and PKD in HF

275 d by a pharmacological block of ryanodine or inositol trisphosphate receptors, indicating that global

276 in group I metabotropic glutamate receptors, inositol trisphosphate receptors, ryanodine receptors, a

277 Specific proteins involved in EDH, such as inositol trisphosphate receptors, small and intermediate

278 group 1 metabotropic glutamate receptors and inositol trisphosphate receptors, thereby coupling these

279 red by release from stores most probably via inositol trisphosphate receptors.

280 ermed Homer, that cross-link the receptor to inositol trisphosphate receptors.

281 ethoxydiphenyl borate, an inhibitor of store inositol trisphosphate receptors.

282 h the concerted opening of tightly clustered inositol trisphosphate receptors/channels (IP3Rs).

283 of Ca2+ from internal stores by caffeine or inositol trisphosphate reduced the EPSCs by 36 +/- 5 and

284 stores that are distinct from G(q)-mediated inositol trisphosphate-regulated stores.

285 n comprising the major storage reservoir for inositol trisphosphate-releasable calcium.

286 or activator, augmented the calcium-elicited inositol trisphosphate response of cloned human keratino

287 which deplete intracellular Ca2+ stores via inositol trisphosphate-sensitive channels, did not activ

288 The depletion of inositol trisphosphate-sensitive intracellular pools of

289 osine kinase activity by releasing Ca++ from inositol trisphosphate-sensitive intracellular stores.

290 taxel does not affect Ca(2+) release from an inositol trisphosphate-sensitive store.

291 nals were due to initial Ca(2+) release from inositol trisphosphate-sensitive stores followed by Ca(2

292 smic/endoplasmic reticulum Ca(2+)-ATPases or inositol trisphosphate signaling had no effect on [Ca(2+

293 Disruption of inositol trisphosphate signaling, but not extracellular-

294 nificantly lose their ability to up-regulate inositol trisphosphate synthesis in response to TCR liga

295 tivation and the Btk-dependent generation of inositol trisphosphate that regulates sustained calcium

296 much larger for Ins(1,4,5)P3 than the other inositol trisphosphates (the fast phase rate constant va

297 on of PLCbeta to generate diacylglycerol and inositol trisphosphate, two known activators of the PKC

298 One selected gene is Itpr2, encoding the inositol trisphosphate type two receptor, which is trans

299 ition between Ca2+ -induced Ca2+ release and inositol trisphosphate waves occurs at higher synaptic i

300 th control T cells, the background levels of inositol trisphosphate were significantly elevated in NT