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 ed sensitive to thapsigargin, ionomycin, and inositol trisphosphate.

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

4 rce of the Ca(2+)-releasing second messenger 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 e second messengers diacylglycerol and 1,4,5-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 Here, we identify Inositol-trisphosphate 3-kinase B (Itpkb) as an essentia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 Simultaneous blockade of inositol trisphosphate and ryanodine receptors abolished

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

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

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

44 Inositol-trisphosphate and inositol-hexaphosphate also p

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

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

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

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

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

50 Inositol trisphosphate binds to the type III inositol tr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 Inositol trisphosphates identified in Arabidopsis includ

75 4-AP also increased the second messenger inositol trisphosphate in both neurons and astrocytes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 In addition to inositol trisphosphate, intracellular messengers include

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 3 blocked the denatonium-induced increase of inositol trisphosphate (IP3) in taste tissue.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 D-Inositol trisphosphate is less potent at inhibiting E54K

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

151 Moreover, an inositol trisphosphate kinase negatively regulates this

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

153 Inositol trisphosphate kinases (IP3Ks) and inositol hexa

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

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

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

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

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

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

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

161 Inositol trisphosphate mobilizes intracellular stores of

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

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

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

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

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

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

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

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

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

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

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

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

174 Inositol trisphosphate production and release of calcium

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

176 This stimulated inositol trisphosphate production, activated an nuclear

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 3O-C12 also appears to directly activate the inositol trisphosphate receptor and release Ca(2+) from

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 between alternative molecular models of the inositol trisphosphate receptor.

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

226 paired protein trafficking downstream of the inositol trisphosphate receptor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 1,4,5-Inositol trisphosphate receptors (IP3Rs) and ryanodine r

243 Tightly clustered inositol trisphosphate receptors (IP3Rs) control localiz

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 The depletion of inositol trisphosphate-sensitive intracellular pools of

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

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

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

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

271 Disruption of inositol trisphosphate signaling, but not extracellular-

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

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

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

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

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

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

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