ライフサイエンスコーパス: IP3

1 IP3 R modulation also regulates Ca(2+) spark parameters,

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

3 IP3 Rs are also substrates for the intracellular cystein

4 IP3 Rs determine the site of initiation and the pattern

5 IP3 uncaging also triggers oscillatory Ca(2+) release, b

6 IP3-induced calcium release (IICR) is increased during E

7 IP3-induced priming was prevented by pretreatment with i

8 ion from enhanced activity in the Galphaq/11-IP3 pathway, resulting in abnormal Ca(2+) release and co

9 In type 2 IP3 R (IP3 R2) knockout atrial myocytes, Ishear was 10-2

10 sociated with increased expression of type 2 IP3-R (IP3-R(2)) and heightened generation of Ins(1,4,5)

11 urther crossed with mice in which the type 2 IP3-R (IP3-R(2)-/-) had been deleted (DCM-2TgxIP3-R(2)-/

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

13 Inhibitors of phospholipase C (U-73122), IP3 (2-APB), ryanodine receptors (Ryanodine) and SERCA p

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

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

16 hibition, and phosphoinositide 3 kinase/Akt (IP3/Akt) inhibition, indicating that PRR regulates NOX a

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

18 aminoethoxydiphenylborane (10 muM, n =6), an IP3 channel antagonist.

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

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

21 SMC stimulation causes an IP3-mediated Ca(2+) transient in the MPs with limited gl

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

23 4,5-trisphosphate (IP3) receptor (ITPR1), an IP3-gated, endoplasmic reticulum (ER)-resident Ca(2+) ch

24 O SAN cells in the presence or absence of an IP3 R blocker (2-aminoethoxydiphenyl borate, 2-APB), or

25 racellular stores following activation of an IP3-dependent pathway-is lacking.

26 sitol 1,4,5-trisphosphate (IP3) receptor, an IP3-gated Ca(2+) channel on the endoplasmic reticulum (E

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

28 cells through Ang II-independent ERK1/2 and IP3/Akt activation.

29 e second messengers diacylglycerol (DAG) and IP3 and ultimately results in microneme secretion.

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

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

32 was undetectable, NHERF-1 mislocalized, and IP3 R3 more intensely stained, along with increased leve

33 of this domain in complex with PI(4,5)P2 and IP3 at resolutions of 1.75 and 1.9 A, respectively, unve

34 Similar increases in Ins(1,4,5)P3 and IP3-R(2) are caused by transverse aortic constriction.

35 plasmic reticulum (ER) through ryanodine and IP3 channels activates the mitochondrial permeability tr

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

37 mity ligation assays revealed that TRPM4 and IP3 R2 were expressed at peripheral sites with co-locali

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

39 activity and/or IP3 metabolism to attenuate IP3 levels and suppress the generation of Ca(2+) oscilla

40 ha-dependent, reciprocal interaction between IP3 and ryanodine receptors that contributes to sex diff

41 s) release Ca(2+) from the ER when they bind IP3 and Ca(2+).

42 ion of a mutated fragment of IP3R that binds IP3 with very high affinity, or blocking formation of th

43 of-function enhancement is sensitive to both IP3 and Ca(2+) and that very small amount of IP3 is requ

44 eric architecture and are still activated by IP3 binding despite the loss of peptide continuity.

45 P3R subtypes are regulated differentially by IP3, Ca(2+), ATP, and various other cellular factors and

46 data indicate that oscillations elicited by IP3 uncaging are driven by the biphasic regulation of th

47 not perturb Ca(2+) oscillations elicited by IP3 uncaging, indicating that reloading of endoplasmic r

48 Modulation of Ca(2+) clock frequency by IP3 signalling in NCX KO SAN cells demonstrates that the

49 tions suggest that the signal is mediated by IP3 rather than Ca(2+) diffusion and that a localized ra

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

51 ii) under resting conditions, propagation by IP3 Rs requires sensitisation by influx of Ca(2+) via re

52 in their ability to be regulated robustly by IP3 .

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

54 phate (IP3) receptors by photolysis of caged IP3 The rate of Ca(2+) removal from the cytosol was unaf

55 tors stimulated with IP3 released from caged-IP3 .

56 ation; stable in zero extracellular calcium; IP3-activatable; and functional SOCE.

57 PLCbeta3 catalyzes IP3 production in T-ALL as opposed to PLCgamma1 in norma

58 In this scenario, stimulation of the cleaved IP3 R may support distinct spatiotemporal Ca(2+) signals

59 clock is uncoupled from the membrane clock, IP3 R agonists and antagonists modulate the rate of spon

60 the order of presentation of its coagonists, IP3 and cytoplasmic calcium.

61 t IP3R model parameters, IP3 concentration ([IP3]) and the recovery rate from Ca(2+) inhibition (rlow

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

63 tified (opioid receptor and PKA/CREB and DAG/IP3 signalling pathways) are genetically associated with

64 their downstream effectors PKA/CREB and DAG/IP3.

65 hol exposure by increasing hormone-dependent IP3 formation, leading to aberrant calcium increases, wh

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

67 evented the induction of priming by low-dose IP3 in females.

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

69 ce of elevated [Ca](i), PA addition elevated IP3 mass to levels equivalent to that induced by sperm (

70 timally placed to be activated by endogenous IP3 and to regulate Ca(2+) entry.

71 Increased pressure suppressed endothelial IP3 -mediated Ca(2+) signals.

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

73 gating scheme with variable non-equilibrium IP3 binding.

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

75 y PGE2, but PGE2 attenuated histamine-evoked IP3 accumulation.

76 For IP3 induced priming, females were also more sensitive.

77 ll death by uncoupling regions important for IP3 binding from the channel domain, leaving an unregula

78 tide continuity is clearly not necessary for IP3 -gating of the channel, we propose that cleavage of

79 ate that RyRs, but not NCX, are required for IP3 to modulate Ca(2+) clock frequency.

80 ddition, there is a specific requirement for IP3 and PKC, as well as protein interacting with C kinas

81 ts in a switch in the enzyme responsible for IP3-induced endoplasmic reticulum Ca(2+) release and oxi

82 more, ITPR1 p.Lys2563del mutant did not form IP3-induced Ca(2+) channels but exerted a negative effec

83 late AHPs by influencing Ca(2+) release from IP3 -triggered Ca(2+) stores, suggesting more direct mod

84 Upon sperm-egg fusion, Ca(2+) release from IP3-sensitive endoplasmic reticulum stores results in cy

85 from dendrites and required both functional IP3 and ryanodine receptor channels.

86 3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors (IP3Rs) located on the endoplasmic reticul

87 l and endoplasmic reticulum Ca(2+) handling, IP3 production, and GTP-binding protein-coupled receptor

88 duration; local sequestration produces high IP3 amplitude, but of short duration.

89 Stimulated synthesis can indeed lead to high IP3 amplitude of long duration; local sequestration prod

90 rol cells stimulated by significantly higher IP3 concentrations.

91 These combined findings implicate IP3-gated Ca(2+) as a key regulator of TDP-43 nucleoplas

92 explicit formulas determining how changes in IP3-mediated Ca(2+) release, under varying conditions of

93 We propose that deficits in IP3-mediated Ca(2+) signaling represent a convergent hub

94 hat E2 stimulates a much greater increase in IP3 levels in females than males, whereas the group I mG

95 Ten-fold increases in IP3 caused saturated calcium mobilization.

96 ripheral localization of TRPM4 was intact in IP3 R2 knockout cells.

97 of phosphoinositides and an 80% reduction in IP3 generation upon platelet activation.

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

99 t mechanisms such as stochastic variation in IP3 binding and channel recruitment by CICR further dete

100 Alternatively, increased IP3 production induced by phenylephrine increased Ca(2+)

101 ediate-term facilitation including increased IP3, Ca(2+), and membrane insertion and recruitment of c

102 c-RAF/MEK/ERK1/2 phosphorylation, increased IP3 amounts, and increased Ca(2+)-dependent calcineurin

103 eas the group I mGluR agonist DHPG increases IP3 levels equivalently in each sex.

104 For increasing IP3 concentration, the release events become modulated a

105 deficiency does not affect receptor-induced IP3 production, but Selk deficiency through genetic dele

106 order polyamines, this interaction inhibited IP3-dependent airway smooth muscle contraction.

107 ling domain of the IP3 receptor and inhibits IP3-dependent channel opening, Ca(2+) release from the E

108 to the supralinear dynamics of intracellular IP3 and that the heterogeneity of the responses may be d

109 eventing formation of its activating ligand, IP3.

110 llowing activation by binding of its ligand, IP3, it releases Ca(2+) from the stores.

111 directly sensitizes the IP3R to its ligand, IP3.

112 ment near IP3 receptor microdomains to limit IP3 -mediated Ca(2+) signals as pressure increased.

113 s the physiological relevance of D1-mediated IP3 production.

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

115 Ca(2+) in response to the second messengers IP3 and cADPR (ER) or NAADP (acidic organelles).

116 -induced generation of the second messengers IP3 and Cai and keratinocyte differentiation.

117 porally control levels of second messengers, IP3, phosphatidylinositol (3,4,5)-triphosphate, and cAMP

118 1, R2, and R3) by key functional modulators (IP3, Ca(2+), and ATP).

119 s obtained under optimal Ca(2+) and multiple IP3 concentrations to gain deeper insights into the enha

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

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

122 In cultured male DRG neurons, IP3 (100 mum) potentiated depolarization-induced transie

123 (2+) store content, IP3 receptor levels, nor IP3 production were altered, indicative of a functional

124 tagonist, and not observed in the absence of IP3 IP3 potentiation was also blocked by ryanodine recep

125 a(2+) triggered by the synergistic action of IP3 and Ca(2+) released by RyRs.

126 The actions of IP3 appear to be confined to the main apical dendrite be

127 ropagation normally depends on activation of IP3 Rs; (ii) under resting conditions, propagation by IP

128 IP3Rs were apparent following activation of IP3/Ca(2+) signaling.

129 cting proteins can determine the activity of IP3 Rs, facilitate their regulation by multiple signalli

130 IP3 and Ca(2+) and that very small amount of IP3 is required to stimulate IP3R channels in the presen

131 ydiphenyl borate, 2-APB), or during block of IP3 production by the phospholipase C inhibitor U73122.

132 evidence shows that large concentrations of IP3 are required for calcium release.

133 f the IP3R revealed a higher contribution of IP3-dependent Ca(2+) release to vascular contraction in

134 To evaluate the contribution of IP3-R(2) to disease progression, the DCM-2Tg mice were f

135 Deletion of IP3-R(2) did not alter the progression of heart failure,

136 These findings support development of IP3 signalling modulators for regulation of heart rate,

137 [Ca(2+)]c rise evoked by submaximal doses of IP3, indicating that O2 directly sensitizes IP3R-mediate

138 n probability, consistent with the effect of IP3 signalling on Ca(2+) clock frequency.

139 fragmentation may represent a novel form of IP3 R regulation, which plays a role in varied adaptive

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

141 e ROCE response, which includes formation of IP3, a store-depleting agent.

142 her, we show that complementary fragments of IP3 R1 assemble into tetrameric structures and retain th

143 out (KO) SAN cells to study the influence of IP3 signalling on cardiac pacemaking in a system where p

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

145 lated mouse SAN cells, whereas inhibition of IP3 Rs slows pacing.

146 uced in unfertilized oocytes by injection of IP3 at concentrations sufficient to induce calcium relea

147 application of ryanodine (2 nm), instead of IP3, also potentiated K20-induced calcium transients in

148 Interactions of IP3 Rs with other proteins contribute to the specificity

149 iated by TRP channels without involvement of IP3 receptors.

150 rs, which led to production of low levels of IP3, caused dissociation of Irbit from IP3Rs and allowed

151 Loss of IP3-R(2) did not alter the progression of hypertrophy af

152 egulation of autophagy through modulation of IP3 signaling.

153 ate (IP) kinases catalyse phosphorylation of IP3 to inositol pyrophosphate, PP-IP5/IP7, which is esse

154 itial puffs evoked following photorelease of IP3-which would not be subject to earlier Ca(2+)-inhibit

155 -out animals, we show that the production of IP3 is mediated by the D1 receptor, but not the D2 recep

156 to shaping the spatio-temporal properties of IP3-mediated Ca(2+) signals has been difficult to evalua

157 e behavior of the channel to a wide range of IP3 and Ca(2+) concentrations and quantify the sensitivi

158 roduce a geometric microdomain regulation of IP3 -mediated Ca(2+) signalling to explain macroscopic p

159 PKC relieves negative feedback regulation of IP3 accumulation and, thereby, shifts Ca(2+) oscillation

160 ould consider the temperature sensitivity of IP3-mediated signal amplitudes when extrapolating from r

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

162 ciated with enhancement and sensitization of IP3-dependent Ca(2+) release, resulting in increased VSM

163 We found that stimulation of IP3 Rs accelerates spontaneous pacing rate in isolated m

164 The suppression of IP3 -mediated Ca(2+) signalling may explain the decrease

165 llowing proteolysis that N- and C-termini of IP3 R1 remain associated, presumably through non-covalen

166 tetanic synaptic stimulation or uncaging of IP3 increased the decay time of spontaneous Ca(2+) event

167 properties likely extend the versatility of IP3-induced Ca(2+) signaling in cells expressing multipl

168 used by using two different combinations of [IP3] and rlow.

169 gest that these effects are not dependent on IP3-dependent increases in astrocytic Ca(2+).

170 GluA2 exit from the ER further depends on IP3 and Ryanodine receptor-controlled Ca(2+) release as

171 nsverse aortic constriction was performed on IP3-R(2)-/- mice.

172 width, and wave velocity were dependent on [IP3] and were not perturbed by phospholipase C (PLC) inh

173 l microscope, was used to uncage Ca(2)(+) or IP3 and conduct photobleaching experiments from multiple

174 protein-coupled receptor PLC activity and/or IP3 metabolism to attenuate IP3 levels and suppress the

175 ms that insect olfaction uses cAMP, cGMP, or IP3 as second messengers; that insect odorant receptors

176 eing due to reducing diacylglycerol (DAG) or IP3 availability, i.e. PIP2 modulation of AHPs is not li

177 1; PLC-gamma1 activity; levels of PI(4,5)P2, IP3, and Cai; and induction of keratinocyte differentiat

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

179 d xi on two important IP3R model parameters, IP3 concentration ([IP3]) and the recovery rate from Ca(

180 e in permeabilized cells, and cell-permeable IP3 ester-induced Ca2+ elevation in intact cells.

181 f inositol phosphate production using a PIP2/IP3 "biosensor" revealed for the first time that IP3 can

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

183 anonical signal transduction via Galphaq-PLC-IP3-Ca(2+) at the expense of canonical DRD1 Galphas cAMP

184 n BAT temperature by sensitizing the TRH-PLC-IP3-calcium release mechanism.

185 ngin C, demonstrating involvement of the PLC/IP3 signal pathway.

186 These cells are endowed with a PLCbeta2/IP3 R3/TRPC6 signal transduction pathway modulating rele

187 ggesting profound alteration of the PLCbeta2/IP3 R3 signaling pathway.

188 response to environmental cues that promote IP3 (inositol 1,4,5-trisphosphate) generation, IP3 recep

189 In type 2 IP3 R (IP3 R2) knockout atrial myocytes, Ishear was 10-20% of t

190 d with increased expression of type 2 IP3-R (IP3-R(2)) and heightened generation of Ins(1,4,5)P3.

191 crossed with mice in which the type 2 IP3-R (IP3-R(2)-/-) had been deleted (DCM-2TgxIP3-R(2)-/-) and

192 ease of Ca(2+) from ER via the IP3 receptor (IP3 R).

193 nhibited by inositol tri-phosphate receptor (IP3 R) blockers.

194 l, the inositol-1,4,5-triphosphate receptor (IP3 R), has been implicated in the generation of spontan

195 r (RyR) and inositol trisphosphate receptor (IP3 R) channels is supported by a complex network of add

196 risphosphate (Ins(1,4,5)P3 [IP3]) receptors (IP3-R) to disease progression in mouse models of dilated

197 s or inositol 1,4,5-trisphosphate receptors (IP3 R) and upon depletion of sarcoplasmic reticulum Ca(2

198 Inositol 1,4,5-trisphosphate receptors (IP3 Rs) are a family of ubiquitously expressed intracell

199 and inositol 1,4,5-trisphosphate receptors (IP3 Rs) are calcium (Ca(2+) ) release channels on the en

200 Inositol 1,4,5-trisphosphate receptors (IP3 Rs) are expressed in nearly all animal cells, where

201 Inositol-1,4,5-trisphosphate receptors (IP3 Rs) modulate pacemaking in embryonic heart, but thei

202 between the endoplasmic reticulum receptors, IP3 and ryanodine, in the induction of priming, regulate

203 ic organelles by NAADP subsequently recruits IP3 or ryanodine receptors on the ER, an anterograde sig

204 electric potential (>-70 mV) and low resting IP3 concentrations.

205 al interaction between endoplasmic reticulum IP3 and ryanodine receptor-mediated calcium signaling is

206 In this review, we focus, not on RyR/IP3 R, but on other ion-channels that are known to be pr

207 By contrast, IgM that stimulates IP3 formation, elicited a [Ca(2+)]c signal in every DKO.

208 tivates Src leading to PLCgamma stimulation, IP3 elevation and [Ca](i) release.

209 al with Dehalogenimonas alkenigignens strain IP3-3.

210 ated the Ca(2+) release evoked by submaximal IP3 in permeabilized DKO1 and DKO2 but was ineffective i

211 uld also facilitate the effect of suboptimal IP3 in TKO transfected with rat IP3R3.

212 attened the endothelial cells and suppressed IP3 -mediated Ca(2+) signals in all activated cells.

213 We conclude that IP3 R-mediated SR Ca(2+) flux is crucial for initiating

214 We conclude that IP3-R(2) do not contribute to the progression of DCM or

215 Our results indicate that IP3 -mediated Ca(2+) release from the endoplasmic reticu

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

217 We suggest that IP3 Rs function as signalling hubs through which diverse

218 of spontaneous Ca(2+) waves, suggesting that IP3 R-mediated Ca(2+) release modulates the Ca(2+) clock

219 "biosensor" revealed for the first time that IP3 can be generated in the nucleus following activation

220 Although the IP3-evoked Ca2+ signals were qualitatively similar at 25

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

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

223 dine receptors and abolished by blocking the IP3 receptors.

224 nduced calcium transients was blocked by the IP3 antagonist, and not observed in the absence of IP3 I

225 dine receptor-dependent and prevented by the IP3 antagonist.

226 The truncation mutants, which encompass the IP3-binding domain and varying lengths of the modulatory

227 urrent by triggering Ca(2+) release from the IP3 R2 in the peripheral domains of atrial myocytes.

228 Cleavage of the IP3 R has been proposed to play a role in apoptotic cell

229 the channel, we propose that cleavage of the IP3 R peptide chain may alter other important regulatory

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

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

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

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

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

235 (2+)]c) signaling, but the exact role of the IP3 receptors (IP3R) in this process remains unclear.

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

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

238 that upon Ca(2+) release from the ER via the IP3 and ryanodine receptors, CaMKII that is activated en

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

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

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

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

243 (PLC)-catalyzed hydrolysis of PI(4,5)P(2) to IP3 and diacylglycerol.

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

245 d Ca(2+) wave velocity, whereas responses to IP3 uncaging are enhanced.

246 nerating a distinct 'blended' sensitivity to IP3 that is likely dictated by the unique IP3 binding af

247 identical ubiquitin ligase activities toward IP3 receptors.

248 (ER) stores via inositol 1,4,5-triphosphate (IP3) binding to the IP3 receptor (IP3R) is particularly

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

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

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

252 was observed in inositol 1,4,5-triphosphate (IP3) type-2 receptor (R2) knock-out (KO) mice, in which

253 mma, generating inositol 1,4,5-triphosphate (IP3), which opens EnR IP3R calcium channels, rapidly dep

254 pling (ECC) and inositol-1,4,5-triphosphate (IP3)-dependent Ca(2+) release in normal and heart failur

255 lateau level of inositol 1,4,5-triphosphate (IP3)-linked calcium signals.

256 Cl(-) ions and inositol 1,4,5-triphosphate (IP3).

257 olipase C, leading to inositol triphosphate (IP3) generation, activation of the IP3 receptor (IP3R),

258 creased production of inositol triphosphate (IP3) in the mouse striatum.

259 urs in the absence of inositol triphosphate (IP3)-dependent release from endoplasmic reticulum arises

260 ormone-induced inositol 1,4,5 trisphosphate (IP3 ) accumulation and phospholipase C (PLC) activity we

261 ormone-induced inositol 1,4,5 trisphosphate (IP3 ) production and does not involve changes in the sen

262 sphate (IP2 ), inositol 1,4,5-trisphosphate (IP3 ), and inositol hexakisphosphate (IP6 ) in T. brucei

263 i triggered by inositol 1,4,5-trisphosphate (IP3 )-induced release of Ca(2+) from ER via the IP3 rece

264 y initiated by inositol 1,4,5-trisphosphate (IP3 )-mobilized Ca(2+) : 8-pCPT-AM fails to induce CaMKI

265 ) release from inositol 1,4,5-trisphosphate (IP3 )-triggered Ca(2+) -store release, or channel modula

266 nt increase in inositol 1,4,5-trisphosphate (IP3) and intracellular calcium (Cai).

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

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

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

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

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

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

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

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

275 reby affecting inositol 1,4,5-trisphosphate (IP3) signaling and calcium levels during salivary gland

276 hich increases inositol 1,4,5-trisphosphate (IP3) to release intracellular calcium ([Ca](i)).

277 cally blocking inositol 1,4,5-trisphosphate (IP3)-dependent Ca(2+) increases in astrocytes failed to

278 Rs) generating inositol 1,4,5-trisphosphate (IP3).

279 complex, propagating inositol trisphosphate (IP3 )-mediated Ca(2+) waves that originated in clusters

280 nduced inhibition of inositol trisphosphate (IP3) production, leading to a decrease in T cell recepto

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

282 a transient rise in inositol trisphosphate (IP3) to trigger calcium mobilization from stores and ele

283 hens the efficacy of inositol trisphosphate (IP3)-induced Ca(2+) transfer from the ER to mitochondria

284 y reported decreased inositol trisphosphate (IP3)-mediated Ca(2+) release from the endoplasmic reticu

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

286 to the main apical dendrite because uncaging IP3 in the oblique dendrites has no effect on the time c

287 fect on Ca(2+) increases induced by uncaging IP3.

288 yl-1-phosphonic acid and CNQX or by uncaging IP3.

289 to IP3 that is likely dictated by the unique IP3 binding affinity of the heteromers.

290 By varying [IP3] and rlow in physiologically plausible ranges, we fi

291 m the ER and transferred to mitochondria via IP3 channels with little cytoplasmic leakage.

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

293 inhibits RNF170 expression and signaling via IP3 receptors.

294 nhibition of IP3R channel activity in vitro, IP3-induced ER Ca2+ release in permeabilized cells, and

295 rt rate, particularly in heart failure where IP3 Rs are upregulated.

296 Whether IP3 R-mediated Ca(2+) release also influences SAN automa

297 ey of the proteins proposed to interact with IP3 Rs and the functional effects that these interaction

298 IP3] receptors binding protein released with IP3), a previously identified activator of pNBC1, activa

299 +) release via IP3 receptors stimulated with IP3 released from caged-IP3 .

300 ilure, because DCM-2Tg mice with and without IP3-R(2) had similarly reduced contractility, increased

301 imilar in the DCM-2Tg mice, with and without IP3-R(2).