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 dary wave of ADP secretion driven by both an IP3/SERCA2b-dependent Ca(2+) stores pathway and the NAAD

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

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

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

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

24 4,5-trisphosphate (IP3) receptor (ITPR1), an IP3-gated, endoplasmic reticulum (ER)-resident Ca(2+) ch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 gating scheme with variable non-equilibrium IP3 binding.

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

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

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

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

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

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

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

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

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

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

83 3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors (IP3Rs) located on the endoplasmic reticul

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

85 rol cells stimulated by significantly higher IP3 concentrations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 while Ca2+ store content and agonist-induced IP3 production were unaltered.

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

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

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

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

105 eventing formation of its activating ligand, IP3.

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

107 directly sensitizes the IP3R to its ligand, IP3.

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

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

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

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

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

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

114 1, R2, and R3) by key functional modulators (IP3, Ca(2+), and ATP).

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

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

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

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

119 (2+) store content, IP3 receptor levels, nor IP3 production were altered, indicative of a functional

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 iated by TRP channels without involvement of IP3 receptors.

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

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

147 egulation of autophagy through modulation of IP3 signaling.

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

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

150 naffected by inhibition of the production of IP3 (inositol-1,4,5-trisphosphate) by phospholipase-C an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 TP; and (4) inhibitors of phospholipase C or IP3 receptors.

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

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

174 Overexpressing IP3 receptor or glucose transporter mitigates the S1RE10

175 1; PLC-gamma1 activity; levels of PI(4,5)P2, IP3, and Cai; and induction of keratinocyte differentiat

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

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

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

179 accordingly were not stimulated by permeant IP3.

180 sphosphate 3-kinase B (Itpkb) phosphorylates IP3 to negatively regulate and thereby tightly control C

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 owed that signaling abnormalities in the PLC/IP3/PKC/ERK pathway (phospholipase C/inositol 1,4,5-trip

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

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

189 c rewiring in chRCC and identifies the PLCG2/IP3/Ca(2+)/PKC axis as a potential therapeutic target in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 al with Dehalogenimonas alkenigignens strain IP3-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

225 dine receptors and abolished by blocking the IP3 receptors.

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

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

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

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

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

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

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

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

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

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

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

237 (2+)]c) signaling, but the exact role of the IP3 receptors (IP3R) in this process remains unclear.

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

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

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

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

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

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

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

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

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

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

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

249 identical ubiquitin ligase activities toward IP3 receptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ation releases inositol 1,4,5-trisphosphate (IP3), inducing cytoplasmic calcium (Ca2+) influx.

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

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

280 amma 2 (PLCG2)/inositol 1,4,5-trisphosphate (IP3)/Ca(2+)/protein kinase C (PKC) pathway significantly

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

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

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

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

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

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

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

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

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

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

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

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

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

294 inhibits RNF170 expression and signaling via IP3 receptors.

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

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

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

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

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).