ライフサイエンスコーパス: IP3R

1 IP3R activation requires phospholipase C (PLC)-catalyzed

2 IP3R activity is regulated by protein-protein interactio

3 IP3R function was determined in human left ventricular m

4 IP3R inactivation by intrathecal xestospongin C attenuat

5 IP3R subtypes are regulated differentially by IP3, Ca(2+

6 IP3R subtypes are seldom expressed in isolation in indiv

7 IP3R up-regulation requires Ca(2+) influx through L-type

8 IP3R-deficient acinar cells accumulate ZGs, but the mice

9 IP3R-mediated Ca(2+)signaling, in turn, was found to inf

10 IP3R-mediated Ca2+ mobilization control hCPC growth and

11 IP3Rs and SERCA were highly expressed in hCPCs, whereas

12 IP3Rs may be activated after Galphaq-protein-coupled rec

13 IP3Rs serve as a potential target of ROS produced by bot

14 IP3Rs tethered close to ER-plasma membrane junctions are

15 -molecule imaging to locate and track type 1 IP3Rs tagged with a photoswitchable fluorescent protein

16 le each isoform can support contacts, type 2 IP3R is the most effective in delivering calcium to the

17 P3Rs and direct attention towards the type 2 IP3R that was previously neglected in the context of ER-

18 O) expressing either type 1 (DKO1) or type 2 IP3Rs (DKO2) showed a [Ca(2+)]c signal, whereas DKO expr

19 Ca2+ signals by Bcl-2, suggesting the Bcl-2-IP3R interaction as a potential therapeutic target in di

20 Here we document Bcl-2-IP3R interaction within cells by FRET and identify a Bcl

21 (2+)]c signal, whereas DKO expressing type 3 IP3R (DKO3) did not.

22 4,5)-triphosphate, the ligand that activates IP3R.

23 In addition, IP3R levels were elevated both in Herpud1-knockout mice

24 um-dependent apoptosis through an ERO1-alpha-IP3R pathway.

25 Also, IP3Rs contain multiple reactive thiols, common molecular

26 to prevent apoptosis, as done instead by an IP3R-derived peptide.

27 structs were expressed in DT40-3KO cells, an IP3R null cell line.

28 s recruited to the ER during apoptosis in an IP3R-dependent manner, and, in addition, a pool of BRCA1

29 s show that a relatively slow recovery of an IP3R from Ca(2+) inhibition is necessary to reproduce mo

30 Using an IP3R-deficient cell model rescued with each of the three

31 function through control of PI(4,5)P(2) and IP3R influences Spry2 function by controlling its distri

32 ced by a decrease in PLC-beta activation and IP3R-mediated calcium store release in the presence of t

33 xamined the impact of astrocytic Gq-GPCR and IP3R-dependent Ca(2+) signaling on cortical blood flow i

34 resistance (Rgj) and the density of IKCa and IP3R in the projection influence the extent of EC respon

35 The positive feedback between PLCbeta and IP3R found here may represent a common feature of the in

36 tors, but not by the blockers of PLCbeta and IP3R.

37 BIN2) as an interaction partner of STIM1 and IP3R in platelets.

38 The content of VDAC1 and IP3R, proteins involved in ER-mitochondria communication

39 a dynamic synergy between TRPV4 channels and IP3Rs in astrocyte endfeet and demonstrate that TRPV4 ch

40 Anti-IP3R-3 immunoprecipitates from cells expressing sigma-1R

41 sponsive mice genetically lacking astrocytic IP3R-dependent Ca(2+) signaling (IP3R2 KO).

42 Signaling via the ouabain/Na,K-ATPase/IP3R/NF-kappaB pathway increases expression of Bcl-xL, a

43 suppressing channel opening and attenuating IP3R-mediated Ca(2+) release.

44 c puff model and a single-channel data-based IP3R model, we establish the dependencies of lambda and

45 Bik also disrupts the Bcl2-IP3R interaction to cause ER Ca(2+) release.

46 on, showing a functional cooperation between IP3R and PLCbeta via released Ca(2+).

47 th the propagation of Ca(2+) signals between IP3Rs and the selective regulation of cellular responses

48 l-XL was protective independently of binding IP3Rs.

49 Furthermore, reducing ER Ca(2+) or blocking IP3Rs caused a dramatic LSD-like lysosome storage phenot

50 With regard to the possible role of Bok-IP3R binding, the following was observed: (i) Bok does n

51 ulate both activation and translocation, but IP3Rs preferentially promote translocation.

52 elease from intracellular stores mediated by IP3R.

53 ons that the relatively longer time spent by IP3R in the H mode leads to the observed higher frequenc

54 Zs requires Ca(2+) microdomains generated by IP3Rs.

55 the notion that increases in Ca(2+) load by IP3Rs promote Ca(2+) extrusion by forward-mode Na(+)/Ca(

56 Calcium release mediated by IP3Rs influences many signaling pathways, including thos

57 ondria tethering was impaired, Ca2+ channels IP3Rs and CACNA1A were downregulated, and Ca2+-dependent

58 by inositol trisphosphate receptor/channels (IP3R) in human neuroblastoma (SH-SY5Y) cells.

59 assumption that IP3 receptor Ca2+ channels (IP3Rs) are globally coupled by a "continuously stirred"

60 sitol 1,4,5-trisphosphate receptor/channels (IP3Rs), whose openings are coordinated by Ca(2+)-induced

61 d inositol trisphosphate receptors/channels (IP3Rs).

62 Therefore, we compared IP3R expression and function between mesenteric arteries

63 dress this question, we created concatenated IP3R linked by short flexible linkers.

64 t simply a blend of those of the constituent IP3R monomers.

65 cysteines to alanines resulted in decreased IP3R palmitoylation and function.

66 event widening is attributable to a delayed IP3R-mediated release of Ca(2+) triggered by the synergi

67 contact formation and whether the different IP3R isoforms have redundant functions.

68 mediated by N=100,000 diffusely distributed IP3Rs, each represented by a four-state Markov chain.

69 nd luminal Ca2+ domains associated with each IP3R.

70 gene editing to fluorescently tag endogenous IP3Rs, and super-resolution microscopy to determine the

71 a(2+) release channels resulting in enhanced IP3R channel gating in an amyloid beta (Abeta) productio

72 e C gamma (PLCgamma)-mediated opening of EnR IP3R calcium channels, enabling passage of calcium from

73 restore EnR Ca(2+) levels, but the open EnR IP3R calcium channel leads to an ATP-depleting futile cy

74 ol 1,4,5-triphosphate (IP3), which opens EnR IP3R calcium channels, rapidly depleting EnR Ca(2+) stor

75 ineffective in DKO3 or in DT40 lacking every IP3R (TKO).

76 hondrial enzymes, which might locally expose IP3Rs at the ER-mitochondrial associations.

77 t polypeptide continuity is not required for IP3R activation and Ca(2+) release.

78 , indicating a higher amount of ankyrin-free IP3R-3.

79 ist-independent dissociation of ANK 220 from IP3R-3, resulting in activation.

80 targeting of apoptotic calcium release from IP3R may enhance tumor cell immunogenicity.

81 inhibitor of apoptotic calcium release from IP3R strongly blocked lymphocyte apoptosis.

82 n cancer cells requires calcium release from IP3R.

83 trigger the dissociation of mature Bok from IP3Rs or Bok degradation, indicating that the role of pr

84 ls of IP3, caused dissociation of Irbit from IP3Rs and allowed translocation of Irbit to CFTR and Slc

85 gnals (blips) arising from single functional IP3Rs are almost immotile (diffusion coefficient<0.003 m

86 Functionally, IP3R up-regulation in VSM is associated with enhancement

87 icant reductions of EAAT4, EAAT1, GluRdelta, IP3R, and NCAM140.

88 Thus, Bok may govern IP3R cleavage and activity during apoptosis.

89 that individual monomers within heteromeric IP3Rs contributed equally toward generating a distinct '

90 the subunit composition of heterotetrameric IP3R channels contributes to shaping the spatio-temporal

91 ight into the regulation of heterotetrameric IP3R of defined composition.

92 ummary, we demonstrate that heterotetrameric IP3R do not necessarily behave as the sum of the constit

93 These findings identify IP3R as a new determinant in HIV-1 trafficking during Ga

94 tic difference provides a way of identifying IP3R kinetic parameters by observing properties of the I

95 generated by a small population of immobile IP3Rs.

96 stable clusters of small numbers of immotile IP3Rs may underlie local Ca(2+) release sites, whereas t

97 verall motility or in clustering of immotile IP3Rs were apparent following activation of IP3/Ca(2+) s

98 A fraction of the immotile IP3Rs were organized in clusters, with dimensions (a few

99 ecreased expression of the IP3R and impaired IP3R-dependent Ca(2+) flux.

100 These defects were a consequence of impaired IP3R function in combination with defective STIM1-mediat

101 pendencies of lambda and xi on two important IP3R model parameters, IP3 concentration ([IP3]) and the

102 Importantly, IP3R channels formed from concatenated dimers were fully

103 In IP3R-deficient photoreceptors, dark bumps were virtually

104 ow expression of the IP3R due to a defect in IP3R palmitoylation.

105 n of the calcineurin-NFAT axis, resulting in IP3R transcription.

106 Individual IP3R monomers are assembled to form homo- and heterotetr

107 Our findings suggest that Spry2 influences IP3R function through control of PI(4,5)P(2) and IP3R in

108 tic variation in numbers of Ca(2+)-inhibited IP3Rs likely contributes to the variability of amplitude

109 ependent apoptosis by binding and inhibiting IP3Rs, although the BH4 domain of Bcl-XL was protective

110 rafficking during Gag assembly and introduce IP3R-regulated Ca(2+) signaling as a potential novel cof

111 o IP3R3, and essentially all cellular Bok is IP3R bound in cells that express substantial amounts of

112 issues, that essentially all cellular Bok is IP3R bound, that it is the helical nature of the Bok BH4

113 lling of lysosomes, but not in cells lacking IP3Rs.

114 The licensed IP3Rs reside alongside ER-plasma membrane junctions wher

115 a demonstrate that astrocytic Gq-GPCR-linked IP3R-dependent Ca(2+) signaling does not mediate neurova

116 ng this process is astrocytic Gq-GPCR-linked IP3R-dependent Ca(2+) signaling, though in vivo tests of

117 Among the three mammalian IP3Rs, IP3R3 appears to be the major player in Ca(2+)-de

118 tation showed that ERalpha-mGluR1 and mGluR1-IP3R complexes exist in both sexes but are regulated by

119 ond, but they do not readily mix with mobile IP3Rs.

120 low occupancy of the low-activity (L) mode, IP3R in FAD-causing mutant PS-expressing cells exhibits

121 Moreover, IP3R was redistributed to the cell periphery and cytosol

122 Most IP3R clusters are mobile, moved by diffusion and microtu

123 ease sites, whereas the more numerous motile IP3Rs appear to be functionally silent.

124 a(2+) signaling in cells expressing multiple IP3R isoforms.

125 We show that native IP3Rs cluster within ER membranes.

126 nary single-channel data, we construct a new IP3R model that includes time-dependent rates of mode sw

127 ) puffs is then constructed based on the new IP3R model and is solved by a hybrid Gillespie method wi

128 to destroy newly synthesized Bok that is not IP3R associated.

129 In the absence of IP3R-mediated Ca(2+) signalling, repression of key Notch

130 y, we focused on Group I mGluR activation of IP3R-mediated intracellular Ca2+ waves and their role in

131 ndicating that the nanoscale architecture of IP3R clusters is important in shaping local Ca2+ signals

132 puffs and waves, we here model a cluster of IP3R channels using a gating scheme with variable non-eq

133 ing from single IP3R (blips) and clusters of IP3R (puffs) showed little temperature dependence, where

134 + signals ("puffs") arising from clusters of IP3R, and patch-clamp studies on isolated oocyte nuclei

135 Combination of IP3R knockdown with reduced PLCbeta catalytic activity r

136 cells often express different complements of IP3R subtypes.

137 However, the contribution of IP3R heterotetramerization to Ca(2+) signal diversity ha

138 Depletion of IP3R and inactivation of phospholipase C (PLC) inhibited

139 Depletion of IP3R by small interfering RNA, sequestration of its acti

140 This gain-of-function enhancement of IP3R activity is considered to be the main reason behind

141 gain deeper insights into the enhancement of IP3R function.

142 igand by expression of a mutated fragment of IP3R that binds IP3 with very high affinity, or blocking

143 3R and reversed Bcl-2-mediated inhibition of IP3R channel activity in vitro, IP3-induced ER Ca2+ rele

144 We also established that inhibition of IP3R or RyR down-regulated T cell proliferation and T-ce

145 s exposed to xestospongin C, an inhibitor of IP3R-mediated calcium release.

146 ist concentrations whereas lowered levels of IP3R and RyR need higher agonist concentration for intra

147 Levels of IP3R transcript and protein were significantly increased

148 Knockdown or inhibition of PLCgamma, or of IP3R, strongly inhibited the estrogen-mediated increases

149 Under conditions where key regulators of IP3R function are optimal for Ca(2+) release, we demonst

150 In this study, we examined the role of IP3R type 2 (IP3R2) using mice deficient in this Ca(2+)

151 ncentrations and quantify the sensitivity of IP3R to its two ligands.

152 to the structural integrity or stability of IP3R tetramers.

153 s questions relating to the stoichiometry of IP3R regulation.

154 When multiple subtypes of IP3R are co-expressed, the subunit composition of channe

155 General suppression of IP3R signaling significantly reduced SW620-mediated Jurk

156 ok does not appear to control the ability of IP3Rs to release ER calcium stores, (ii) Bok regulates I

157 in cells that express substantial amounts of IP3Rs.

158 a small region within the coupling domain of IP3Rs (amino acids 1895-1903 of IP3R1) that is adjacent

159 ivary gland ducts expressing mutant forms of IP3Rs that could not undergo protein kinase A-mediated p

160 time scales between the stochastic gating of IP3Rs and the dynamics of domain Ca2+.

161 ts likely result from asynchronous gating of IP3Rs distributed within clusters that have an overall d

162 ion microscopy to determine the geography of IP3Rs and Ca(2+) signals within living cells.

163 tagged IP3Rs have shown that the majority of IP3Rs are freely motile.

164 Furthermore, we find that, as the number of IP3Rs increases, the average duration of puffs initially

165 The spatial organization of IP3Rs determines both the propagation of Ca(2+) signals

166 -coupled receptors led to phosphorylation of IP3Rs, which increased their affinity for InsP3 and redu

167 of this binding appears to be protection of IP3Rs from proteolysis.

168 oocyte nuclei have yielded extensive data on IP3R gating kinetics.

169 mined the effect of superoxide anion (O2) on IP3R-mediated Ca(2+) signaling.

170 y induced intercellular Ca(2+) waves rely on IP3R-mediated Ca(2+)-induced Ca(2+) release and propagat

171 ibody targeted to the ligand-binding site on IP3R, blocked plasma membrane accumulation of Gag.

172 ed" bulk cytosolic [Ca2+], when in fact open IP3Rs experience elevated "domain" Ca2+ concentrations.

173 Overall, IP3R-mediated Ca2+ release in ESdCs is translated into a

174 oteasome pathway, in a manner that parallels IP3R degradation, and (iv) Bok protects IP3Rs from prote

175 ; P<0.001) was found to be unable to promote IP3R signaling and calcium store release.

176 lels IP3R degradation, and (iv) Bok protects IP3Rs from proteolysis, either by chymotrypsin in vitro

177 osphorylation of the MAM associated proteins IP3R, Hexokinase 2, and phosphofurin acidic cluster sort

178 Galphaq signaling, leading to IP3 receptor (IP3R) activation at the growth cone of differentiating P

179 phosphate (IP3) binding to the IP3 receptor (IP3R) is particularly important for the activation and f

180 generation, activation of the IP3 receptor (IP3R), and postsynaptic endocannabinoid release, likely

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

182 RC2 at MAM interacted with the IP3 receptor (IP3R)-Grp75-voltage-dependent anion-selective channel 1

183 kyrin B 220 (ANK 220) from the IP3 receptor (IP3R-3), releasing it from inhibition.

184 inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) Ca(2+) release channels resulting in enhanced IP3R

185 inositol 1,4,5-triphosphate (IP3) receptor (IP3R) via CHOP-induced ERO1-alpha (ER oxidase 1 alpha).

186 The inositol (1,4,5)-triphosphate receptor (IP3R) gates intracellular Ca(2+) stores.

187 of the inositol 1,4,5-triphosphate receptor (IP3R) is required for efficient HIV-1 Gag trafficking an

188 ts and inositol 1,4,5-triphosphate receptor (IP3R) levels at day 10 postinfection.

189 of the inositol 1,4,5-triphosphate receptor (IP3R), a protein that "gates" Ca(2+) release from intrac

190 pump, inositol-1,4,5-triphosphate receptor (IP3R), and Ryanodine receptor (RyR), plays a major role

191 Grp75)/inositol 1,4,5-triphosphate receptor (IP3R)-1 complex, and regulating energy metabolism.

192 ns and inositol 1,4,5-triphosphate receptor (IP3R)-induced cytosolic signals is based on attenuating

193 ation of the inositol triphosphate receptor (IP3R).

194 Bcl2 and the inositol triphosphate receptor (IP3R).

195 annel inositol 1,4,5-trisphosphate receptor (IP3R) affects progression to cardiac hypertrophy.

196 PLC/inositol trisphosphate receptor (IP3R) and estrogen receptor co-regulation in spinal cord

197 Inositol 1,4,5-trisphosphate receptor (IP3R) antagonists (xestospongin D or 2-aminoethoxydiphen

198 more, inositol 1,4,5-trisphosphate receptor (IP3R) but not ryanodine receptor (RyR) expression was hi

199 h the inositol 1,4,5-trisphosphate receptor (IP3R) Ca2+ channel localized with Bcl-2 on the ER.

200 s the inositol 1,4,5-trisphosphate receptor (IP3R) channel, whose regulation of intracellular Ca(2+)

201 r (RyR) and inositol trisphosphate receptor (IP3R) channels is supported by a complex network of addi

202 angement of inositol trisphosphate receptor (IP3R) channels underlying local Ca2+ puffs.

203 The inositol 1,4,5-trisphosphate receptor (IP3R) is a ubiquitously expressed endoplasmic reticulum

204 The inositol 1,4,5 trisphosphate receptor (IP3R) is an intracellular Ca(2+) release channel express

205 ts of inositol 1,4,5-trisphosphate receptor (IP3R) or ryanodine receptor (RyR), respectively, facilit

206 y the inositol 1,4,5-trisphosphate receptor (IP3R) types 2 and 3.

207 ai1 and the inositol trisphosphate receptor (IP3R), thereby linking the endo-/sarcoplasmic reticulum

208 Inositol 1, 4, 5-trisphosphate receptor (IP3R)-mediated Ca(2+) release from the endoplasmic retic

209 beta]- inositol 1,4,5-triphosphate receptor [IP3R]), and are not sufficient to impact airway contract

210 The Galphaq-protein/coupled receptor/IP3R axis modulates the electromechanical properties of

211 calcium signals between the IP(3) receptors (IP3R) and the mitochondrial calcium uniporter, and are c

212 ng, but the exact role of the IP3 receptors (IP3R) in this process remains unclear.

213 y of inositol 1,4,5-trisphosphate receptors (IP3R) to precisely initiate and generate a diverse varie

214 s, Irbit was sequestered by InsP3 receptors (IP3Rs) in the endoplasmic reticulum.

215 potassium channels (IKCa) and IP3 receptors (IP3Rs) in the MPs.

216 ,5-trisphosphate) generation, IP3 receptors (IP3Rs) located on the endoplasmic reticulum allow the 'q

217 ecifically, antagonists of ER IP3 receptors (IP3Rs) rapidly and completely blocked Ca(2+) refilling o

218 IP3 receptors (IP3Rs) release Ca(2+) from the ER when they bind IP3 and

219 on of inositol 1,4,5-triphosphate receptors (IP3Rs) and the reuptake of Ca2+ by the sarco-/endoplasmi

220 hough inositol 1,4,5-triphosphate receptors (IP3Rs) are abundant in VSM, their role in the molecular

221 ow that the inositol triphosphate receptors (IP3Rs) Ca(2+) ion channels are required for proliferatio

222 1,4,5-Inositol trisphosphate receptors (IP3Rs) and ryanodine receptors (RyRs) mediate release of

223 ized inositol 1,4,5-trisphosphate receptors (IP3Rs) and the voltage-dependent anion channel 1 (VDAC1)

224 clustered inositol trisphosphate receptors (IP3Rs) control localized Ca(2+) liberation from the endo

225 n of inositol 1,4,5-trisphosphate receptors (IP3Rs) in the adult heart experimentally.

226 y to inositol 1,4,5-trisphosphate receptors (IP3Rs), proteins that form tetrameric calcium channels i

227 with inositol 1,4,5-trisphosphate receptors (IP3Rs), suggesting that it may contribute to the structu

228 lease from inositol trisphosphate receptors (IP3Rs).

229 r of inositol 1,4,5-trisphosphate receptors (IP3Rs).

230 (RyRs) and inositol trisphosphate receptors (IP3Rs).

231 from inositol 1,4,5-trisphosphate receptors (IP3Rs).

232 in inositol 1, 4, 5-trisphosphate receptors (IP3Rs).

233 elease ER calcium stores, (ii) Bok regulates IP3R expression, (iii) persistent activation of inositol

234 , suggesting that Spry2 negatively regulates IP3R by preventing formation of its activating ligand, I

235 gulator of cardiac hypertrophy by regulating IP3R protein levels.

236 logical hypertrophic phenotype by regulating IP3R protein levels.

237 r5 cells as a cellular model that replicates IP3R up-regulation during hypertension by depolarizing t

238 STEP activation by M1R stimulation requires IP3Rs and can depress NMDA-evoked currents with modest i

239 These findings reveal IP3R palmitoylation as a critical regulator of Ca(2+) fl

240 In this review, we focus, not on RyR/IP3R, but on other ion-channels that are known to be pre

241 Thus, ROS seem to specifically sensitize IP3Rs through a thiol group(s) within the IP3R, which is

242 IP3, indicating that O2 directly sensitizes IP3R-mediated Ca(2+) release.

243 the significance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynamics of V

244 be modified by changing the levels of SERCA, IP3R, and/or RyR.

245 Here we report that Bok is similarly IP3R-assocated in mouse tissues, that essentially all ce

246 spread of local signals arising from single IP3R (blips) and clusters of IP3R (puffs) showed little

247 we employed computational modeling of single IP3R channel activity records obtained under optimal Ca(

248 s depend on the kinetic parameters of single IP3Rs in a cluster is still unclear.

249 Agents that stimulate IP3R activity, apoptosis, phosphorylation, and endoplasm

250 small amount of IP3 is required to stimulate IP3R channels in the presence of FAD-causing mutant PS t

251 oying overexpression of fluorescently tagged IP3Rs have shown that the majority of IP3Rs are freely m

252 We demonstrate here that IP3R function is required for efficient release of HIV-1

253 These data indicate that IP3R-mediated Ca(2+) signalling reinforces Tcf-1 activit

254 We further show that IP3R-dependent calcium transients in the glutamatergic n

255 trastructural approaches we demonstrate that IP3Rs are required for maintaining ER-mitochondrial cont

256 We report that IP3Rs are expressed and operative in human left ventricu

257 ion was high in enamel cells suggesting that IP3Rs are the main ER Ca(2+) release mechanism.

258 , which is prevented by JNK1/2 siRNA and the IP3R inhibitor xestospongin C.

259 This molecular interaction disrupts the IP3R's 'head-tail' interaction, thereby suppressing chan

260 arable to those previously estimated for the IP3R clusters underlying functional puff sites.

261 this IP3R sequence displaced Bcl-2 from the IP3R and reversed Bcl-2-mediated inhibition of IP3R chan

262 Although the Ca(2+) release from the IP3R can be activated by TCR stimulation, the Ca(2+) rel

263 ease via IP3R and/or RyR, and identified the IP3R and RyR as potential targets for manipulation of Ca

264 and binding and conformational change in the IP3R at the subunit level.

265 ell lines led to decreased expression of the IP3R and impaired IP3R-dependent Ca(2+) flux.

266 culture media leads to low expression of the IP3R due to a defect in IP3R palmitoylation.

267 hotometric and bioinformatic analyses of the IP3R protein identified two palmitoylated cysteine resid

268 imals, and pharmacological inhibition of the IP3R revealed a higher contribution of IP3-dependent Ca(

269 4A mutant and blocked by an inhibitor of the IP3R, suggesting that calcium flow through the alpha7 ch

270 carboxyl-terminal gate-keeping domain of the IP3R.

271 in the regulatory and coupling domain of the IP3R.

272 Based on the IP3R model (which is determined by fitting to stationary

273 BRCA1 binding directly sensitizes the IP3R to its ligand, IP3.

274 Here we show that the IP3R binds to the tumor suppressor BRCA1.

275 lso controlled T cell activation through the IP3R/calcium/NFAT pathway.

276 RIP140 localizes to the ER by binding to the IP3R.

277 ze IP3Rs through a thiol group(s) within the IP3R, which is probably inaccessible in the chicken IP3R

278 eal a non-canonical, structural role for the IP3Rs and direct attention towards the type 2 IP3R that

279 These IP3Rs are licensed to respond, but they do not readily m

280 A peptide based on this IP3R sequence displaced Bcl-2 from the IP3R and reversed

281 nse to X+XO, DT40 cells lacking two of three IP3R isoforms (DKO) expressing either type 1 (DKO1) or t

282 nt cell model rescued with each of the three IP3R isoforms and an array of super-resolution and ultra

283 2+) transfer from ER to mitochondria through IP3R under normoxic conditions.

284 probability of the channel in comparison to IP3R in cells expressing wild-type PS.

285 Binding to IP3Rs appears to be mediated by the putative BH4 domain

286 raded by the proteasome, and that binding to IP3Rs limits the pro-apoptotic effect of overexpressed B

287 ecific amino acids, that mediates binding to IP3Rs, that Bok is dramatically stabilized by binding to

288 Bok is dramatically stabilized by binding to IP3Rs, that unbound Bok is ubiquitinated and degraded by

289 rd restricting Bok to that which is bound to IP3Rs, implies that unbound Bok is deleterious to cell v

290 hat Bok binds strongly and constitutively to IP3Rs and that the most significant consequence of this

291 and on blue native gels exactly as wild type IP3R.

292 s, that is SOCE-dependent Ca(2+) release via IP3R and/or RyR, and identified the IP3R and RyR as pote

293 ations are preceded by ER Ca(2+) release via IP3R channels and mitochondrial Ca(2+) uptake.

294 to the current dogma that Ca(2+) release via IP3R does not participate in light excitation, we show t

295 obilized from the sarcoplasmic reticulum via IP3Rs contributes to the decrease in resting membrane po

296 Our studies indicate that signalling via IP3Rs represses Sox13, an antagonist of the developmenta

297 It remains unclear whether IP3Rs also have a structural role in contact formation a

298 myocytes to identify the mechanisms by which IP3Rs influence the electric and mechanical properties o

299 minal domain [Ca2+] jointly distributed with IP3R state.

300 Thus, the interaction of Bcl-2 with IP3Rs contributes to the regulation of proapoptotic Ca2+