ライフサイエンスコーパス: RyR

1 RyR density at the ends of lateral left ventricular card

2 RyR density exhibits remarkable subcellular heterogeneit

3 RyR remodeling occurred in lateral and anterior cardiomy

4 RyR-mediated function is also impaired, as indicated by

5 RyRs are so named because they bind the plant alkaloid r

6 RyRs are the largest known ion channels, with a homotetr

7 RyRs play a major role in excitation-contraction couplin

8 complex of the rabbit skeletal muscle type 1 RyR (RyR1), solved by single-particle electron cryomicro

9 reveals the most prominent juxtaposed Kv2.1:RyR clusters in indirect pathway MSNs.

10 tis elegans, we find that mutation of unc-68/RyR greatly impedes both outgrowth and guidance of the r

11 tomy and completely eliminated within unc-68/RyR mutants.

12 n and can be blocked by disruption of UNC-68/RyR.

13 el approach by which the spark fidelity of a RyR cluster can be predicted from structural information

14 ects of modulators for TMEM16A or VDCCs on a RyR-mediated rise in global [Ca(2+)]i and impairs the to

15 al development and Rac1 activation through a RyR-mediated mechanism, which in turn activates NOX thro

16 s caused by a global rise in [Ca(2+)]i via a RyR-TMEM16A-VDCC signalling module sets the basal tone.

17 EADs are promoted by aberrant RyR-mediated Ca(2+) releases that are present despite a

18 hologic conditions, thus precluding abnormal RyR-mediated Ca(2+) release.

19 one of the NOX subunits, was activated after RyR-mediated Ca(2+) release, suggesting a feedforward me

20 e-sensing gate structure is conserved in all RyR and inositol 1,4,5-trisphosphate receptor isoforms.

21 Nevertheless, submicromolar S100A1 can alter RyR function, an effect that is influenced by both [Ca(2

22 the molecular mechanisms underlying altered RyR-mediated intracellular Ca(2+) release in AD remain t

23 hanism that integrates both NOX activity and RyR-mediated Ca(2+) release to support cellular mechanis

24 lic Ca diffusion, SERCA uptake activity, and RyR open probability.

25 nist-induced calcium release from the ER and RyR-mediated synaptic responses in the absence of PS.

26 ntrations whereas lowered levels of IP3R and RyR need higher agonist concentration for intracellular

27 icance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynamics of VSMC and to

28 the contribution of the link between NOX and RyR-mediated Ca(2+) release toward axonal specification

29 ting a feedforward mechanism between NOX and RyR.

30 interaction between activation of IP(3)R and RyR near the sarcolemmal membrane.

31 Characterization of TRPA1 and RyR demonstrates that Ca(2+) signaling is required for o

32 direct cytoplasmic regulator of IP(3)Rs and RyRs and propose that CHERP acts in the nucleus to impac

33 rating functional segregation of IP(3)Rs and RyRs.

34 the SR Ca(2+)-stimulated ATPase (SERCA) and RyRs by K201.

35 The aphid RyR shares many of the features of other insect and vert

36 hese data suggest an interdependence between RyR and InsP3 R in the generation of Ca(2+) transients.

37 A similar interplay between RyR sensitivity and SR content was observed during treat

38 During VF, [Ca(2+)]SR was high, but RyR remained nearly continuously refractory, resulting i

39 y an increase of RyR2 oxidation, but also by RyR-S2814 phosphorylation, and by CaMKII oxidation.

40 that late aberrant Ca(2+) releases caused by RyR hyperactivity promote EADs and underlie the enhanced

41 pecific localized calcium signal mediated by RyR channel activity that stimulates regenerative outgro

42 We find that small ions are preferred by RyR because they can fit into this crowded environment m

43 ral features explain high ion conductance by RyRs and the long-range allosteric regulation of channel

44 NCX; (iii) propagation can be maintained by RyRs if they have been sensitised to Ca(2+).

45 cates a lack of competition by S100A1 on CaM/RyR binding under normal physiological conditions.

46 s, high micromolar S100A1 does alter the CaM/RyR interaction, without involving competition.

47 odel is consistent with the RyR1 and cardiac RyR (RyR2) open-channel structures reported while this p

48 3778-4201) that contains a number of cardiac RyR (RyR2) mutations associated with catecholaminergic p

49 ytoplasmic region in the function of cardiac RyR (RyR2) via structure-guided site-directed mutagenesi

50 the agonistic action of caffeine on cardiac RyR gating (i.e., stabilized long openings characteristi

51 s driven by stochastic Ca2+ release channel (RyR) gating and is used to study mechanisms of DAD varia

52 eptor intracellular calcium release channel (RyR) with high (fM) potency and provides a functional li

53 Ryanodine receptor channels (RyR) are key components of striated muscle excitation-co

54 ryanodine receptor/Ca(2+)-release channels (RyRs) of skeletal and cardiac muscle are essential for C

55 ryanodine receptor Ca(2+) release channels (RyRs), causing enhanced vascular tone.

56 Like other calcium channels, RyR has four aspartate residues in its GGGIGDE selectivi

57 n species scavenging, also prevented coupled RyR modulation.

58 Coupled RyRs have a distinct modulation by Ca(2+)/calmodulin-dep

59 driven and occurred as a result of decreased RyR inactivation which led to increased steepness of the

60 ough to produce frequent firings, decreasing RyR open probability counter-intuitively promotes long-l

61 In this setting, decreasing RyR open probability further suppresses long-lasting spa

62 have shown that a phosphorylation defective RyR mutant mouse (RyRS2808A) does not respond normally t

63 espondence between DHPR positioning and DHPR/RyR functional interactions.

64 blished literature showing that dysregulated RyRs contribute to the altered Ca(2+) regulatory phenoty

65 Each RyR opens stochastically and is regulated by cytosolic a

66 ndritic calcium release mediated by enhanced RyR calcium release.

67 These results are illustrated for RyR clusters based on super-resolution stimulated emissi

68 ) maps, we obtained pseudo-atomic models for RyR fragments consisting of residues 850-1,056 in rabbit

69 Instead, MBED's affinity for RyRs (EC50 approximately 0.5 muM) was much larger than f

70 on is influenced by the number of functional RyRs in a junctional cluster (which is reduced by tetrac

71 We varied the number of functional RyRs in the single cluster, diffusion within the SR netw

72 ng clear functional evidence that the G4946E RyR mutation impairs diamide insecticide binding.

73 ally, using our unique method for generating RyR cluster distributions, we demonstrate the robustness

74 In intact hearts, RyR refractoriness initiates SR Ca(2+) release alternans

75 , we found a similar degree of heterogeneous RyR remodeling, despite preserved t-system.

76 yR cluster contains a few to several hundred RyRs, and we use a four-state Markov RyR gating model.

77 Hyperactive, hyperphosphorylated RyRs because of reduced local phosphatase activity enhan

78 We conclude: (i) RyRs are required for the initiation of Ca(2+) waves, bu

79 s in the [Ca2+]i transient to differences in RyR cluster distributions measured between rat and human

80 of the mechanisms and structures involved in RyR function.

81 ibers, suggesting a possible role of SepN in RyR regulation.

82 nto how Ryd interacts with major residues in RyRs that were experimentally determined to be critical

83 o help identify the caffeine-binding site in RyRs.

84 results suggest synergism between increased RyR sensitivity and decreased IK1 in contributing to foc

85 ition suggesting synergism between increased RyR sensitivity and decreased IK1 in contributing to foc

86 Neither increased RyR sensitivity or decreased IK1 alone led to significan

87 nases appears necessary to observe increased RyR sensitivity.

88 we sought to determine the role of increased RyR sensitivity and decreased IK1 in contributing to foc

89 We studied the role of increased RyR sensitivity and decreased IK1 in contributing to foc

90 is a feedforward cycle between the increased RyR calcium release seen in presymptomatic AD mice and a

91 c reticulum (SR) Ca load is high, increasing RyR open probability promotes long-lasting sparks by pot

92 of Ca(2+) sparks originating from individual RyR clusters.

93 s of Ca2+ sparks originating from individual RyR clusters.

94 By inducing RyR intersubunit cross-linking, ROS can increase SR Ca(2

95 by 50 muM Ca(2+), Ln(3+) potently inhibited RyR's open probability (Kd Eu(3+) = 167 +/- 5 nM and Kd

96 elease properties due to variations in inter-RyR coupling via local subspace Ca(2+) concentration ([C

97 a membrane sites juxtaposed to intracellular RyRs, as well as in Kv2.1 phosphorylation state.

98 cryo-EM and with FRET measurements involving RyR and FK506-binding protein (FKBP).

99 ictory reports in muscle fibers and isolated RyRs, where Mg(2+) is present or absent, respectively, a

100 vates local [Ca(2+) ]SR , leading to luminal RyR sensitization and lowering of the activation thresho

101 +) inside the SR locally, leading to luminal RyR sensitization and lowering of the cytosolic Ca(2+) a

102 hundred RyRs, and we use a four-state Markov RyR gating model.

103 cells stably expressing the G4946E modified RyR, providing clear functional evidence that the G4946E

104 SERCA at concentrations required to modulate RyRs.

105 ICC express transcripts of multiple RyRs and InsP3 Rs, with Itpr1 and Ryr2 subtypes displayi

106 2460-2495 segment within the cardiac muscle RyR isoform (RyR2) central domain.

107 Mutations in skeletal muscle RyR (RyR1) are associated with congenital diseases such

108 novel information on the structural basis of RyR gating, identifying both similarities with, and diff

109 en by changes in the underlying behaviour of RyR channels.

110 ly combine confocal-scale (~ 200 nm) data of RyR clusters with 3D electron microscopy data (~ 30 nm)

111 but also to heterogeneous local densities of RyR clusters.

112 thod to simulate the spatial distribution of RyR clusters, which act as the major mediators of contra

113 g protein 12.6) on the cytoplasmic domain of RyR in isolated sarcoplasmic reticulum vesicles.

114 Here we show that the predominant form of RyR in skeletal muscle, RyR1, is subject to Cys-directed

115 as associated with marginal heterogeneity of RyR density.

116 rs, is required for dantrolene inhibition of RyR channels.

117 Inhibition of RyR, CREB, or miR132 as well as expression of a mutant p

118 support a model in which the interaction of RyR with CaM is nonuniform along the peptide, and the pr

119 Furthermore, knockdown of RyR expression in wild-type hippocampal neurons by two i

120 ence using a previously established model of RyR permeation and selectivity.

121 Thus, post-translational modifications of RyR occur downstream of Abeta through a beta2-adrenergic

122 D mice and is reversed upon normalization of RyR-evoked calcium release with chronic dantrolene treat

123 analyses showed increased phosphorylation of RyR in LQT2 myocytes versus controls.

124 trating the existence of an optimal range of RyR open probability favoring long-lasting sparks.

125 central vestibule and corner clamp region of RyR, resulting in a good match of the secondary structur

126 tion (I4790M) in highly conserved regions of RyR.

127 ight into the Ca(2+)-dependent regulation of RyR by CaM.

128 probes to investigate the Ca(2+) sensors of RyR, because they specifically bind to Ca(2+)-binding pr

129 oxin maurocalcine on the cytoplasmic side of RyR.

130 placing Kv2.1 in close proximity to sites of RyR-mediated Ca2+ release.

131 solved FRET detects two structural states of RyR-bound CaM, which respond to [Ca(2+)] and are isoform

132 In addition, we find that the structure of RyR clusters also influences Ca(2+) release properties d

133 ructural detail has impeded understanding of RyR gating and regulation.

134 cle SR microsomes as well as the function of RyRs in planar bilayers.

135 mapping and pharmacological manipulation of RyRs and IK1.

136 terminates the release; 2) if the number of RyRs is too large, the depletion of Ca from the junction

137 We found the following: 1) if the number of RyRs is too small, it is difficult to maintain consecuti

138 etected in recent cryo-EM reconstructions of RyRs.

139 spring could attribute to down-regulation of RyRs-BKCa, providing new information for further underst

140 different mechanisms underlie remodeling of RyRs and t-system.

141 Finally, acute stimulation of RyRs in heterologous cells causes a rapid hyperpolarizin

142 isms explaining functional data collected on RyR blockade.

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

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

145 -LITX-Lw1a), has a similar mode of action on RyRs as scorpion calcines, although with significantly g

146 derivatives displayed mild to no agonism on RyRs, SR Ca(2+) leak, or [(3)H]ryanodine binding studies

147 inding-site hypothesis of scorpion toxins on RyRs.

148 One RyR cluster contains a few to several hundred RyRs, and

149 ing, suggesting potential SERCA block and/or RyR agonism.

150 y changing the levels of SERCA, IP3R, and/or RyR.

151 cale approach may be useful in mapping other RyR sites of mechanistic interest within FRET range of F

152 However, unlike the other RyRs characterised to date, the M. persicae channel does

153 on increases coimmunoprecipitation between P-RyR and cardiac spliced BIN1+13+17 (with exons 13 and 17

154 imaging, we identified that BIN1 clusters P-RyR and CaV1.2.

155 BIN1 is also 50% reduced, with diminished P-RyR association with BIN1.

156 o concentrate BIN1 to t-tubules, impairing P-RyR recruitment.

157 tion of BIN1-induced microdomains recruits P-RyR into dyads, increasing the calcium transient while p

158 Phosphorylated RyRs (P-RyR) have increased calcium sensitivity and open probabi

159 edistributes BIN1 to t-tubules, recruiting P-RyRs and improving the calcium transient.

160 The resultant accumulation of uncoupled P-RyRs increases the incidence of spontaneous calcium rele

161 n was associated with a decrease in parallel RyR-mediated Ca2+ transients.

162 Phosphorylated RyRs (P-RyR) have increased calcium sensitivity and open

163 othesis that calmodulin (CaM), a physiologic RyR binding partner that is lost during incorporation in

164 In conclusion, MBED is a potent RyR agonist and, potentially, a better choice than caffe

165 ations of PCB 95, a NDL congener with potent RyR activity, significantly increased spine density and

166 Preventing RyR cross-linking with N-ethylmaleimide decreased the pr

167 resting RyR2 but is accelerated by promoting RyR opening or unzipping (by unlabeled DPc10).

168 ssue model is used to investigate how random RyR gating gives rise to probabilistic triggered activit

169 amino acid mutations in ryanodine receptor (RyR) and elevated activity of detoxification enzymes hav

170 r Ca(2+) release through ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3 R) channel

171 lar Ca2+ release through ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3R) channels

172 ts signaling between the ryanodine receptor (RyR) and the dihydropyridine receptor (DHPR), two protei

173 d phosphorylation of the Ryanodine Receptor (RyR) at a single serine (RyRS2808) is essential for norm

174 r peptide DPc10 bound to ryanodine receptor (RyR) Ca(2+) channels, we developed an approach that comb

175 does not inhibit single ryanodine receptor (RyR) Ca(2+) release channels in lipid bilayers.

176 release (CICR) from j-SR ryanodine receptor (RyR) Ca(2+) release channels.

177 lusters of intracellular ryanodine receptor (RyR) Ca2+ -release channels in mouse brain neurons, most

178 ion with each other, the ryanodine receptor (RyR) calcium channel preferentially conducts smaller cat

179 n neurons by stabilizing ryanodine receptor (RyR) calcium release channels in the open configuration,

180 Ryanodine receptor (RyR) calcium release channels showed lower sensitivity t

181 The ryanodine receptor (RyR) channel pore is formed by four S6 inner helices, wi

182 e receptor (InsP3 R) and ryanodine receptor (RyR) channels blocked ICC Ca(2+) transients.

183 s localized closely with ryanodine receptor (RyR) channels in the SR terminal cisternae.

184 ndoplasmic reticulum via ryanodine receptor (RyR) channels is critical in stimulating initial regener

185 ed by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that ar

186 ellular heterogeneity of ryanodine receptor (RyR) density and the transverse tubular system (t-system

187 receptor (IP3R) but not ryanodine receptor (RyR) expression was high in enamel cells suggesting that

188 s are believed to affect ryanodine receptor (RyR) gating in a "caffeine-like" manner, no single-chann

189 Cardiac ryanodine receptor (RyR) gating in rats and sheep was recorded at physiologi

190 biophysical model of the ryanodine receptor (RyR) in the computer model.

191 ted, only decreasing the ryanodine receptor (RyR) inactivation rate constant (kiCa) produced action p

192 Calcium leak from the ryanodine receptor (RyR) is regulated by reactive oxygen species (ROS), whic

193 ng sparks can occur when ryanodine receptor (RyR) open probability is either increased or decreased.

194 structural dynamics of a ryanodine receptor (RyR) peptide bound to calmodulin (CaM).

195 ic reticulum through the ryanodine receptor (RyR) reduces the amplitude of the Ca transient and slows

196 Ryanodine receptor (RyR) refractoriness played a key role in the onset of SR

197 d the sensitivity of the ryanodine receptor (RyR) release channels that produce sparks.

198 d the sensitivity of the ryanodine receptor (RyR) release channels that produce sparks.

199 te receptor (IP(3)R) and ryanodine receptor (RyR) represents a critical component of intracellular Ca

200 at the central domain of ryanodine receptor (RyR) serves as a transducer that converts long-range con

201 ulfide bonds between two ryanodine receptor (RyR) subunits, referred to as intersubunit cross-linking

202 cid mutation (G4946E) in ryanodine receptor (RyR) was highly correlated to diamide insecticide resist

203 hese diamides act on the ryanodine receptor (RyR), a large endoplasmic calcium release channel.

204 ate receptor (IP3R), and Ryanodine receptor (RyR), plays a major role in agonist-induced intracellula

205 tation in the Drosophila ryanodine receptor (RyR), which inhibits activity-induced increase in cytoso

206 h as with suppression of ryanodine receptor (RyR)-evoked calcium signaling.

207 axonal growth, through a ryanodine receptor (RyR)-mediated Ca(2+) release mechanism.

208 a2+ channel activity and ryanodine receptor (RyR)-mediated Ca2+ release, but underlying molecular mec

209 e latter is activated by ryanodine receptor (RyR)-mediated calcium (Ca(2+) ) release from the sarcopl

210 Alteration of ryanodine receptor (RyR)-mediated calcium (Ca(2+)) signaling has been report

211 or demonstrated enhanced ryanodine receptor (RyR)-mediated sarcoplasmic reticulum Ca(2+) leak in LQT2

212 s on the skeletal muscle ryanodine receptor (RyR).

213 potential A1 (TRPA1) and ryanodine receptor (RyR).

214 a(2+) sensitivity of the ryanodine receptor (RyRs) Ca(2+) release channel is low and it is unclear ho

215 ticulum (SR) Ca channel (ryanodine receptor, RyR) and/or decreased activity of the SR Ca ATPase (SERC

216 Ryanodine receptors (RyR) are calcium release channels, playing a major role

217 gests they may regulate ryanodine receptors (RyR) via multiple mechanisms.

218 rises from a cluster of ryanodine receptors (RyR).

219 ncreased sensitivity of ryanodine receptors (RyRs) and decreased inward rectifying K(+) current (IK1)

220 Ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3 Rs

221 mechanisms involve both ryanodine receptors (RyRs) and inositol triphosphate receptors (InsP3 Rs).

222 smic reticulum (ER) via ryanodine receptors (RyRs) and, while they often remained localised, they som

223 ver, when a fraction of ryanodine receptors (RyRs) are blocked by tetracaine or ruthenium red, Ca spa

224 The ryanodine receptors (RyRs) are high-conductance intracellular Ca(2+) channels

225 Ryanodine receptors (RyRs) are intracellular membrane channels playing key ro

226 at dyads consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels

227 Ryanodine receptors (RyRs) form calcium release channels located in the membr

228 taplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC.

229 e receptors (IP3Rs) and ryanodine receptors (RyRs) mediate release of Ca(2+) from internal stores in

230 Ryanodine receptors (RyRs) mediate the rapid release of calcium (Ca(2+)) from

231 ncreased sensitivity of ryanodine receptors (RyRs) to Ca(2+) release and down-regulation of the inwar

232 d) irreversibly targets ryanodine receptors (RyRs), a family of intracellular calcium release channel

233 cological regulation of ryanodine receptors (RyRs), L-type voltage-dependent Ca(2+) channels (VDCCs)

234 Activation of ryanodine receptors (RyRs), which can lead to activation of alphaCaMKII, also

235 ve activators of insect ryanodine receptors (RyRs).

236 events originating from ryanodine receptors (RyRs).

237 SkM) by stabilizing the ryanodine receptors (RyRs; RyR1 and RyR2, respectively).

238 on is also impaired, as indicated by reduced RyR agonist-induced calcium release from the ER and RyR-

239 ivery, we explored whether beta-AR-regulated RyRs are also affected by BIN1.

240 st to that of cardiac sarcoplasmic reticulum RyR.

241 ion by increasing the activity of ryanodine (RyR)-sensitive release channels on the peripheral sarcop

242 Ca(2+) regulates ryanodine receptor's (RyR) activity through an activating and an inhibiting Ca

243 IK1, or 200 muM caffeine (Caff) to sensitize RyRs, both alone and in combination.

244 Sensitizing RyR suppresses spatially concordant but not discordant S

245 Sensitizing RyR with caffeine (200 mumol/L) significantly reduced th

246 explains why dantrolene inhibition of single RyR channels has not been previously observed.

247 elease events require relatively small-sized RyR clusters (reducing flux as seen experimentally with

248 ters the single-channel function of skeletal RyR (RyR1).

249 ty, i.e., the probability that a spontaneous RyR opening triggers a Ca(2+) spark.

250 KBP1b), a small immunophilin that stabilizes RyR-mediated Ca2+ release in cardiomyocytes, declines in

251 Stimulating RyRs with 1 mm caffeine restored propagation.

252 the presence of beta-adrenergic stimulation, RyR-mediated Ca leak produces a biphasic decay of the Ca

253 ated by cytosolic and luminal Ca(2+) (tandem RyR activation) via a novel 'fire-diffuse-uptake-fire' (

254 We conclude that targeting RyR-mediated Ca(2+) leakage may be a therapeutic approac

255 We propose that RyR-mediated metaplastic mechanisms can be considered as

256 These experiments showed that RyR lost reactivity to changing cytosolic [Ca(2+)] from

257 It has been shown that RyR activity is regulated by dynamic post-translational

258 These findings suggest that RyR kinetics may play a critical role in altered Ca2+ ho

259 ts in NCX KO SAN cells also demonstrate that RyRs, but not NCX, are required for IP3 to modulate Ca(2

260 A number of ligands are able to activate the RyR channel, but whether these structurally diverse liga

261 Although the RyR is involved in heart failure-related Ca(2+) disturba

262 s does not involve direct competition at the RyR CaM binding site.

263 simulated-annealing constrained by both the RyR cryo-EM map and the FKBP atomic structure docked to

264 lease response in HEK293 cells and bound the RyR-specific ligand [(3)H]ryanodine.

265 establishing that, with ryanodine bound, the RyR pore adopts an extremely stable open conformation.

266 itial rate of [Ca(2+) ]i rise induced by the RyR activator caffeine without significantly affecting t

267 en peroxide induced SR calcium leak from the RyR and activation of CaMKII.

268 tein phosphatases type 1 and type 2 from the RyR complex.

269 s describe clear binding modes of Ryd in the RyR cavity and offer structural mechanisms explaining fu

270 is crucial for initiating and modulating the RyR-mediated Ca(2+) cycling that regulates SAN pacemakin

271 ne is to increase the Mg(2+) affinity of the RyR (or "stabilize" the resting state of the channel) an

272 ver, the Mg(2+)-dependent enhancement of the RyR adaptation was not evident in this RyR-type channel,

273 elays; (4) preventing phosphorylation of the RyR at serine 2808 with a knock-in mouse prevented the d

274 elays; (4) preventing phosphorylation of the RyR at serine 2808 with a knock-in mouse prevented the d

275 site located on the cytoplasmic side of the RyR channel.

276 oding the complete open reading frame of the RyR from M. persicae.

277 R luminal Ca(2+)-dependent regulation of the RyR is not critical for spark termination, but it can ex

278 nuously because the typical open time of the RyR is only a few milliseconds.

279 ated within the trans-membrane domain of the RyR, though the exact role of this mutation has not yet

280 rial ROS emission and S-nitrosylation of the RyR, whereas hydrogen peroxide induced SR calcium leak f

281 In particular, the RyR-mediated Ca(2+) upregulation within synaptic compart

282 leak with either caffeine (to sensitise the RyR to Ca activation) or ryanodine (non-sensitising) had

283 scent ligand binding assay revealed that the RyR containing multiple mutations displayed a significan

284 and the FKBP atomic structure docked to the RyR.

285 e in SkM SR Ca(2+) release observed with the RyR agonist caffeine.

286 pendent shRNAs to levels comparable with the RyR protein reduction in PS-deficient hippocampal neuron

287 CC that is based on tandem activation of the RyRs by cytosolic and luminal Ca(2+) through a 'fire-dif

288 Opening of these RyR clusters is triggered to produce a local, regenerati

289 f the RyR adaptation was not evident in this RyR-type channel, in contrast to that of cardiac sarcopl

290 nflux triggers Ca(2+) release solely through RyRs to generate SK-dependent slow afterhyperpolarizatio

291 (without altering the amount of CaM bound to RyR).

292 the atomistic details about how Ryd binds to RyRs.

293 sitising leak can be reversed by traditional RyR inhibitors such as tetracaine.

294 the features of other insect and vertebrate RyRs, including a highly conserved transmembrane region.

295 PCB 95 also induced spine formation via RyR- and miR132-dependent mechanisms in hippocampal slic

296 m of PCB developmental neurotoxicity whereby RyR sensitization modulates spine formation and synaptog

297 lines stably expressing either the wildtype RyR or the G4946E variant, in order to test the sensitiv

298 sed to trilaterate the acceptor locus within RyR.

299 Results locate the DPc10 probe within RyR domain 3, ?35 A from the previously docked N-termina

300 full-length cDNA encoding the P. xylostella RyR and established clonal Sf9 cell lines stably express

301 The up-regulation of P. xylostella RyR mRNA (PxRyR) expression has also been reported in fi