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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                                              RyRs are so named because they bind the plant alkaloid r
5                                              RyRs are the largest known ion channels, with a homotetr
6                                              RyRs play a major role in excitation-contraction couplin
7 complex of the rabbit skeletal muscle type 1 RyR (RyR1), solved by single-particle electron cryomicro
8 ts, CRUs), contained an average of 18 and 23 RyRs at the surface and interior, respectively, although
9 tis elegans, we find that mutation of unc-68/RyR greatly impedes both outgrowth and guidance of the r
10 ects of modulators for TMEM16A or VDCCs on a RyR-mediated rise in global [Ca(2+)]i and impairs the to
11 al development and Rac1 activation through a RyR-mediated mechanism, which in turn activates NOX thro
12 s caused by a global rise in [Ca(2+)]i via a RyR-TMEM16A-VDCC signalling module sets the basal tone.
13 hologic conditions, thus precluding abnormal RyR-mediated Ca(2+) release.
14 one of the NOX subunits, was activated after RyR-mediated Ca(2+) release, suggesting a feedforward me
15 tes, as erroneous merging of axially aligned RyRs was circumvented.
16 e-sensing gate structure is conserved in all RyR and inositol 1,4,5-trisphosphate receptor isoforms.
17 Nevertheless, submicromolar S100A1 can alter RyR function, an effect that is influenced by both [Ca(2
18 termine whether diabetogenic stressors alter RyR or IP(3)R function.
19  the molecular mechanisms underlying altered RyR-mediated intracellular Ca(2+) release in AD remain t
20 les and similarly 'orphaned' in HF, although RyR distribution along Z-lines was relatively sparse.
21        MG53 inhibits IFNbeta induction in an RyR-dependent manner.
22 hanism that integrates both NOX activity and RyR-mediated Ca(2+) release to support cellular mechanis
23 lic Ca diffusion, SERCA uptake activity, and RyR open probability.
24                 In line with CaMKIIdelta and RyR inhibition, SN treatment decreased Ca(2+) spark freq
25 ntrations whereas lowered levels of IP3R and RyR need higher agonist concentration for intracellular
26 icance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynamics of VSMC and to
27 the contribution of the link between NOX and RyR-mediated Ca(2+) release toward axonal specification
28 ting a feedforward mechanism between NOX and RyR.
29                Characterization of TRPA1 and RyR demonstrates that Ca(2+) signaling is required for o
30 inated packing of L-type Ca(2+) channels and RyRs into dyadic junctions during development, and order
31  the SR Ca(2+)-stimulated ATPase (SERCA) and RyRs by K201.
32 hese data suggest an interdependence between RyR and InsP3 R in the generation of Ca(2+) transients.
33 t inactivation, or physical coupling between RyRs when Ca(2+) flux is below a threshold value.
34          During VF, [Ca(2+)]SR was high, but RyR remained nearly continuously refractory, resulting i
35 pecific localized calcium signal mediated by RyR channel activity that stimulates regenerative outgro
36 ral features explain high ion conductance by RyRs and the long-range allosteric regulation of channel
37  NCX; (iii) propagation can be maintained by RyRs if they have been sensitised to Ca(2+).
38 cates a lack of competition by S100A1 on CaM/RyR binding under normal physiological conditions.
39 s, high micromolar S100A1 does alter the CaM/RyR interaction, without involving competition.
40 odel is consistent with the RyR1 and cardiac RyR (RyR2) open-channel structures reported while this p
41 3778-4201) that contains a number of cardiac RyR (RyR2) mutations associated with catecholaminergic p
42 ytoplasmic region in the function of cardiac RyR (RyR2) via structure-guided site-directed mutagenesi
43 s driven by stochastic Ca2+ release channel (RyR) gating and is used to study mechanisms of DAD varia
44  ryanodine receptor Ca(2+) release channels (RyRs), causing enhanced vascular tone.
45                                Consequently, RyR is recognized as a high-value target for drug discov
46 driven and occurred as a result of decreased RyR inactivation which led to increased steepness of the
47 ough to produce frequent firings, decreasing RyR open probability counter-intuitively promotes long-l
48                  In this setting, decreasing RyR open probability further suppresses long-lasting spa
49  have shown that a phosphorylation defective RyR mutant mouse (RyRS2808A) does not respond normally t
50 f hearts and inhibited CaMKIIdelta-dependent RyR phosphorylation.
51 bled quantification of dyadic and non-dyadic RyR populations.
52 blished literature showing that dysregulated RyRs contribute to the altered Ca(2+) regulatory phenoty
53                                         Each RyR opens stochastically and is regulated by cytosolic a
54 ndritic calcium release mediated by enhanced RyR calcium release.
55 to create a calibration curve for estimating RyR number based on recorded fluorescence blinks.
56 l perturbation of CaM, with implications for RyR regulation and the decay of muscle function in aging
57                 Instead, MBED's affinity for RyRs (EC50 approximately 0.5 muM) was much larger than f
58  IP(3) receptors, spatial amplification from RyRs and ongoing refilling of ER via the sarcoplasmic/en
59 on is influenced by the number of functional RyRs in a junctional cluster (which is reduced by tetrac
60           We varied the number of functional RyRs in the single cluster, diffusion within the SR netw
61 ng clear functional evidence that the G4946E RyR mutation impairs diamide insecticide binding.
62 ally, using our unique method for generating RyR cluster distributions, we demonstrate the robustness
63 y reduced [Ca(2+)] likely reflecting gradual RyR inactivation with >=1.0 mM caffeine.
64  Here, we tested the impact of heterogeneous RyR cluster size on the initiation of Ca waves.
65 , we found a similar degree of heterogeneous RyR remodeling, despite preserved t-system.
66                                     However, RyR blockade distinctly prevented beta-cell death, propa
67 yR cluster contains a few to several hundred RyRs, and we use a four-state Markov RyR gating model.
68  variable size from a few to several hundred RyRs, creating a spatially nonuniform intracellular dist
69                             We conclude: (i) RyRs are required for the initiation of Ca(2+) waves, bu
70      These data support evidence implicating RyRs as targets in environmentally triggered NDDs and su
71 s in the [Ca2+]i transient to differences in RyR cluster distributions measured between rat and human
72 nto how Ryd interacts with major residues in RyRs that were experimentally determined to be critical
73  results suggest synergism between increased RyR sensitivity and decreased IK1 in contributing to foc
74 ition suggesting synergism between increased RyR sensitivity and decreased IK1 in contributing to foc
75 vidual congeners (50 nM to 50 muM) increased RyR activity by 2.4-19.2-fold.
76                            Neither increased RyR sensitivity or decreased IK1 alone led to significan
77 nases appears necessary to observe increased RyR sensitivity.
78 we sought to determine the role of increased RyR sensitivity and decreased IK1 in contributing to foc
79             We studied the role of increased RyR sensitivity and decreased IK1 in contributing to foc
80 is a feedforward cycle between the increased RyR calcium release seen in presymptomatic AD mice and a
81 c reticulum (SR) Ca load is high, increasing RyR open probability promotes long-lasting sparks by pot
82 hesis implicating Epac actions in increasing RyR-mediated SR Ca(2+) release resulting in a Ca(2+)-med
83 of Ca(2+) sparks originating from individual RyR clusters.
84                                  By inducing RyR intersubunit cross-linking, ROS can increase SR Ca(2
85 that dantrolene also requires ATP to inhibit RyR.
86  by 50 muM Ca(2+), Ln(3+) potently inhibited RyR's open probability (Kd Eu(3+) = 167 +/- 5 nM and Kd
87  the fungal natural product and known insect RyR antagonist (-)-verticilide and several congeners to
88 e data provide novel, nanoscale insight into RyR organization and function across cardiomyocytes.
89 ictory reports in muscle fibers and isolated RyRs, where Mg(2+) is present or absent, respectively, a
90                                       Larger RyR clusters have lower SR Ca release threshold for loca
91  wave initiation and propagation from larger RyR clusters.
92                              However, larger RyR clusters tend to lower SR Ca load because of the hig
93                      This enabled Kv2.1-LTCC-RyR triads to generate localized Ca(2+) release events (
94 vates local [Ca(2+) ]SR , leading to luminal RyR sensitization and lowering of the activation thresho
95 +) inside the SR locally, leading to luminal RyR sensitization and lowering of the cytosolic Ca(2+) a
96 hundred RyRs, and we use a four-state Markov RyR gating model.
97                  Experimentally, we measured RyR cluster sizes at Ca spark sites in rat ventricular m
98 nd constituted ~75% of the roughly 1 million RyRs present in an average cardiomyocyte.
99  cells stably expressing the G4946E modified RyR, providing clear functional evidence that the G4946E
100 SERCA at concentrations required to modulate RyRs.
101                 Internal CRUs contained more RyRs in more clusters than CRUs on the cell surface, and
102  a recruitment bias in favor of opening more RyRs.
103  but consistent bias against recruiting more RyRs to open during the middle of a Ca(2+) release event
104          ICC express transcripts of multiple RyRs and InsP3 Rs, with Itpr1 and Ryr2 subtypes displayi
105                        In a cardiac myocyte, RyRs group into clusters of variable size from a few to
106 nism in which fluxed Ca(2+) activates nearby RyRs.
107 ), i.e. functional groupings of neighbouring RyR clusters, were similarly observed to be smaller than
108 ace CRUs, contained larger and more numerous RyR clusters, and constituted ~75% of the roughly 1 mill
109                      Complex arrangements of RyR clusters were observed in 3D space, both at the cell
110 en by changes in the underlying behaviour of RyR channels.
111 ly combine confocal-scale (~ 200 nm) data of RyR clusters with 3D electron microscopy data (~ 30 nm)
112 but also to heterogeneous local densities of RyR clusters.
113 at a spatially heterogeneous distribution of RyR cluster size under pathological conditions may poten
114 thod to simulate the spatial distribution of RyR clusters, which act as the major mediators of contra
115 e corresponding to the CaM-binding domain of RyR (RyRp).
116 g protein 12.6) on the cytoplasmic domain of RyR in isolated sarcoplasmic reticulum vesicles.
117                      Functional groupings of RyR clusters (Ca(2+) release units, CRUs), contained an
118           It is unclear how heterogeneity of RyR cluster size alters spontaneous sarcoplasmic reticul
119 as associated with marginal heterogeneity of RyR density.
120 rs, is required for dantrolene inhibition of RyR channels.
121  support a model in which the interaction of RyR with CaM is nonuniform along the peptide, and the pr
122 hippocampal slices, and expression levels of RyR in the hippocampus that were altered in the 3xTg mic
123  this using simulations with three models of RyR gating that have identical open probabilities: the c
124    Thus, post-translational modifications of RyR occur downstream of Abeta through a beta2-adrenergic
125 D mice and is reversed upon normalization of RyR-evoked calcium release with chronic dantrolene treat
126 surface showed an undulating organization of RyR clusters, resulting in their frequent overlap in the
127 as lost during the purification procedure of RyR.
128 trating the existence of an optimal range of RyR open probability favoring long-lasting sparks.
129  significant negative feedback regulation of RyR activity on Na(v)1.4 properties through increased or
130 ight into the Ca(2+)-dependent regulation of RyR by CaM.
131 n CaM structure and functional regulation of RyR in physiologically relevant conditions is largely un
132  probes to investigate the Ca(2+) sensors of RyR, because they specifically bind to Ca(2+)-binding pr
133 oxin maurocalcine on the cytoplasmic side of RyR.
134                           The simulations of RyR clusters that utilize the multiexponential gating mo
135 litude increase nonlinearly with the size of RyR clusters.
136 solved FRET detects two structural states of RyR-bound CaM, which respond to [Ca(2+)] and are isoform
137 ructural detail has impeded understanding of RyR gating and regulation.
138 sm relies on the asymmetric distributions of RyRs and sarco/ER calcium-ATPase (SERCA) pumps that we p
139 clamp were utilized to measure engagement of RyRs as a direct target of DM.
140 cle SR microsomes as well as the function of RyRs in planar bilayers.
141 ry was underscored by correlative imaging of RyRs and t-tubules, which enabled quantification of dyad
142         However, the precise localization of RyRs remains unknown, due to shortcomings of imaging tec
143  mapping and pharmacological manipulation of RyRs and IK1.
144  terminates the release; 2) if the number of RyRs is too large, the depletion of Ca from the junction
145  We found the following: 1) if the number of RyRs is too small, it is difficult to maintain consecuti
146 o determine the 3D nanoscale organization of RyRs in rat cardiomyocytes by employing direct stochasti
147 etected in recent cryo-EM reconstructions of RyRs.
148 spring could attribute to down-regulation of RyRs-BKCa, providing new information for further underst
149  different mechanisms underlie remodeling of RyRs and t-system.
150 isms explaining functional data collected on RyR blockade.
151             In this review, we focus, not on RyR/IP3 R, but on other ion-channels that are known to b
152  derivatives displayed mild to no agonism on RyRs, SR Ca(2+) leak, or [(3)H]ryanodine binding studies
153                                          One RyR cluster contains a few to several hundred RyRs, and
154 (2+) release events with relatively few open RyRs.
155 asmic reticulum (SR), and another, with open RyRs and a depleted SR.
156 ing, suggesting potential SERCA block and/or RyR agonism.
157 y changing the levels of SERCA, IP3R, and/or RyR.
158 on increases coimmunoprecipitation between P-RyR and cardiac spliced BIN1+13+17 (with exons 13 and 17
159  imaging, we identified that BIN1 clusters P-RyR and CaV1.2.
160  BIN1 is also 50% reduced, with diminished P-RyR association with BIN1.
161 o concentrate BIN1 to t-tubules, impairing P-RyR recruitment.
162 tion of BIN1-induced microdomains recruits P-RyR into dyads, increasing the calcium transient while p
163                       Phosphorylated RyRs (P-RyR) have increased calcium sensitivity and open probabi
164 edistributes BIN1 to t-tubules, recruiting P-RyRs and improving the calcium transient.
165    The resultant accumulation of uncoupled P-RyRs increases the incidence of spontaneous calcium rele
166 ct mechanism of action compared with the pan-RyR inhibitors dantrolene and tetracaine and the antiarr
167 n was associated with a decrease in parallel RyR-mediated Ca2+ transients.
168                               Phosphorylated RyRs (P-RyR) have increased calcium sensitivity and open
169 othesis that calmodulin (CaM), a physiologic RyR binding partner that is lost during incorporation in
170                                   Preventing RyR cross-linking with N-ethylmaleimide decreased the pr
171 ssue model is used to investigate how random RyR gating gives rise to probabilistic triggered activit
172  amino acid mutations in ryanodine receptor (RyR) and elevated activity of detoxification enzymes hav
173 r Ca(2+) release through ryanodine receptor (RyR) and inositol trisphosphate receptor (IP3 R) channel
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          Here, we report ryanodine receptor (RyR) channel activity and Ca(2+) release both are increa
179                      The ryanodine receptor (RyR) channel pore is formed by four S6 inner helices, wi
180 e receptor (InsP3 R) and ryanodine receptor (RyR) channels blocked ICC Ca(2+) transients.
181 s localized closely with ryanodine receptor (RyR) channels in the SR terminal cisternae.
182 ed by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that ar
183  stores via dysregulated ryanodine receptor (RyR) channels.
184 ellular heterogeneity of ryanodine receptor (RyR) density and the transverse tubular system (t-system
185 (2+) channels (LTCCs) to ryanodine receptor (RyR) ER Ca(2+) release channels.
186  receptor (IP3R) but not ryanodine receptor (RyR) expression was high in enamel cells suggesting that
187          Dantrolene is a ryanodine receptor (RyR) inhibitor, which is used to relax muscles in malign
188 estigated effects of the ryanodine receptor (RyR) modulator caffeine on Na(+) current (I(Na)) activat
189 ng sparks can occur when ryanodine receptor (RyR) open probability is either increased or decreased.
190 specific role for either ryanodine receptor (RyR) or inositol 1,4,5-triphosphate receptor (IP(3)R) dy
191 structural dynamics of a ryanodine receptor (RyR) peptide bound to calmodulin (CaM).
192 ic reticulum through the ryanodine receptor (RyR) reduces the amplitude of the Ca transient and slows
193 d the sensitivity of the ryanodine receptor (RyR) release channels that produce sparks.
194 at the central domain of ryanodine receptor (RyR) serves as a transducer that converts long-range con
195 ulfide bonds between two ryanodine receptor (RyR) subunits, referred to as intersubunit cross-linking
196 ate receptor (IP3R), and Ryanodine receptor (RyR), plays a major role in agonist-induced intracellula
197 has been associated with ryanodine receptor (RyR), such that spines lacking SP release less calcium f
198 tation in the Drosophila ryanodine receptor (RyR), which inhibits activity-induced increase in cytoso
199 h as with suppression of ryanodine receptor (RyR)-evoked calcium signaling.
200 axonal growth, through a ryanodine receptor (RyR)-mediated Ca(2+) release mechanism.
201 a2+ channel activity and ryanodine receptor (RyR)-mediated Ca2+ release, but underlying molecular mec
202 e latter is activated by ryanodine receptor (RyR)-mediated calcium (Ca(2+) ) release from the sarcopl
203            Alteration of ryanodine receptor (RyR)-mediated calcium (Ca(2+)) signaling has been report
204 potential A1 (TRPA1) and ryanodine receptor (RyR).
205 s on the skeletal muscle ryanodine receptor (RyR).
206 calcium release channel, ryanodine receptor (RyR).
207 rmone receptor (THR) and ryanodine receptor (RyR).
208  oscillation mediated by ryanodine receptor (RyR).
209 lcium ions arriving at a Ryanodyne receptor (RyR).
210 a(2+) sensitivity of the ryanodine receptor (RyRs) Ca(2+) release channel is low and it is unclear ho
211 ticulum (SR) Ca channel (ryanodine receptor, RyR) and/or decreased activity of the SR Ca ATPase (SERC
212 states, one with closed ryanodine receptors (RyR) and most calcium in the cell stored in the sarcopla
213                         Ryanodine receptors (RyR) are calcium release channels, playing a major role
214 gests they may regulate ryanodine receptors (RyR) via multiple mechanisms.
215 ncreased sensitivity of ryanodine receptors (RyRs) and decreased inward rectifying K(+) current (IK1)
216                         Ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3 Rs
217 mechanisms involve both ryanodine receptors (RyRs) and inositol triphosphate receptors (InsP3 Rs).
218 smic reticulum (ER) via ryanodine receptors (RyRs) and, while they often remained localised, they som
219 ver, when a fraction of ryanodine receptors (RyRs) are blocked by tetracaine or ruthenium red, Ca spa
220                     The ryanodine receptors (RyRs) are high-conductance intracellular Ca(2+) channels
221  at dyads consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels
222                         Ryanodine receptors (RyRs) form calcium release channels located in the membr
223           Historically, ryanodine receptors (RyRs) have presented unique challenges for high-resoluti
224 ale, 3D organization of ryanodine receptors (RyRs) in cardiomyocytes.
225 taplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC.
226                         Ryanodine receptors (RyRs) mediate calcium (Ca)-induced Ca release and intrac
227                         Ryanodine receptors (RyRs) mediate the rapid release of calcium (Ca(2+)) from
228 ncreased sensitivity of ryanodine receptors (RyRs) to Ca(2+) release and down-regulation of the inwar
229                         Ryanodine receptors (RyRs) were observed to be laid down in advance of develo
230 d) irreversibly targets ryanodine receptors (RyRs), a family of intracellular calcium release channel
231 cological regulation of ryanodine receptors (RyRs), L-type voltage-dependent Ca(2+) channels (VDCCs)
232 ve activators of insect ryanodine receptors (RyRs).
233 events originating from ryanodine receptors (RyRs).
234  on Ca(2+) release from ryanodine receptors (RyRs).
235 SkM) by stabilizing the ryanodine receptors (RyRs; RyR1 and RyR2, respectively).
236             Namely, 10 uM dantrolene reduced RyR channel open probability by ~50% in the presence of
237 ivery, we explored whether beta-AR-regulated RyRs are also affected by BIN1.
238  of all CRUs contained only a single 'rogue' RyR.
239 ion by increasing the activity of ryanodine (RyR)-sensitive release channels on the peripheral sarcop
240       Ca(2+) regulates ryanodine receptor's (RyR) activity through an activating and an inhibiting Ca
241 IK1, or 200 muM caffeine (Caff) to sensitize RyRs, both alone and in combination.
242                                  Sensitizing RyR suppresses spatially concordant but not discordant S
243  (SR) vesicles, but failed to inhibit single RyR channel currents in bilayers.
244 explains why dantrolene inhibition of single RyR channels has not been previously observed.
245 e understood, less is known about how single-RyR gating properties define the RyR group dynamics in a
246                  Thus, the details of single-RyR gating can profoundly affect SR Ca(2+) release even
247 ence stems from the two-state model's single-RyR OT and CT distributions being qualitatively differen
248 elease events require relatively small-sized RyR clusters (reducing flux as seen experimentally with
249 ters the single-channel function of skeletal RyR (RyR1).
250                  Mixtures of large and small RyR clusters potentiates Ca waves because the enhanced S
251  myocyte level, homogeneously large or small RyR clusters limit Ca waves (because of low load for lar
252 e cell surface and interior revealed smaller RyR clusters than 2D estimates, as erroneous merging of
253 KBP1b), a small immunophilin that stabilizes RyR-mediated Ca2+ release in cardiomyocytes, declines in
254                                  Stimulating RyRs with 1 mm caffeine restored propagation.
255 the presence of beta-adrenergic stimulation, RyR-mediated Ca leak produces a biphasic decay of the Ca
256 ated by cytosolic and luminal Ca(2+) (tandem RyR activation) via a novel 'fire-diffuse-uptake-fire' (
257                   We conclude that targeting RyR-mediated Ca(2+) leakage may be a therapeutic approac
258   Collectively, these findings indicate that RyR dysfunction shapes ER Ca(2+) dynamics in beta cells
259                              We propose that RyR-mediated metaplastic mechanisms can be considered as
260                These experiments showed that RyR lost reactivity to changing cytosolic [Ca(2+)] from
261 R activation and cell death, suggesting that RyR-mediated loss of ER Ca(2+) may be an early pathogeni
262 ts in NCX KO SAN cells also demonstrate that RyRs, but not NCX, are required for IP3 to modulate Ca(2
263                  Our findings suggested that RyRs were sensitive molecular targets of DM with functio
264                                 Although the RyR is involved in heart failure-related Ca(2+) disturba
265 s does not involve direct competition at the RyR CaM binding site.
266  simulated-annealing constrained by both the RyR cryo-EM map and the FKBP atomic structure docked to
267 lease response in HEK293 cells and bound the RyR-specific ligand [(3)H]ryanodine.
268 itial rate of [Ca(2+) ]i rise induced by the RyR activator caffeine without significantly affecting t
269  how single-RyR gating properties define the RyR group dynamics in an array of many channels.
270 en peroxide induced SR calcium leak from the RyR and activation of CaMKII.
271 at depend on both ER Ca(2+) leakage from the RyR and plasma membrane depolarization.
272 tein phosphatases type 1 and type 2 from the RyR complex.
273 s describe clear binding modes of Ryd in the RyR cavity and offer structural mechanisms explaining fu
274 is crucial for initiating and modulating the RyR-mediated Ca(2+) cycling that regulates SAN pacemakin
275 ne is to increase the Mg(2+) affinity of the RyR (or "stabilize" the resting state of the channel) an
276 elays; (4) preventing phosphorylation of the RyR at serine 2808 with a knock-in mouse prevented the d
277 hibian muscles endowed with isoform 3 of the RyR channel, Ca(2+) spark frequency is correlated with t
278  site located on the cytoplasmic side of the RyR channel.
279 nuously because the typical open time of the RyR is only a few milliseconds.
280 servation, pharmacological inhibition of the RyR with ryanodine and inhibition of the IP(3)R with xes
281 ated within the trans-membrane domain of the RyR, though the exact role of this mutation has not yet
282 rial ROS emission and S-nitrosylation of the RyR, whereas hydrogen peroxide induced SR calcium leak f
283 ts were abolished by further addition of the RyR-inhibitor dantrolene (10 uM).
284  leak with either caffeine (to sensitise the RyR to Ca activation) or ryanodine (non-sensitising) had
285                Our results revealed that the RyR is sensitive mainly to ER stress-induced dysfunction
286        Adding a small amount of noise to the RyR behavior increases the parameter region where oscill
287             Although dantrolene binds to the RyR protein, its mechanism of action is unknown, mainly
288  and the FKBP atomic structure docked to the RyR.
289 e in SkM SR Ca(2+) release observed with the RyR agonist caffeine.
290 CC that is based on tandem activation of the RyRs by cytosolic and luminal Ca(2+) through a 'fire-dif
291                                        Thus, RyR clusters were found to be significantly smaller than
292 (without altering the amount of CaM bound to RyR).
293 the atomistic details about how Ryd binds to RyRs.
294 gher potency than the parent congener toward RyR.
295 sitising leak can be reversed by traditional RyR inhibitors such as tetracaine.
296  lines stably expressing either the wildtype RyR or the G4946E variant, in order to test the sensitiv
297 ed after establishing the patch seal or with RyR block by 10 muM dantrolene.
298 ion to the dyads, where they colocalize with RyRs.
299  full-length cDNA encoding the P. xylostella RyR and established clonal Sf9 cell lines stably express
300           The up-regulation of P. xylostella RyR mRNA (PxRyR) expression has also been reported in fi

 
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