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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.
14 one of the NOX subunits, was activated after RyR-mediated Ca(2+) release, suggesting a feedforward me
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
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.
22 hanism that integrates both NOX activity and RyR-mediated Ca(2+) release to support cellular mechanis
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
30 inated packing of L-type Ca(2+) channels and RyRs into dyadic junctions during development, and order
32 hese data suggest an interdependence between RyR and InsP3 R in the generation of Ca(2+) transients.
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
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
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
49 have shown that a phosphorylation defective RyR mutant mouse (RyRS2808A) does not respond normally t
52 blished literature showing that dysregulated RyRs contribute to the altered Ca(2+) regulatory phenoty
56 l perturbation of CaM, with implications for RyR regulation and the decay of muscle function in aging
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
62 ally, using our unique method for generating RyR cluster distributions, we demonstrate the robustness
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
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
78 we sought to determine 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
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
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
99 cells stably expressing the G4946E modified RyR, providing clear functional evidence that the G4946E
103 but consistent bias against recruiting more RyRs to open during the middle of a Ca(2+) release event
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
111 ly combine confocal-scale (~ 200 nm) data of RyR clusters with 3D electron microscopy data (~ 30 nm)
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
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
129 significant negative feedback regulation of RyR activity on Na(v)1.4 properties through increased or
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
136 solved FRET detects two structural states of RyR-bound CaM, which respond to [Ca(2+)] and are isoform
138 sm relies on the asymmetric distributions of RyRs and sarco/ER calcium-ATPase (SERCA) pumps that we p
141 ry was underscored by correlative imaging of RyRs and t-tubules, which enabled quantification of dyad
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
148 spring could attribute to down-regulation of RyRs-BKCa, providing new information for further underst
152 derivatives displayed mild to no agonism on RyRs, SR Ca(2+) leak, or [(3)H]ryanodine binding studies
158 on increases coimmunoprecipitation between P-RyR and cardiac spliced BIN1+13+17 (with exons 13 and 17
162 tion of BIN1-induced microdomains recruits P-RyR into dyads, increasing the calcium transient while p
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
169 othesis that calmodulin (CaM), a physiologic RyR binding partner that is lost during incorporation in
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
177 lusters of intracellular ryanodine receptor (RyR) Ca2+ -release channels in mouse brain neurons, most
182 ed by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that ar
184 ellular heterogeneity of ryanodine receptor (RyR) density and the transverse tubular system (t-system
186 receptor (IP3R) but not ryanodine receptor (RyR) expression was high in enamel cells suggesting that
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
192 ic reticulum through the ryanodine receptor (RyR) reduces the amplitude of the Ca transient and slows
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
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
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
215 ncreased sensitivity of ryanodine receptors (RyRs) and decreased inward rectifying K(+) current (IK1)
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
221 at dyads consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels
225 taplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC.
228 ncreased sensitivity of ryanodine receptors (RyRs) to Ca(2+) release and down-regulation of the inwar
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)
239 ion by increasing the activity of ryanodine (RyR)-sensitive release channels on the peripheral sarcop
245 e understood, less is known about how single-RyR gating properties define the RyR group dynamics in a
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
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
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' (
258 Collectively, these findings indicate that RyR dysfunction shapes ER Ca(2+) dynamics in beta cells
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
266 simulated-annealing constrained by both the RyR cryo-EM map and the FKBP atomic structure docked to
268 itial rate of [Ca(2+) ]i rise induced by the RyR activator caffeine without significantly affecting t
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
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
284 leak with either caffeine (to sensitise the RyR to Ca activation) or ryanodine (non-sensitising) had
290 CC that is based on tandem activation of the RyRs by cytosolic and luminal Ca(2+) through a 'fire-dif
296 lines stably expressing either the wildtype RyR or the G4946E variant, in order to test the sensitiv
299 full-length cDNA encoding the P. xylostella RyR and established clonal Sf9 cell lines stably express