ライフサイエンスコーパス: sarcoplasmic

1 B6a localized to myonuclei while DNAJB6b was sarcoplasmic.

2 Similarly, hnRNPA1 and hnRNPA2/B1 formed sarcoplasmic aggregates in patients with LGMD1D.

3 ase channels located in the membranes of the sarcoplasmic and endoplasmic reticulum.

4 d ryanodine receptor type 2 (RyR2)-dependent sarcoplasmic Ca(2+) leak.

5 y early pathogenesis, including dysregulated sarcoplasmic calcium and increased lethality.

6 gargin, a subnanomolar inhibitor of the endo/sarcoplasmic calcium ATPase (SERCA), is presented.

7 Sarcoplasmic calcium dysregulation in dys-1 worms preced

8 It remains unresolved whether increased sarcoplasmic calcium observed in dystrophic muscles foll

9 myosin, arginine kinase, myosin light chain, sarcoplasmic calcium-binding protein, and hemocyanin are

10 oxide synthase 2-positive muscle fibers with sarcoplasmic colocalization of markers of regeneration a

11 to sarcomere mutation-positive HCM, whereas sarcoplasmic endoplasmic reticular calcium ATPase 2 abun

12 educed in HCM regardless of genotype, as was sarcoplasmic endoplasmic reticular calcium ATPase 2/phos

13 (45)Ca sarcoplasmic endoplasmic reticular calcium ATPaseuptake

14 This compound is a potent inhibitor of the sarcoplasmic-endoplasmic reticulum Ca(2+)-ATPase calcium

15 channels that are known to be present in the sarcoplasmic/endoplasmic reticulum (ER/SR) membranes.

16 Sarcoplasmic/endoplasmic reticulum Ca(2+) adenosine trip

17 (RyR1), dihydropyridine receptor (DHPR), and sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA)

18 ticulum Ca(2+) content via rescue of control sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase levels

19 Sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA2

20 ciparum with differential sensitivity to the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pump in

21 ase and influx elicited by inhibitors of the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pumps,

22 Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) a

23 ular partners, including the ER calcium pump sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA

24 ng, increased contractile function, elevated sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SER

25 concentration regulatory proteins, that is, sarcoplasmic/endoplasmic reticulum calcium ATPase 2 and

26 kinase-domain, which in turn phosphorylates sarcoplasmic/endoplasmic reticulum calcium-ATPase 2a (SE

27 argets the ryanodine receptor present in the sarcoplasmic/endoplasmic reticulum to promote Ca(2+) rel

28 rom RyRs and ongoing refilling of ER via the sarcoplasmic/endoplasmic-reticulum-Ca(2+) -ATPase.

29 ticulum (EnR) homeostasis through preserving sarcoplasmic/EnR calcium ATPase 2b (SERCA2b) function in

30 that LGMD1D mutations in DNAJB6 disrupt its sarcoplasmic function suggesting a role for DNAJB6b in Z

31 gressive myopathy with highly characteristic sarcoplasmic inclusions in skeletal and cardiac muscle.

32 tural abnormalities including ringed fibres, sarcoplasmic masses or Z-band disorganization, which are

33 ixed muscle protein and the myofibrillar and sarcoplasmic muscle fractions.

34 induced by thapsigargin, an inhibitor of the sarcoplasmic or endoplasmic reticulum calcium ATPase fam

35 P, this processing modified the 1-D SDS-PAGE sarcoplasmic patterns in a direct-dependent manner and e

36 ical role in vertebrates, and as the primary sarcoplasmic pigment in meat, influences quality percept

37 ns, namely mince (M), washed mince (WM), and sarcoplasmic protein (SP), were investigated.

38 nd tryptophan fluorescence spectra indicated sarcoplasmic protein denaturation in drip due to freezin

39 However, sarcoplasmic protein denaturation was independent of fre

40 veral peptides derived from myofibrillar and sarcoplasmic proteins are sufficiently resistant to proc

41 od for evaluating proteolytic degradation of sarcoplasmic proteins during the processing of dry-cured

42 al sodium dodecyl sulphate (SDS)-soluble and sarcoplasmic proteins in frozen (-10 degrees C for 3 mon

43 nvestigated denaturation of myofibrillar and sarcoplasmic proteins of pork loins caused by freezing-t

44 inhibitor from common carp (Cyprinus carpio) sarcoplasmic proteins resulted in 2.8% yield with purifi

45 rolox/g), whereas the ex vivo hydrolysate of sarcoplasmic proteins showed the highest DPPH scavenging

46 dentification and relative quantification of sarcoplasmic proteins through individual quantification

47 antify changes in the abundance of the major sarcoplasmic proteins throughout the ham dry-curing proc

48 For this purpose, extraction of sarcoplasmic proteins was followed by trypsin digestion

49 ivo hydrolysate, whereas the peptide PW from sarcoplasmic proteins was identified only in the in vitr

50 The sarcoplasmic proteins were hydrolyzed faster than the my

51 differences in abundance of myofibrillar and sarcoplasmic proteins were observed between samples and

52 total of five non-redundant myofibrillar and sarcoplasmic proteins.

53 18 differentially abundant myofibrillar and sarcoplasmic proteins/isoforms contributing to proteomic

54 We propose that VCP sustains sarcoplasmic proteostasis, in part, by controlling the i

55 Dysregulated sarcoplasmic RBM20 RNP granules displayed liquid-like ma

56 iprotein complexes at discrete plasmalemmal, sarcoplasmic reticular and myofilament sites, reveals di

57 ntain close contacts between the endoplasmic/sarcoplasmic reticulum (ER/SR) and the plasma membrane i

58 omal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum (ER/SR) Ca(2+) sensor, is unclear

59 lcium (Ca(2+) ) release channels on the endo/sarcoplasmic reticulum (ER/SR).

60 that lysosomes form close contacts with the sarcoplasmic reticulum (separation approximately 25 nm).

61 sed on the activity of an ATPase pump in the sarcoplasmic reticulum (SERCA1a) and is controlled by th

62 arcolemma triggering Ca(2+) release from the sarcoplasmic reticulum (SR) - a process termed Ca(2+) -i

63 d Ca(2+) release from central non-junctional sarcoplasmic reticulum (SR) and centripetal propagation

64 action depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)ad

65 ]i , in particular the relative roles of the sarcoplasmic reticulum (SR) and surface membrane, are un

66 Calcium cycling between the sarcoplasmic reticulum (SR) and the cytosol via the sarc

67 associated membrane (MAM) signaling from the sarcoplasmic reticulum (SR) and the endoplasmic reticulu

68 reviously unidentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs)

69 d spontaneous Ca(2+) release events from the sarcoplasmic reticulum (SR) as a potential cause of proa

70 unction can by caused by Ca leak through the sarcoplasmic reticulum (SR) Ca channel (ryanodine recept

71 f systolic Ca(2+) decrease with age, whereas sarcoplasmic reticulum (SR) Ca content increases.

72 We find that when CRU firings are sparse and sarcoplasmic reticulum (SR) Ca load is high, increasing

73 f Ca wave initiation sites), cellular scale (sarcoplasmic reticulum (SR) Ca load), and tissue scale (

74 Calcium (Ca) sparks are the fundamental sarcoplasmic reticulum (SR) Ca release events in cardiac

75 neity of RyR cluster size alters spontaneous sarcoplasmic reticulum (SR) Ca releases (Ca sparks) and

76 y of beta-adrenergic stimulation to regulate sarcoplasmic reticulum (SR) Ca(2+) -release.

77 ial cardiomyocytes are caused by a decreased sarcoplasmic reticulum (SR) Ca(2+) ATPase (SERCA2)-media

78 Sarcoplasmic reticulum (SR) Ca(2+) content increased dur

79 it a higher open probability of RyR2, higher sarcoplasmic reticulum (SR) Ca(2+) leak in diastole and

80 nodine receptor 2 (RyR2) phosphorylation and sarcoplasmic reticulum (SR) Ca(2+) leak.

81 V is associated with rapid remodeling of the sarcoplasmic reticulum (SR) Ca(2+) release channel/ryano

82 KEY POINTS: Spontaneous sarcoplasmic reticulum (SR) Ca(2+) release events increa

83 ransverse (t) tubule depolarization triggers sarcoplasmic reticulum (SR) Ca(2+) release through ryano

84 ack a transverse tubule system, dividing the sarcoplasmic reticulum (SR) Ca(2+) store into the periph

85 e by Ca(2+) -induced Ca(2+) release from the sarcoplasmic reticulum (SR) Ca(2+) store.

86 Depletion of sarcoplasmic reticulum (SR) Ca(2+) stores activates stor

87 ation in RyR1 decreases the amplitude of the sarcoplasmic reticulum (SR) Ca(2+) transient, resting cy

88 Ang II-stimulated Nox2 activity increased sarcoplasmic reticulum (SR) Ca(2+) uptake in transgenic

89 Sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA) and ph

90 ulate ryanodine receptor 2 (RYR2), the major sarcoplasmic reticulum (SR) Ca(2+)-release channel in th

91 amplitude was smaller, although spontaneous sarcoplasmic reticulum (SR) Ca(2+)-release events and L-

92 ation, which was accompanied by an increased sarcoplasmic reticulum (SR) Ca2+ content and Ca2+ transi

93 Sarcoplasmic reticulum (SR) calcium (Ca(2+) ) release is

94 Because sarcoplasmic reticulum (SR) calcium has been shown to pl

95 to modulate activity of the skeletal muscle sarcoplasmic reticulum (SR) calcium release channel (rya

96 To address this question, sarcoplasmic reticulum (SR) calcium release in a mouse s

97 nctions in skeletal muscle between stacks of sarcoplasmic reticulum (SR) cisternae and extensions of

98 Abnormal calcium (Ca(2+)) release from the sarcoplasmic reticulum (SR) contributes to the pathogene

99 l to the amount of calcium released from the Sarcoplasmic Reticulum (SR) during systole.

100 Although abnormal Ca(2+) release from the sarcoplasmic reticulum (SR) has been linked to arrhythmo

101 tion is triggered by Ca(2+) release from the sarcoplasmic reticulum (SR) in response to plasma membra

102 nhancement of Ca(2+) uptake and release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (S

103 X-1 (HS-associated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts w

104 9) may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and sk

105 lysosomes are intimately associated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a m

106 Calcium (Ca2+) released from the sarcoplasmic reticulum (SR) is crucial for excitation-co

107 and type 1 ryanodine receptor (RyR1) in the sarcoplasmic reticulum (SR) is thought to underlie both

108 Imaging at ~100 nm resolution located GPa at sarcoplasmic reticulum (SR) junctional cisternae, and ap

109 ith the nucleus at its centre, demarcated by sarcoplasmic reticulum (SR) junctions (<=400 nm across)

110 TRIC-A and TRIC-B, represent two subtypes of sarcoplasmic reticulum (SR) K(+) -channel but their indi

111 s in function between native skeletal muscle sarcoplasmic reticulum (SR) K(+) -channels from wild-typ

112 eceptor Ca(2+) release channel (RyR2) in the sarcoplasmic reticulum (SR) membrane and the SR Ca(2+) b

113 C-A) is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and ske

114 Does this rule apply inside the sarcoplasmic reticulum (SR) of a working cell?

115 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori

116 Intracellular Local Ca releases (LCRs) from sarcoplasmic reticulum (SR) regulate cardiac pacemaker c

117 l matrix includes local Ca(2+) delivery from sarcoplasmic reticulum (SR) ryanodine receptors (RyR2) t

118 RC protein triadin (T95) is localized in the sarcoplasmic reticulum (SR) subdomain of triads where it

119 zed membrane network of smooth ER called the sarcoplasmic reticulum (SR) surrounding myofibrils and s

120 ubules (ATs) with extensive junctions to the sarcoplasmic reticulum (SR) that include ryanodine recep

121 ous intracellular release of Ca(2+) from the sarcoplasmic reticulum (SR) through RyR2 generates local

122 s mediated by increased Ca(2+) leak from the sarcoplasmic reticulum (SR) through the RyR1.

123 Altered calcium transfer from sarcoplasmic reticulum (SR) to mitochondria has been cau

124 tophilin isoforms (JPH1 and JPH2) tether the sarcoplasmic reticulum (SR) to transverse tubule (T-tubu

125 ibited Ca(2+) release from intact fibers and sarcoplasmic reticulum (SR) vesicles, but failed to inhi

126 ne receptors (RyR2s) release Ca(2+) from the sarcoplasmic reticulum (SR) via a positive feedback mech

127 P(i) diffuses into the sarcoplasmic reticulum (SR) where it is believed to form

128 Precise Ca cycling through the sarcoplasmic reticulum (SR), a Ca storage organelle, is

129 activated by a synchronized Ca release from sarcoplasmic reticulum (SR), a major intracellular Ca st

130 ) and most calcium in the cell stored in the sarcoplasmic reticulum (SR), and another, with open RyRs

131 R2), a Ca(2+) release channel located in the sarcoplasmic reticulum (SR), or calsequestrin 2 (CASQ2),

132 ated 'pathological' calcium release from the sarcoplasmic reticulum (SR), the major calcium storage o

133 coupling of the contractile apparatus to the sarcoplasmic reticulum (SR), which serves as the reservo

134 e channel ryanodine receptor 1 (RyR1) in the sarcoplasmic reticulum (SR).

135 in muscle and alters the composition of the sarcoplasmic reticulum (SR).

136 KAP18 in a multiprotein signalosome in human sarcoplasmic reticulum (SR).

137 -mediated calcium (Ca(2+) ) release from the sarcoplasmic reticulum (SR).

138 axation by regulating Ca(2+) uptake into the sarcoplasmic reticulum (SR).

139 ults in markedly increased Ca content of the sarcoplasmic reticulum (SR).

140 ue by precipitating calcium salts inside the sarcoplasmic reticulum (SR).

141 ith type 2 ryanodine receptors (RyR2) on the sarcoplasmic reticulum (SR).

142 er beating rate, disorganised sarcomeres and sarcoplasmic reticulum and a blunted response to isopren

143 se in the amount of Ca(2+) stored within the sarcoplasmic reticulum and activated Ca(2+)/calmodulin-d

144 hondria but exhibited only a small effect on sarcoplasmic reticulum and cytosolic Ca(2+) levels under

145 the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of C

146 the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of

147 hat can prolong the AP duration and load the sarcoplasmic reticulum and likely contributes to the alt

148 e underwent extensive remodeling of both the sarcoplasmic reticulum and mitochondria, including alter

149 ultrastructural abnormalities of junctional sarcoplasmic reticulum and transverse tubules, and (4) a

150 consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels at t-tub

151 similar to those present in the lumen of the sarcoplasmic reticulum at rest, whereas Ca(2+) concentra

152 cell shortening, Ca transient amplitude and sarcoplasmic reticulum Ca content compared with sham car

153 cell shortening, Ca transient amplitude, and sarcoplasmic reticulum Ca content in colon ascendens ste

154 ak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum Ca content, Ca transient amplitud

155 t the T tubules and regulates arrhythmogenic sarcoplasmic reticulum Ca leak.

156 waves is a highly nonlinear function of the sarcoplasmic reticulum Ca load.

157 mined the subcellular mechanisms involved in sarcoplasmic reticulum Ca loss that mediate altered Ca h

158 sim) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca release, by simultaneous live

159 icantly reduced the frequency of spontaneous sarcoplasmic reticulum Ca release, while QX-flecainide a

160 mic reticular calcium ATPase 2 abundance and sarcoplasmic reticulum Ca uptake are depressed in both s

161 hate receptors (IP3 R) and upon depletion of sarcoplasmic reticulum Ca(2+) .

162 Sarcolipin (SLN) is a novel regulator of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) in muscle.

163 ease models have shown that dysregulation of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) pump is one

164 fects and that murine PDE3A1 associates with sarcoplasmic reticulum Ca(2+) ATPase 2 (SERCA2), phospho

165 e-type versus Fork-type; P<0.01), because of sarcoplasmic reticulum Ca(2+) ATPase pump potentiation c

166 Calsequestrin1 (CSQ1), a sarcoplasmic reticulum Ca(2+) buffering protein, inhibit

167 dling proteins, intracellular [Ca(2+)]i, and sarcoplasmic reticulum Ca(2+) content and increases in p

168 n of transient outward potassium current and sarcoplasmic reticulum Ca(2+) content via rescue of cont

169 2+) transient amplitude, 50% decay rate, and sarcoplasmic reticulum Ca(2+) content were not different

170 , reduced Ca(2+) spark dimensions, increased sarcoplasmic reticulum Ca(2+) content, and augmented the

171 reased [Ca(2+)] transient amplitude, reduced sarcoplasmic reticulum Ca(2+) content, and short action

172 activation caused a compensatory increase in sarcoplasmic reticulum Ca(2+) content, Ca(2+) transient

173 arcoplasmic reticulum Ca(2+) leak, augmented sarcoplasmic reticulum Ca(2+) content, increased the mag

174 2+) current but had no significant impact on sarcoplasmic reticulum Ca(2+) content.

175 , sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic reticulum Ca(2+) handling proteins in post-

176 vation of neuronal nitric oxide synthase and sarcoplasmic reticulum Ca(2+) handling proteins, and ide

177 osphorylated neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) handling proteins, intrace

178 iculum Ca(2+) release, and the expression of sarcoplasmic reticulum Ca(2+) handling proteins.

179 SN also reduced sarcoplasmic reticulum Ca(2+) leak, augmented sarcoplasm

180 loss without marked changes in cytosolic and sarcoplasmic reticulum Ca(2+) levels, likely owing to al

181 Ca(2+)-dependent mechanism without altering sarcoplasmic reticulum Ca(2+) load and by increasing uns

182 Ca(2+) concentration transients and a lesser sarcoplasmic reticulum Ca(2+) load due to a down-regulat

183 use STIM1 binding to phospholamban increases sarcoplasmic reticulum Ca(2+) load independent of store-

184 Sarcoplasmic reticulum Ca(2+) load was not changed with

185 f mutant ryanodine receptor type 2 channels, sarcoplasmic reticulum Ca(2+) load, measured by caffeine

186 There are reduced Ca(2+) transient and sarcoplasmic reticulum Ca(2+) load, together with decrea

187 lic cytosolic Ca(2+), RyR2 inactivation, and sarcoplasmic reticulum Ca(2+) release (ie, Ca(2+) altern

188 hese models: one relies mainly on fractional sarcoplasmic reticulum Ca(2+) release and uptake, and th

189 orylation of neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic

190 pterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and the expressio

191 The resultant RyR2 inactivation diminishes sarcoplasmic reticulum Ca(2+) release, which, in turn, r

192 l, flecainide did not inhibit RyR2-dependent sarcoplasmic reticulum Ca(2+) release.

193 omal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum Ca(2+) sensor.

194 (fl/fl) mice post HF revealed both increased sarcoplasmic reticulum Ca(2+) spark frequency and disrup

195 Ca(2+) load due to a down-regulation of the sarcoplasmic reticulum Ca(2+)-adenosine triphosphatase p

196 h there is some evidence that suppression of sarcoplasmic reticulum Ca(2+)-ATP-ase (SERCA2) contribut

197 The calcium pump sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) counter-tra

198 The sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) transports

199 namics (MD) simulations of the calcium pump (sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)) in complex

200 Down-regulation of sarcoplasmic reticulum Ca(2+)-ATPase 2a (SERCA2a) in the

201 merization of phospholamban, which activates sarcoplasmic reticulum Ca(2+)-ATPase and increases cytos

202 The sarcoplasmic reticulum Ca(2+)-ATPase SERCA promotes musc

203 s improved function was coupled to increased sarcoplasmic reticulum Ca(2+)ATPase activity in the R92W

204 Sarcoplasmic reticulum Ca(2+)ATPase activity was measure

205 sine formation in lymphocytes as an index of sarcoplasmic reticulum Ca-release-induced adenosine 5'-t

206 een linked to Ca2+ cycling proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in

207 nction of calcium transport ATPase increases sarcoplasmic reticulum Ca2+ concentration, thereby enhan

208 D amplitude and timing include cytosolic and sarcoplasmic reticulum Ca2+ concentrations, inwardly rec

209 sed, activation of X-ROS signaling increases sarcoplasmic reticulum Ca2+ leak and contributes to glob

210 d stretching does not significantly increase sarcoplasmic reticulum Ca2+ leak; and 4) when the chemic

211 atrial alternans mainly due to the increased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake

212 In adult skeletal muscle, depletion of sarcoplasmic reticulum calcium activates STIM1/Orai1-dep

213 eased activity and expression of the cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a), a criti

214 eticulum stress, as well as an activation of sarcoplasmic reticulum calcium ATPase isoform 2 and citr

215 e activity in Runx1-deficient mice increased sarcoplasmic reticulum calcium content and sarcoplasmic

216 ibitor, consistent with a role for decreased sarcoplasmic reticulum calcium flux in Tbx5-dependent AF

217 This work defines a link between Tbx5 dose, sarcoplasmic reticulum calcium flux, and AF propensity.

218 forms raise the interesting possibility that sarcoplasmic reticulum calcium handling and cardiac cont

219 onged calcium-transient duration and reduced sarcoplasmic reticulum calcium loading and release, cons

220 phorylation of Ser(16) acutely stimulate the sarcoplasmic reticulum calcium pump (SERCA) by relieving

221 The sarcoplasmic reticulum calcium pump (SERCA) is regulated

222 nance of myofilament calcium sensitivity and sarcoplasmic reticulum calcium pumping.

223 o-cell differences through intracellular and sarcoplasmic reticulum calcium regulation.

224 Calcium transient amplitude and fractional sarcoplasmic reticulum calcium release were larger and a

225 Flecainide acetate directly suppresses sarcoplasmic reticulum calcium release-the cellular mech

226 are strongly correlated with fluctuations in sarcoplasmic reticulum calcium, because of strong releas

227 as associated with altered protein levels of sarcoplasmic reticulum calcium-regulatory proteins parti

228 the elevated diastolic Ca(2+) leak from the sarcoplasmic reticulum can be normalized by the cardiac

229 effect on the mechanisms responsible for the sarcoplasmic reticulum charge-compensating counter curre

230 We found that CFTR localizes to the sarcoplasmic reticulum compartment of airway smooth musc

231 -signaling nanodomains between lysosomes and sarcoplasmic reticulum dependent on NAADP and TPC2 compr

232 liable activation of Ca(2+) release from the sarcoplasmic reticulum during the plateau of the ventric

233 dyads (triads that have lost one junctional sarcoplasmic reticulum element); both results suggest a

234 VT VMs and PCs than respective controls, and sarcoplasmic reticulum fractional release was greater in

235 ]i is increased by manoeuvres that decrease sarcoplasmic reticulum function.

236 t to prevent global calcium release from the sarcoplasmic reticulum in LV myocytes, without affecting

237 l role of abnormal calcium releases from the sarcoplasmic reticulum in producing repetitive electrica

238 rotein, obscurin, and stabilizes the network sarcoplasmic reticulum in skeletal muscle.

239 efine a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junctions as unexpected but major

240 Importantly, a mismatch between sarcoplasmic reticulum load and L-type Ca(2+) trigger ca

241 nm) pore connects the transport sites to the sarcoplasmic reticulum lumen through a chain of water mo

242 and modulate sequestration of Ca(2+) in the sarcoplasmic reticulum lumen.

243 nd nearly fully opened at 2 mum cytosolic or sarcoplasmic reticulum luminal Ca(2+), and Ca(2+)- and v

244 rs of Ca(2+) release channels located in the sarcoplasmic reticulum membrane (ryanodine receptors and

245 ated that sAnk1 and SLN can associate in the sarcoplasmic reticulum membrane and after exogenous expr

246 g sites (ECC couplons) comprising plasma and sarcoplasmic reticulum membrane calcium channels are imp

247 he intracellular calcium gradient across the sarcoplasmic reticulum membrane.

248 a lattice to form clusters in the junctional sarcoplasmic reticulum membrane.

249 under conditions that mimic environments in sarcoplasmic reticulum membranes.

250 spryn and RyR2 co-localise at the junctional sarcoplasmic reticulum of isolated cardiomyocytes.

251 dantrolene inhibits Ca(2+) release from the sarcoplasmic reticulum of skeletal and cardiac muscle pr

252 the principal Ca(2+) storage protein of the sarcoplasmic reticulum of skeletal muscle.

253 A2a, the protein that pumps calcium into the sarcoplasmic reticulum of the cardiomyocyte, seems promi

254 tivity of channels in the plasma membrane or sarcoplasmic reticulum of vascular cells.

255 increased distance between mitochondria and sarcoplasmic reticulum on electron microscopy, and 3) ni

256 Immunostaining showed mislocalization of the sarcoplasmic reticulum proteins Serca1 and Ryr1 in a pat

257 ainide or riluzole) acting primarily through sarcoplasmic reticulum stabilization.

258 rtly results from increased Ca(2+) leak from sarcoplasmic reticulum stores via dysregulated ryanodine

259 An approach was developed to model the sarcoplasmic reticulum structure at the whole-cell scale

260 of the calcium release channel (RyR1) in the sarcoplasmic reticulum that supplies the calcium signal

261 Ca leak from the sarcoplasmic reticulum through the ryanodine receptor (R

262 ciation between T-tubules and the junctional sarcoplasmic reticulum to ensure efficient CICR.

263 ptor (RyR1) mediates Ca(2+) release from the sarcoplasmic reticulum to initiate skeletal muscle contr

264 ne receptors (RyR1s) release Ca(2+) from the sarcoplasmic reticulum to initiate skeletal muscle contr

265 es bidirectional proton transport across the sarcoplasmic reticulum to maintain the charge balance of

266 e receptor (IP3R), thereby linking the endo-/sarcoplasmic reticulum to the plasma membrane.

267 sAnk1 interacts specifically with SERCA1 in sarcoplasmic reticulum vesicles isolated from rabbit ske

268 on the cytoplasmic domain of RyR in isolated sarcoplasmic reticulum vesicles.

269 The Ca(2+) pool in the sarcoplasmic reticulum was increased, the activity of ca

270 adic junctions between the cell membrane and sarcoplasmic reticulum were progressively 'packed' with

271 se during systole, gradually overloading the sarcoplasmic reticulum with Ca(2+).

272 ease from intracellular Ca(2+) stores (e.g., sarcoplasmic reticulum) need to be examined.

273 bules), the intracellular calcium store (the sarcoplasmic reticulum), and the co-localisation of thes

274 KCNQ1 mainly resides in the jSR (junctional sarcoplasmic reticulum), whereas KCNE1 resides on the ce

275 are caused by cyclic Ca(2+) release from the sarcoplasmic reticulum, although Ca(2+) influx via plasm

276 r in the regulation of calcium uptake in the sarcoplasmic reticulum, and by probing its dynamical act

277 ban is a small phosphoprotein in the cardiac sarcoplasmic reticulum, and it is the major regulator of

278 channels (ryanodine receptors, RyR2) in the sarcoplasmic reticulum, and the frequency of Ca(2+) spar

279 leading to inhibition of Ca-uptake into the sarcoplasmic reticulum, are linked to inherited DCM.

280 rm shape show changes in the location of the sarcoplasmic reticulum, inter-organelle distances, and d

281 tructural bridge between the plasmalemma and sarcoplasmic reticulum, is essential for precise Ca(2+)-

282 initiated by the release of calcium from the sarcoplasmic reticulum, muscle relaxation involves the a

283 nger function, reduction of Ca(2+) uptake to sarcoplasmic reticulum, reduced K(+) currents, and incre

284 dine receptor would lead to Ca leak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum

285 o RyR1 that triggers Ca(2+) release from the sarcoplasmic reticulum, retrograde signaling from RyR1 t

286 ed force production, fatigue resistance, and sarcoplasmic reticulum-Ca(2+) uptake, which were associa

287 d sarcoplasmic reticulum calcium content and sarcoplasmic reticulum-mediated calcium release, preserv

288 ing calcium ions from the cytoplasm into the sarcoplasmic reticulum.

289 lease probably due to Ca(2+) overload in the sarcoplasmic reticulum.

290 sensitive release channels on the peripheral sarcoplasmic reticulum.

291 erize structural changes in mitochondria and sarcoplasmic reticulum.

292 A/DDD and controls in calcium content of the sarcoplasmic reticulum.

293 current mediated by Ca(2+) released from the sarcoplasmic reticulum.

294 iculum Ca2+ ATPase (SERCA2a), located in the sarcoplasmic reticulum.

295 ith type 1 ryanodine receptors (RyR1) in the sarcoplasmic reticulum.

296 he active transport of calcium back into the sarcoplasmic reticulum.

297 duit for passive proton transport across the sarcoplasmic reticulum.

298 vitro, along with Ca(2+) uptake in isolated sarcoplasmic reticulum.

299 tracellular fluxes in both the cytoplasm and sarcoplasmic reticulum.

300 accumulated and co-localized with DNAJB6 at sarcoplasmic stress granules suggesting that these prote