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1 tracellular fluxes in both the cytoplasm and sarcoplasmic reticulum.
2 iculum Ca2+ ATPase (SERCA2a), located in the sarcoplasmic reticulum.
3 ith type 1 ryanodine receptors (RyR1) in the sarcoplasmic reticulum.
4 rticularly spontaneous Ca2+ release from the sarcoplasmic reticulum.
5 alignment with the terminal cisternae of the sarcoplasmic reticulum.
6 r Thr-17 relieves this inhibition in cardiac sarcoplasmic reticulum.
7 mall space between sarcolemma and junctional sarcoplasmic reticulum.
8 ious rates in the release of Ca(2+) from the sarcoplasmic reticulum.
9 es detachment of transverse tubules from the sarcoplasmic reticulum.
10 ing calcium ions from the cytoplasm into the sarcoplasmic reticulum.
11 mainly dependent on [Ca2+]i release from the sarcoplasmic reticulum.
12 ific inhibition of IRE-1 signaling at the ER/sarcoplasmic reticulum.
13 res such as the endoplasmic reticulum or the sarcoplasmic reticulum.
14 lease probably due to Ca(2+) overload in the sarcoplasmic reticulum.
15 sensitive release channels on the peripheral sarcoplasmic reticulum.
16 erize structural changes in mitochondria and sarcoplasmic reticulum.
17 current mediated by Ca(2+) released from the sarcoplasmic reticulum.
18 are caused by cyclic Ca(2+) release from the sarcoplasmic reticulum, although Ca(2+) influx via plasm
19 tors of the release of calcium ions from the sarcoplasmic reticulum, an essential step in muscle exci
20 er beating rate, disorganised sarcomeres and sarcoplasmic reticulum and a blunted response to isopren
21 se in the amount of Ca(2+) stored within the sarcoplasmic reticulum and activated Ca(2+)/calmodulin-d
23 uscles of SHR showed reduced activity of the sarcoplasmic reticulum and decreased sarcolemmal calcium
24 tudies uncovered progressive dilation of the sarcoplasmic reticulum and ectopic and misaligned transv
25 the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of C
26 the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of
27 hat can prolong the AP duration and load the sarcoplasmic reticulum and likely contributes to the alt
28 e underwent extensive remodeling of both the sarcoplasmic reticulum and mitochondria, including alter
31 contact, of the junctions between junctional sarcoplasmic reticulum and T tubules (couplons), and of
32 ultrastructural abnormalities of junctional sarcoplasmic reticulum and transverse tubules, and (4) a
33 bules), the intracellular calcium store (the sarcoplasmic reticulum), and the co-localisation of thes
34 r in the regulation of calcium uptake in the sarcoplasmic reticulum, and by probing its dynamical act
35 channels (ryanodine receptors, RyR2) in the sarcoplasmic reticulum, and the frequency of Ca(2+) spar
36 consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels at t-tub
38 similar to those present in the lumen of the sarcoplasmic reticulum at rest, whereas Ca(2+) concentra
39 cell shortening, Ca transient amplitude and sarcoplasmic reticulum Ca content compared with sham car
40 cell shortening, Ca transient amplitude, and sarcoplasmic reticulum Ca content in colon ascendens ste
41 ak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum Ca content, Ca transient amplitud
44 mined the subcellular mechanisms involved in sarcoplasmic reticulum Ca loss that mediate altered Ca h
45 sim) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca release, by simultaneous live
46 mic reticular calcium ATPase 2 abundance and sarcoplasmic reticulum Ca uptake are depressed in both s
48 Our results demonstrate that despite severe sarcoplasmic reticulum Ca(2)(+) leak, PLN-KO suppresses
53 fects and that murine PDE3A1 associates with sarcoplasmic reticulum Ca(2+) ATPase 2 (SERCA2), phospho
54 e-type versus Fork-type; P<0.01), because of sarcoplasmic reticulum Ca(2+) ATPase pump potentiation c
55 o changes in expression of phospholamban and sarcoplasmic reticulum Ca(2+) ATPase, increased levels o
57 dling proteins, intracellular [Ca(2+)]i, and sarcoplasmic reticulum Ca(2+) content and increases in p
58 crease in amplitude of Ca(2+) transients and sarcoplasmic reticulum Ca(2+) content in LQT2 myocytes.
59 n of transient outward potassium current and sarcoplasmic reticulum Ca(2+) content via rescue of cont
60 , reduced Ca(2+) spark dimensions, increased sarcoplasmic reticulum Ca(2+) content, and augmented the
61 arcoplasmic reticulum Ca(2+) leak, augmented sarcoplasmic reticulum Ca(2+) content, increased the mag
63 , sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic reticulum Ca(2+) handling proteins in post-
64 vation of neuronal nitric oxide synthase and sarcoplasmic reticulum Ca(2+) handling proteins, and ide
65 osphorylated neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) handling proteins, intrace
69 )]Bulk=100 nmol/L) is dictated mainly by the sarcoplasmic reticulum Ca(2+) leak rather than sarcolemm
71 also increased ryanodine receptor activity (sarcoplasmic reticulum Ca(2+) leak/load relationship) an
72 loss without marked changes in cytosolic and sarcoplasmic reticulum Ca(2+) levels, likely owing to al
73 Ca(2+)-dependent mechanism without altering sarcoplasmic reticulum Ca(2+) load and by increasing uns
74 Ca(2+) concentration transients and a lesser sarcoplasmic reticulum Ca(2+) load due to a down-regulat
76 lasmic reticulum which, in turn, changes the sarcoplasmic reticulum Ca(2+) load, diastolic Ca(2+) rel
77 f mutant ryanodine receptor type 2 channels, sarcoplasmic reticulum Ca(2+) load, measured by caffeine
79 infrequently occurring Ca(2+) sparks, larger sarcoplasmic reticulum Ca(2+) loads, and spontaneous Ca(
80 eceptor agonists by preventing cytosolic and sarcoplasmic reticulum Ca(2+) overload and calcium/calmo
81 otoxin (but not ranolazine), suggesting that sarcoplasmic reticulum Ca(2+) release and Na(+) current
83 L-type Ca(2+) current (ICaL) reactivation or sarcoplasmic reticulum Ca(2+) release and Na(+)/Ca(2+) e
85 hese models: one relies mainly on fractional sarcoplasmic reticulum Ca(2+) release and uptake, and th
87 s CaMKII-dependent activation of spontaneous sarcoplasmic reticulum Ca(2+) release events that can co
88 ure for synchronization and stabilization of sarcoplasmic reticulum Ca(2+) release in healthy cardiom
89 enge slowed late repolarization, potentiated sarcoplasmic reticulum Ca(2+) release, and initiated EAD
90 orylation of neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic
91 pterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and the expressio
94 (fl/fl) mice post HF revealed both increased sarcoplasmic reticulum Ca(2+) spark frequency and disrup
95 crease Ca(2+) influx to enhance refilling of sarcoplasmic reticulum Ca(2+) stores, slow muscle fatigu
96 Ca(2+) load due to a down-regulation of the sarcoplasmic reticulum Ca(2+)-adenosine triphosphatase p
97 h there is some evidence that suppression of sarcoplasmic reticulum Ca(2+)-ATP-ase (SERCA2) contribut
98 The membrane protein complex between the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and phospho
100 namics (MD) simulations of the calcium pump (sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)) in complex
101 injury is associated with downregulation of sarcoplasmic reticulum Ca(2+)-ATPase 2a (SERCA2a) and al
103 merization of phospholamban, which activates sarcoplasmic reticulum Ca(2+)-ATPase and increases cytos
104 ed myocardial oxidative stress and decreased sarcoplasmic reticulum Ca(2+)-ATPase protein expression
111 embrane proteins, such as bacteriorhodopsin, sarcoplasmic reticulum Ca(2+)ATPase (SERCA1a), and its a
113 Patients with mutations in RyR2 or in the sarcoplasmic reticulum Ca-binding protein calsequestrin
114 sine formation in lymphocytes as an index of sarcoplasmic reticulum Ca-release-induced adenosine 5'-t
115 ally, EHD3-deficient myocytes show increased sarcoplasmic reticulum [Ca], increased spark frequency,
116 vidence has suggested a role for spontaneous sarcoplasmic reticulum Ca2+ -release events in long-stan
117 ent AF, but the occurrence and mechanisms of sarcoplasmic reticulum Ca2+ -release events in paroxysma
118 creased sarcoplasmic reticulum Ca2+ leak and sarcoplasmic reticulum Ca2+ -release events, causing del
119 However, mRNA and protein levels of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory pr
120 een linked to Ca2+ cycling proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in
121 D amplitude and timing include cytosolic and sarcoplasmic reticulum Ca2+ concentrations, inwardly rec
122 sed, activation of X-ROS signaling increases sarcoplasmic reticulum Ca2+ leak and contributes to glob
124 enhanced SERCA2a activity promote increased sarcoplasmic reticulum Ca2+ leak and sarcoplasmic reticu
126 d stretching does not significantly increase sarcoplasmic reticulum Ca2+ leak; and 4) when the chemic
128 studies point to a combination of increased sarcoplasmic reticulum Ca2+ load related to phospholamba
129 role in the normal sympathetic regulation of sarcoplasmic reticulum Ca2+ release or cardiac contracti
131 state contractions and increased spontaneous sarcoplasmic reticulum Ca2+ sparks mediated by enhanced
133 eased activity and expression of the cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a), a criti
134 virus serotype 1 (AAV1) vector carrying the sarcoplasmic reticulum calcium ATPase gene (AAV1/SERCA2a
135 eticulum stress, as well as an activation of sarcoplasmic reticulum calcium ATPase isoform 2 and citr
136 raction of interstitial fibrosis, normalized sarcoplasmic reticulum calcium ATPase-2a activity and ex
137 ss volume fraction of interstitial fibrosis, sarcoplasmic reticulum calcium ATPase-2a activity, expre
138 e activity in Runx1-deficient mice increased sarcoplasmic reticulum calcium content and sarcoplasmic
139 forms raise the interesting possibility that sarcoplasmic reticulum calcium handling and cardiac cont
140 onged calcium-transient duration and reduced sarcoplasmic reticulum calcium loading and release, cons
143 Calcium transient amplitude and fractional sarcoplasmic reticulum calcium release were larger and a
145 interacting with messenger RNA encoding the sarcoplasmic reticulum calcium uptake pump SERCA2a (also
146 are strongly correlated with fluctuations in sarcoplasmic reticulum calcium, because of strong releas
147 as associated with altered protein levels of sarcoplasmic reticulum calcium-regulatory proteins parti
148 effect on the mechanisms responsible for the sarcoplasmic reticulum charge-compensating counter curre
151 -signaling nanodomains between lysosomes and sarcoplasmic reticulum dependent on NAADP and TPC2 compr
153 liable activation of Ca(2+) release from the sarcoplasmic reticulum during the plateau of the ventric
155 omal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum (ER/SR) Ca(2+) sensor, is unclear
157 VT VMs and PCs than respective controls, and sarcoplasmic reticulum fractional release was greater in
161 rastructural alterations of mitochondria and sarcoplasmic reticulum in muscle and abnormal collagen f
162 l role of abnormal calcium releases from the sarcoplasmic reticulum in producing repetitive electrica
165 Orai1 channels in complex with STIM1 in the sarcoplasmic reticulum is one such potential disease mec
166 tructural bridge between the plasmalemma and sarcoplasmic reticulum, is essential for precise Ca(2+)-
168 efine a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junctions as unexpected but major
170 nm) pore connects the transport sites to the sarcoplasmic reticulum lumen through a chain of water mo
172 nd nearly fully opened at 2 mum cytosolic or sarcoplasmic reticulum luminal Ca(2+), and Ca(2+)- and v
173 d sarcoplasmic reticulum calcium content and sarcoplasmic reticulum-mediated calcium release, preserv
174 ated that sAnk1 and SLN can associate in the sarcoplasmic reticulum membrane and after exogenous expr
175 g sites (ECC couplons) comprising plasma and sarcoplasmic reticulum membrane calcium channels are imp
182 dantrolene inhibits Ca(2+) release from the sarcoplasmic reticulum of skeletal and cardiac muscle pr
184 A2a, the protein that pumps calcium into the sarcoplasmic reticulum of the cardiomyocyte, seems promi
185 ediated release of Ca(2+) (J(leak)) from the sarcoplasmic reticulum of ventricular myocytes occurs in
186 increased distance between mitochondria and sarcoplasmic reticulum on electron microscopy, and 3) ni
189 Immunostaining showed mislocalization of the sarcoplasmic reticulum proteins Serca1 and Ryr1 in a pat
190 nger function, reduction of Ca(2+) uptake to sarcoplasmic reticulum, reduced K(+) currents, and incre
191 dine receptor would lead to Ca leak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum
192 o RyR1 that triggers Ca(2+) release from the sarcoplasmic reticulum, retrograde signaling from RyR1 t
193 e include the Ca(2+) release channels of the sarcoplasmic reticulum (ryanodine receptors or RyR2s) an
195 that lysosomes form close contacts with the sarcoplasmic reticulum (separation approximately 25 nm).
196 arcolemma triggering Ca(2+) release from the sarcoplasmic reticulum (SR) - a process termed Ca(2+) -i
197 tromal-interacting molecule 1 (STIM1) in the sarcoplasmic reticulum (SR) and Ca(2)(+) selective Orai1
198 d Ca(2+) release from central non-junctional sarcoplasmic reticulum (SR) and centripetal propagation
199 action depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)ad
200 ]i , in particular the relative roles of the sarcoplasmic reticulum (SR) and surface membrane, are un
202 reviously unidentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs)
203 d spontaneous Ca(2+) release events from the sarcoplasmic reticulum (SR) as a potential cause of proa
204 unction can by caused by Ca leak through the sarcoplasmic reticulum (SR) Ca channel (ryanodine recept
206 We find that when CRU firings are sparse and sarcoplasmic reticulum (SR) Ca load is high, increasing
207 f Ca wave initiation sites), cellular scale (sarcoplasmic reticulum (SR) Ca load), and tissue scale (
208 Calcium (Ca) sparks are the fundamental sarcoplasmic reticulum (SR) Ca release events in cardiac
210 in Ca(2+) transient amplitudes and increased sarcoplasmic reticulum (SR) Ca(2+) content, without chan
213 determined by measuring cytosolic and intra-sarcoplasmic reticulum (SR) Ca(2+) dynamics in intact an
214 The charge translocation associated with sarcoplasmic reticulum (SR) Ca(2+) efflux is compensated
215 PH2 is believed to have an important role in sarcoplasmic reticulum (SR) Ca(2+) handling and modulati
216 isoproterenol were associated with increased sarcoplasmic reticulum (SR) Ca(2+) leak and frequent dia
217 it a higher open probability of RyR2, higher sarcoplasmic reticulum (SR) Ca(2+) leak in diastole and
221 ased intracellular Ca(2+) leak and increased sarcoplasmic reticulum (SR) Ca(2+) load compared with ag
222 ise showed an extensive fragmentation of the sarcoplasmic reticulum (SR) Ca(2+) release channel, the
223 V is associated with rapid remodeling of the sarcoplasmic reticulum (SR) Ca(2+) release channel/ryano
224 myocytes ensures synchronized activation of sarcoplasmic reticulum (SR) Ca(2+) release during systol
226 vation can induce potentially arrhythmogenic sarcoplasmic reticulum (SR) Ca(2+) release that involves
227 o explore whether subclinical alterations of sarcoplasmic reticulum (SR) Ca(2+) release through cardi
228 ransverse (t) tubule depolarization triggers sarcoplasmic reticulum (SR) Ca(2+) release through ryano
229 ack a transverse tubule system, dividing the sarcoplasmic reticulum (SR) Ca(2+) store into the periph
232 on of STIM1 in mice resulted in depletion of sarcoplasmic reticulum (SR) Ca(2+) stores of SANCs and l
233 ation in RyR1 decreases the amplitude of the sarcoplasmic reticulum (SR) Ca(2+) transient, resting cy
234 Ang II-stimulated Nox2 activity increased sarcoplasmic reticulum (SR) Ca(2+) uptake in transgenic
235 Ca2+ sparks, arrhythmogenic Ca2+ waves, sarcoplasmic reticulum (SR) Ca2+ leak, and SR Ca2+ conte
236 alaemia, increased Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load, SR Ca2+ leak and
238 ctivity was not altered, implicating altered sarcoplasmic reticulum (SR) calcium leak in the activati
240 usceptibility has been attributed to a leaky sarcoplasmic reticulum (SR) caused by missense mutations
241 pin (SLN) is a regulatory peptide present in sarcoplasmic reticulum (SR) from skeletal muscle of anim
243 Although abnormal Ca(2+) release from the sarcoplasmic reticulum (SR) has been linked to arrhythmo
245 tion is triggered by Ca(2+) release from the sarcoplasmic reticulum (SR) in response to plasma membra
246 nhancement of Ca(2+) uptake and release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (S
247 X-1 (HS-associated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts w
248 9) may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and sk
249 lysosomes are intimately associated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a m
251 and type 1 ryanodine receptor (RyR1) in the sarcoplasmic reticulum (SR) is thought to underlie both
252 HYD alone or in combination with NTG reduced sarcoplasmic reticulum (SR) leak, improved SR Ca(2+) reu
254 ndence of RyR closed time, with the measured sarcoplasmic reticulum (SR) lumen Ca(2+) dependence of R
255 uestrin (CASQ) is the major component of the sarcoplasmic reticulum (SR) lumen in skeletal and cardia
256 eceptor Ca(2+) release channel (RyR2) in the sarcoplasmic reticulum (SR) membrane and the SR Ca(2+) b
257 C-A) is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and ske
260 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori
261 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori
262 Intracellular Local Ca releases (LCRs) from sarcoplasmic reticulum (SR) regulate cardiac pacemaker c
263 l matrix includes local Ca(2+) delivery from sarcoplasmic reticulum (SR) ryanodine receptors (RyR2) t
264 ubules (ATs) with extensive junctions to the sarcoplasmic reticulum (SR) that include ryanodine recep
265 ian skeletal muscle, Ca(2+) release from the sarcoplasmic reticulum (SR) through the ryanodine recept
268 ts in Ca2+ cycling occur at the level of the sarcoplasmic reticulum (SR), a Ca2+ storage organelle in
269 R2), a Ca(2+) release channel located in the sarcoplasmic reticulum (SR), or calsequestrin 2 (CASQ2),
271 coupling of the contractile apparatus to the sarcoplasmic reticulum (SR), which serves as the reservo
282 Depletion of the intracellular Ca store (sarcoplasmic reticulum, SR) may play an important role,
285 urce of reactive oxygen species (ROS) in the sarcoplasmic reticulum that may reduce SERCA2a function.
286 le are essential for Ca(2+) release from the sarcoplasmic reticulum that mediates excitation-contract
287 of the calcium release channel (RyR1) in the sarcoplasmic reticulum that supplies the calcium signal
289 ne receptors (RyR1s) release Ca(2+) from the sarcoplasmic reticulum to initiate skeletal muscle contr
290 ptor (RyR1) mediates Ca(2+) release from the sarcoplasmic reticulum to initiate skeletal muscle contr
292 on RyR1 channel activity after incorporating sarcoplasmic reticulum vesicles into lipid bilayers.
293 sAnk1 interacts specifically with SERCA1 in sarcoplasmic reticulum vesicles isolated from rabbit ske
295 ceptor activation, Ca(2+) mobilized from the sarcoplasmic reticulum via IP3Rs contributes to the decr
296 and T tubules (couplons), and of junctional sarcoplasmic reticulum volume; (4) have a propensity to
298 KCNQ1 mainly resides in the jSR (junctional sarcoplasmic reticulum), whereas KCNE1 resides on the ce
299 changes in Ca(2+) available for pumping into sarcoplasmic reticulum which, in turn, changes the sarco
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