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1 lease probably due to Ca(2+) overload in the sarcoplasmic reticulum.
2 sensitive release channels on the peripheral sarcoplasmic reticulum.
3 erize structural changes in mitochondria and sarcoplasmic reticulum.
4 A/DDD and controls in calcium content of the sarcoplasmic reticulum.
5 current mediated by Ca(2+) released from the sarcoplasmic reticulum.
6 iculum Ca2+ ATPase (SERCA2a), located in the sarcoplasmic reticulum.
7 ith type 1 ryanodine receptors (RyR1) in the sarcoplasmic reticulum.
8 rticularly spontaneous Ca2+ release from the sarcoplasmic reticulum.
9 alignment with the terminal cisternae of the sarcoplasmic reticulum.
10 r Thr-17 relieves this inhibition in cardiac sarcoplasmic reticulum.
11 mall space between sarcolemma and junctional sarcoplasmic reticulum.
12 ious rates in the release of Ca(2+) from the sarcoplasmic reticulum.
13 he active transport of calcium back into the sarcoplasmic reticulum.
14 duit for passive proton transport across the sarcoplasmic reticulum.
15 vitro, along with Ca(2+) uptake in isolated sarcoplasmic reticulum.
16 tracellular fluxes in both the cytoplasm and sarcoplasmic reticulum.
17 ing calcium ions from the cytoplasm into the sarcoplasmic reticulum.
18 are caused by cyclic Ca(2+) release from the sarcoplasmic reticulum, although Ca(2+) influx via plasm
19 er beating rate, disorganised sarcomeres and sarcoplasmic reticulum and a blunted response to isopren
20 se in the amount of Ca(2+) stored within the sarcoplasmic reticulum and activated Ca(2+)/calmodulin-d
22 hondria but exhibited only a small effect on sarcoplasmic reticulum and cytosolic Ca(2+) levels under
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
29 ultrastructural abnormalities of junctional sarcoplasmic reticulum and transverse tubules, and (4) a
30 bules), the intracellular calcium store (the sarcoplasmic reticulum), and the co-localisation of thes
31 r in the regulation of calcium uptake in the sarcoplasmic reticulum, and by probing its dynamical act
32 ban is a small phosphoprotein in the cardiac sarcoplasmic reticulum, and it is the major regulator of
33 channels (ryanodine receptors, RyR2) in the sarcoplasmic reticulum, and the frequency of Ca(2+) spar
34 consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels at t-tub
36 similar to those present in the lumen of the sarcoplasmic reticulum at rest, whereas Ca(2+) concentra
37 cell shortening, Ca transient amplitude and sarcoplasmic reticulum Ca content compared with sham car
38 cell shortening, Ca transient amplitude, and sarcoplasmic reticulum Ca content in colon ascendens ste
39 ak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum Ca content, Ca transient amplitud
42 mined the subcellular mechanisms involved in sarcoplasmic reticulum Ca loss that mediate altered Ca h
43 sim) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca release, by simultaneous live
44 icantly reduced the frequency of spontaneous sarcoplasmic reticulum Ca release, while QX-flecainide a
45 mic reticular calcium ATPase 2 abundance and sarcoplasmic reticulum Ca uptake are depressed in both s
48 ease models have shown that dysregulation of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) pump is one
49 fects and that murine PDE3A1 associates with sarcoplasmic reticulum Ca(2+) ATPase 2 (SERCA2), phospho
50 e-type versus Fork-type; P<0.01), because of sarcoplasmic reticulum Ca(2+) ATPase pump potentiation c
52 dling proteins, intracellular [Ca(2+)]i, and sarcoplasmic reticulum Ca(2+) content and increases in p
53 crease in amplitude of Ca(2+) transients and sarcoplasmic reticulum Ca(2+) content in LQT2 myocytes.
54 n of transient outward potassium current and sarcoplasmic reticulum Ca(2+) content via rescue of cont
55 2+) transient amplitude, 50% decay rate, and sarcoplasmic reticulum Ca(2+) content were not different
56 , reduced Ca(2+) spark dimensions, increased sarcoplasmic reticulum Ca(2+) content, and augmented the
57 reased [Ca(2+)] transient amplitude, reduced sarcoplasmic reticulum Ca(2+) content, and short action
58 activation caused a compensatory increase in sarcoplasmic reticulum Ca(2+) content, Ca(2+) transient
59 arcoplasmic reticulum Ca(2+) leak, augmented sarcoplasmic reticulum Ca(2+) content, increased the mag
61 , sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic reticulum Ca(2+) handling proteins in post-
62 vation of neuronal nitric oxide synthase and sarcoplasmic reticulum Ca(2+) handling proteins, and ide
63 osphorylated neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) handling proteins, intrace
66 )]Bulk=100 nmol/L) is dictated mainly by the sarcoplasmic reticulum Ca(2+) leak rather than sarcolemm
68 loss without marked changes in cytosolic and sarcoplasmic reticulum Ca(2+) levels, likely owing to al
69 Ca(2+)-dependent mechanism without altering sarcoplasmic reticulum Ca(2+) load and by increasing uns
70 Ca(2+) concentration transients and a lesser sarcoplasmic reticulum Ca(2+) load due to a down-regulat
71 use STIM1 binding to phospholamban increases sarcoplasmic reticulum Ca(2+) load independent of store-
73 f mutant ryanodine receptor type 2 channels, sarcoplasmic reticulum Ca(2+) load, measured by caffeine
75 lic cytosolic Ca(2+), RyR2 inactivation, and sarcoplasmic reticulum Ca(2+) release (ie, Ca(2+) altern
76 otoxin (but not ranolazine), suggesting that sarcoplasmic reticulum Ca(2+) release and Na(+) current
79 hese models: one relies mainly on fractional sarcoplasmic reticulum Ca(2+) release and uptake, and th
81 ure for synchronization and stabilization of sarcoplasmic reticulum Ca(2+) release in healthy cardiom
82 enge slowed late repolarization, potentiated sarcoplasmic reticulum Ca(2+) release, and initiated EAD
83 orylation of neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic
84 pterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and the expressio
85 The resultant RyR2 inactivation diminishes sarcoplasmic reticulum Ca(2+) release, which, in turn, r
88 (fl/fl) mice post HF revealed both increased sarcoplasmic reticulum Ca(2+) spark frequency and disrup
89 crease Ca(2+) influx to enhance refilling of sarcoplasmic reticulum Ca(2+) stores, slow muscle fatigu
90 Ca(2+) load due to a down-regulation of the sarcoplasmic reticulum Ca(2+)-adenosine triphosphatase p
91 h there is some evidence that suppression of sarcoplasmic reticulum Ca(2+)-ATP-ase (SERCA2) contribut
94 namics (MD) simulations of the calcium pump (sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)) in complex
96 merization of phospholamban, which activates sarcoplasmic reticulum Ca(2+)-ATPase and increases cytos
101 embrane proteins, such as bacteriorhodopsin, sarcoplasmic reticulum Ca(2+)ATPase (SERCA1a), and its a
102 s improved function was coupled to increased sarcoplasmic reticulum Ca(2+)ATPase activity in the R92W
105 Patients with mutations in RyR2 or in the sarcoplasmic reticulum Ca-binding protein calsequestrin
106 sine formation in lymphocytes as an index of sarcoplasmic reticulum Ca-release-induced adenosine 5'-t
107 ally, EHD3-deficient myocytes show increased sarcoplasmic reticulum [Ca], increased spark frequency,
108 ed force production, fatigue resistance, and sarcoplasmic reticulum-Ca(2+) uptake, which were associa
109 However, mRNA and protein levels of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory pr
110 een linked to Ca2+ cycling proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in
111 nction of calcium transport ATPase increases sarcoplasmic reticulum Ca2+ concentration, thereby enhan
112 D amplitude and timing include cytosolic and sarcoplasmic reticulum Ca2+ concentrations, inwardly rec
113 sed, activation of X-ROS signaling increases sarcoplasmic reticulum Ca2+ leak and contributes to glob
116 d stretching does not significantly increase sarcoplasmic reticulum Ca2+ leak; and 4) when the chemic
118 studies point to a combination of increased sarcoplasmic reticulum Ca2+ load related to phospholamba
119 role in the normal sympathetic regulation of sarcoplasmic reticulum Ca2+ release or cardiac contracti
120 state contractions and increased spontaneous sarcoplasmic reticulum Ca2+ sparks mediated by enhanced
121 atrial alternans mainly due to the increased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake
123 eased activity and expression of the cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a), a criti
124 eticulum stress, as well as an activation of sarcoplasmic reticulum calcium ATPase isoform 2 and citr
125 e activity in Runx1-deficient mice increased sarcoplasmic reticulum calcium content and sarcoplasmic
126 ibitor, consistent with a role for decreased sarcoplasmic reticulum calcium flux in Tbx5-dependent AF
127 This work defines a link between Tbx5 dose, sarcoplasmic reticulum calcium flux, and AF propensity.
128 forms raise the interesting possibility that sarcoplasmic reticulum calcium handling and cardiac cont
129 onged calcium-transient duration and reduced sarcoplasmic reticulum calcium loading and release, cons
130 phorylation of Ser(16) acutely stimulate the sarcoplasmic reticulum calcium pump (SERCA) by relieving
134 Calcium transient amplitude and fractional sarcoplasmic reticulum calcium release were larger and a
136 are strongly correlated with fluctuations in sarcoplasmic reticulum calcium, because of strong releas
137 as associated with altered protein levels of sarcoplasmic reticulum calcium-regulatory proteins parti
138 the elevated diastolic Ca(2+) leak from the sarcoplasmic reticulum can be normalized by the cardiac
139 effect on the mechanisms responsible for the sarcoplasmic reticulum charge-compensating counter curre
142 -signaling nanodomains between lysosomes and sarcoplasmic reticulum dependent on NAADP and TPC2 compr
143 liable activation of Ca(2+) release from the sarcoplasmic reticulum during the plateau of the ventric
144 dyads (triads that have lost one junctional sarcoplasmic reticulum element); both results suggest a
146 ntain close contacts between the endoplasmic/sarcoplasmic reticulum (ER/SR) and the plasma membrane i
147 omal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum (ER/SR) Ca(2+) sensor, is unclear
149 VT VMs and PCs than respective controls, and sarcoplasmic reticulum fractional release was greater in
152 t to prevent global calcium release from the sarcoplasmic reticulum in LV myocytes, without affecting
153 rastructural alterations of mitochondria and sarcoplasmic reticulum in muscle and abnormal collagen f
154 l role of abnormal calcium releases from the sarcoplasmic reticulum in producing repetitive electrica
156 rm shape show changes in the location of the sarcoplasmic reticulum, inter-organelle distances, and d
157 Orai1 channels in complex with STIM1 in the sarcoplasmic reticulum is one such potential disease mec
158 tructural bridge between the plasmalemma and sarcoplasmic reticulum, is essential for precise Ca(2+)-
159 efine a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junctions as unexpected but major
161 nm) pore connects the transport sites to the sarcoplasmic reticulum lumen through a chain of water mo
163 nd nearly fully opened at 2 mum cytosolic or sarcoplasmic reticulum luminal Ca(2+), and Ca(2+)- and v
164 d sarcoplasmic reticulum calcium content and sarcoplasmic reticulum-mediated calcium release, preserv
165 rs of Ca(2+) release channels located in the sarcoplasmic reticulum membrane (ryanodine receptors and
166 ated that sAnk1 and SLN can associate in the sarcoplasmic reticulum membrane and after exogenous expr
167 g sites (ECC couplons) comprising plasma and sarcoplasmic reticulum membrane calcium channels are imp
172 initiated by the release of calcium from the sarcoplasmic reticulum, muscle relaxation involves the a
175 dantrolene inhibits Ca(2+) release from the sarcoplasmic reticulum of skeletal and cardiac muscle pr
177 A2a, the protein that pumps calcium into the sarcoplasmic reticulum of the cardiomyocyte, seems promi
179 increased distance between mitochondria and sarcoplasmic reticulum on electron microscopy, and 3) ni
180 Immunostaining showed mislocalization of the sarcoplasmic reticulum proteins Serca1 and Ryr1 in a pat
181 nger function, reduction of Ca(2+) uptake to sarcoplasmic reticulum, reduced K(+) currents, and incre
182 dine receptor would lead to Ca leak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum
183 o RyR1 that triggers Ca(2+) release from the sarcoplasmic reticulum, retrograde signaling from RyR1 t
184 e include the Ca(2+) release channels of the sarcoplasmic reticulum (ryanodine receptors or RyR2s) an
186 that lysosomes form close contacts with the sarcoplasmic reticulum (separation approximately 25 nm).
187 sed on the activity of an ATPase pump in the sarcoplasmic reticulum (SERCA1a) and is controlled by th
188 arcolemma triggering Ca(2+) release from the sarcoplasmic reticulum (SR) - a process termed Ca(2+) -i
189 d Ca(2+) release from central non-junctional sarcoplasmic reticulum (SR) and centripetal propagation
190 action depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)ad
191 ]i , in particular the relative roles of the sarcoplasmic reticulum (SR) and surface membrane, are un
193 associated membrane (MAM) signaling from the sarcoplasmic reticulum (SR) and the endoplasmic reticulu
194 reviously unidentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs)
195 d spontaneous Ca(2+) release events from the sarcoplasmic reticulum (SR) as a potential cause of proa
196 unction can by caused by Ca leak through the sarcoplasmic reticulum (SR) Ca channel (ryanodine recept
198 We find that when CRU firings are sparse and sarcoplasmic reticulum (SR) Ca load is high, increasing
199 f Ca wave initiation sites), cellular scale (sarcoplasmic reticulum (SR) Ca load), and tissue scale (
200 Calcium (Ca) sparks are the fundamental sarcoplasmic reticulum (SR) Ca release events in cardiac
201 neity of RyR cluster size alters spontaneous sarcoplasmic reticulum (SR) Ca releases (Ca sparks) and
203 ial cardiomyocytes are caused by a decreased sarcoplasmic reticulum (SR) Ca(2+) ATPase (SERCA2)-media
207 isoproterenol were associated with increased sarcoplasmic reticulum (SR) Ca(2+) leak and frequent dia
208 it a higher open probability of RyR2, higher sarcoplasmic reticulum (SR) Ca(2+) leak in diastole and
211 ased intracellular Ca(2+) leak and increased sarcoplasmic reticulum (SR) Ca(2+) load compared with ag
212 ise showed an extensive fragmentation of the sarcoplasmic reticulum (SR) Ca(2+) release channel, the
213 V is associated with rapid remodeling of the sarcoplasmic reticulum (SR) Ca(2+) release channel/ryano
215 o explore whether subclinical alterations of sarcoplasmic reticulum (SR) Ca(2+) release through cardi
216 ransverse (t) tubule depolarization triggers sarcoplasmic reticulum (SR) Ca(2+) release through ryano
217 ack a transverse tubule system, dividing the sarcoplasmic reticulum (SR) Ca(2+) store into the periph
220 on of STIM1 in mice resulted in depletion of sarcoplasmic reticulum (SR) Ca(2+) stores of SANCs and l
221 ation in RyR1 decreases the amplitude of the sarcoplasmic reticulum (SR) Ca(2+) transient, resting cy
222 Ang II-stimulated Nox2 activity increased sarcoplasmic reticulum (SR) Ca(2+) uptake in transgenic
224 ulate ryanodine receptor 2 (RYR2), the major sarcoplasmic reticulum (SR) Ca(2+)-release channel in th
225 amplitude was smaller, although spontaneous sarcoplasmic reticulum (SR) Ca(2+)-release events and L-
226 ation, which was accompanied by an increased sarcoplasmic reticulum (SR) Ca2+ content and Ca2+ transi
227 alaemia, increased Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load, SR Ca2+ leak and
231 to modulate activity of the skeletal muscle sarcoplasmic reticulum (SR) calcium release channel (rya
233 nctions in skeletal muscle between stacks of sarcoplasmic reticulum (SR) cisternae and extensions of
234 Abnormal calcium (Ca(2+)) release from the sarcoplasmic reticulum (SR) contributes to the pathogene
236 Although abnormal Ca(2+) release from the sarcoplasmic reticulum (SR) has been linked to arrhythmo
237 tion is triggered by Ca(2+) release from the sarcoplasmic reticulum (SR) in response to plasma membra
238 nhancement of Ca(2+) uptake and release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (S
239 X-1 (HS-associated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts w
240 9) may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and sk
241 lysosomes are intimately associated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a m
243 and type 1 ryanodine receptor (RyR1) in the sarcoplasmic reticulum (SR) is thought to underlie both
244 Imaging at ~100 nm resolution located GPa at sarcoplasmic reticulum (SR) junctional cisternae, and ap
245 ith the nucleus at its centre, demarcated by sarcoplasmic reticulum (SR) junctions (<=400 nm across)
246 TRIC-A and TRIC-B, represent two subtypes of sarcoplasmic reticulum (SR) K(+) -channel but their indi
247 s in function between native skeletal muscle sarcoplasmic reticulum (SR) K(+) -channels from wild-typ
249 eceptor Ca(2+) release channel (RyR2) in the sarcoplasmic reticulum (SR) membrane and the SR Ca(2+) b
250 C-A) is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and ske
252 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori
253 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori
254 Intracellular Local Ca releases (LCRs) from sarcoplasmic reticulum (SR) regulate cardiac pacemaker c
255 l matrix includes local Ca(2+) delivery from sarcoplasmic reticulum (SR) ryanodine receptors (RyR2) t
256 RC protein triadin (T95) is localized in the sarcoplasmic reticulum (SR) subdomain of triads where it
257 zed membrane network of smooth ER called the sarcoplasmic reticulum (SR) surrounding myofibrils and s
258 ubules (ATs) with extensive junctions to the sarcoplasmic reticulum (SR) that include ryanodine recep
259 ous intracellular release of Ca(2+) from the sarcoplasmic reticulum (SR) through RyR2 generates local
262 tophilin isoforms (JPH1 and JPH2) tether the sarcoplasmic reticulum (SR) to transverse tubule (T-tubu
263 ibited Ca(2+) release from intact fibers and sarcoplasmic reticulum (SR) vesicles, but failed to inhi
264 ne receptors (RyR2s) release Ca(2+) from the sarcoplasmic reticulum (SR) via a positive feedback mech
267 activated by a synchronized Ca release from sarcoplasmic reticulum (SR), a major intracellular Ca st
268 ) and most calcium in the cell stored in the sarcoplasmic reticulum (SR), and another, with open RyRs
269 R2), a Ca(2+) release channel located in the sarcoplasmic reticulum (SR), or calsequestrin 2 (CASQ2),
270 ated 'pathological' calcium release from the sarcoplasmic reticulum (SR), the major calcium storage o
271 coupling of the contractile apparatus to the sarcoplasmic reticulum (SR), which serves as the reservo
283 rtly results from increased Ca(2+) leak from sarcoplasmic reticulum stores via dysregulated ryanodine
285 urce of reactive oxygen species (ROS) in the sarcoplasmic reticulum that may reduce SERCA2a function.
286 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
291 es bidirectional proton transport across the sarcoplasmic reticulum to maintain the charge balance of
294 on RyR1 channel activity after incorporating sarcoplasmic reticulum vesicles into lipid bilayers.
295 sAnk1 interacts specifically with SERCA1 in sarcoplasmic reticulum vesicles isolated from rabbit ske
298 adic junctions between the cell membrane and sarcoplasmic reticulum were progressively 'packed' with
299 KCNQ1 mainly resides in the jSR (junctional sarcoplasmic reticulum), whereas KCNE1 resides on the ce