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1 B6a localized to myonuclei while DNAJB6b was sarcoplasmic.
4 t was shown that radicals were formed in the sarcoplasmic and myofibrillar fractions as well as in th
5 myosin, arginine kinase, myosin light chain, sarcoplasmic calcium-binding protein, and hemocyanin are
6 oxide synthase 2-positive muscle fibers with sarcoplasmic colocalization of markers of regeneration a
7 to sarcomere mutation-positive HCM, whereas sarcoplasmic endoplasmic reticular calcium ATPase 2 abun
8 educed in HCM regardless of genotype, as was sarcoplasmic endoplasmic reticular calcium ATPase 2/phos
11 r assist device-supported hearts, S100A1 and sarcoplasmic endoplasmic reticulum Ca(2+)ATPase showed n
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 channels that are known to be present in the sarcoplasmic/endoplasmic reticulum (ER/SR) membranes.
18 (RyR1), dihydropyridine receptor (DHPR), and sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA)
19 ticulum Ca(2+) content via rescue of control sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase levels
20 y that resemble PII-type ATPases such as the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA)
22 concentration regulatory proteins, that is, sarcoplasmic/endoplasmic reticulum calcium ATPase 2 and
23 argets the ryanodine receptor present in the sarcoplasmic/endoplasmic reticulum to promote Ca(2+) rel
24 ticulum (EnR) homeostasis through preserving sarcoplasmic/EnR calcium ATPase 2b (SERCA2b) function in
25 that LGMD1D mutations in DNAJB6 disrupt its sarcoplasmic function suggesting a role for DNAJB6b in Z
27 tural abnormalities including ringed fibres, sarcoplasmic masses or Z-band disorganization, which are
28 P, this processing modified the 1-D SDS-PAGE sarcoplasmic patterns in a direct-dependent manner and e
29 ical role in vertebrates, and as the primary sarcoplasmic pigment in meat, influences quality percept
31 veral peptides derived from myofibrillar and sarcoplasmic proteins are sufficiently resistant to proc
32 od for evaluating proteolytic degradation of sarcoplasmic proteins during the processing of dry-cured
33 al sodium dodecyl sulphate (SDS)-soluble and sarcoplasmic proteins in frozen (-10 degrees C for 3 mon
34 inhibitor from common carp (Cyprinus carpio) sarcoplasmic proteins resulted in 2.8% yield with purifi
35 rolox/g), whereas the ex vivo hydrolysate of sarcoplasmic proteins showed the highest DPPH scavenging
36 dentification and relative quantification of sarcoplasmic proteins through individual quantification
37 antify changes in the abundance of the major sarcoplasmic proteins throughout the ham dry-curing proc
39 ivo hydrolysate, whereas the peptide PW from sarcoplasmic proteins was identified only in the in vitr
41 differences in abundance of myofibrillar and sarcoplasmic proteins were observed between samples and
44 iprotein complexes at discrete plasmalemmal, sarcoplasmic reticular and myofilament sites, reveals di
45 omal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum (ER/SR) Ca(2+) sensor, is unclear
48 e include the Ca(2+) release channels of the sarcoplasmic reticulum (ryanodine receptors or RyR2s) an
49 that lysosomes form close contacts with the sarcoplasmic reticulum (separation approximately 25 nm).
50 arcolemma triggering Ca(2+) release from the sarcoplasmic reticulum (SR) - a process termed Ca(2+) -i
51 d Ca(2+) release from central non-junctional sarcoplasmic reticulum (SR) and centripetal propagation
52 action depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)ad
53 ]i , in particular the relative roles of the sarcoplasmic reticulum (SR) and surface membrane, are un
55 reviously unidentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs)
56 d spontaneous Ca(2+) release events from the sarcoplasmic reticulum (SR) as a potential cause of proa
57 unction can by caused by Ca leak through the sarcoplasmic reticulum (SR) Ca channel (ryanodine recept
59 We find that when CRU firings are sparse and sarcoplasmic reticulum (SR) Ca load is high, increasing
60 f Ca wave initiation sites), cellular scale (sarcoplasmic reticulum (SR) Ca load), and tissue scale (
65 isoproterenol were associated with increased sarcoplasmic reticulum (SR) Ca(2+) leak and frequent dia
66 it a higher open probability of RyR2, higher sarcoplasmic reticulum (SR) Ca(2+) leak in diastole and
69 ased intracellular Ca(2+) leak and increased sarcoplasmic reticulum (SR) Ca(2+) load compared with ag
70 ise showed an extensive fragmentation of the sarcoplasmic reticulum (SR) Ca(2+) release channel, the
71 V is associated with rapid remodeling of the sarcoplasmic reticulum (SR) Ca(2+) release channel/ryano
72 myocytes ensures synchronized activation of sarcoplasmic reticulum (SR) Ca(2+) release during systol
74 o explore whether subclinical alterations of sarcoplasmic reticulum (SR) Ca(2+) release through cardi
75 ransverse (t) tubule depolarization triggers sarcoplasmic reticulum (SR) Ca(2+) release through ryano
76 ack a transverse tubule system, dividing the sarcoplasmic reticulum (SR) Ca(2+) store into the periph
79 on of STIM1 in mice resulted in depletion of sarcoplasmic reticulum (SR) Ca(2+) stores of SANCs and l
80 ation in RyR1 decreases the amplitude of the sarcoplasmic reticulum (SR) Ca(2+) transient, resting cy
81 Ang II-stimulated Nox2 activity increased sarcoplasmic reticulum (SR) Ca(2+) uptake in transgenic
83 alaemia, increased Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load, SR Ca2+ leak and
85 ctivity was not altered, implicating altered sarcoplasmic reticulum (SR) calcium leak in the activati
87 pin (SLN) is a regulatory peptide present in sarcoplasmic reticulum (SR) from skeletal muscle of anim
88 Although abnormal Ca(2+) release from the sarcoplasmic reticulum (SR) has been linked to arrhythmo
89 tion is triggered by Ca(2+) release from the sarcoplasmic reticulum (SR) in response to plasma membra
90 nhancement of Ca(2+) uptake and release from sarcoplasmic reticulum (SR) in sinoatrial nodal cells (S
91 X-1 (HS-associated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts w
92 9) may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and sk
93 lysosomes are intimately associated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a m
95 and type 1 ryanodine receptor (RyR1) in the sarcoplasmic reticulum (SR) is thought to underlie both
97 eceptor Ca(2+) release channel (RyR2) in the sarcoplasmic reticulum (SR) membrane and the SR Ca(2+) b
98 C-A) is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and ske
100 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori
101 ry of spark amplitude is controlled by local sarcoplasmic reticulum (SR) refilling whereas refractori
102 Intracellular Local Ca releases (LCRs) from sarcoplasmic reticulum (SR) regulate cardiac pacemaker c
103 l matrix includes local Ca(2+) delivery from sarcoplasmic reticulum (SR) ryanodine receptors (RyR2) t
104 ubules (ATs) with extensive junctions to the sarcoplasmic reticulum (SR) that include ryanodine recep
107 R2), a Ca(2+) release channel located in the sarcoplasmic reticulum (SR), or calsequestrin 2 (CASQ2),
108 coupling of the contractile apparatus to the sarcoplasmic reticulum (SR), which serves as the reservo
118 ally, EHD3-deficient myocytes show increased sarcoplasmic reticulum [Ca], increased spark frequency,
119 er beating rate, disorganised sarcomeres and sarcoplasmic reticulum and a blunted response to isopren
120 se in the amount of Ca(2+) stored within the sarcoplasmic reticulum and activated Ca(2+)/calmodulin-d
122 uscles of SHR showed reduced activity of the sarcoplasmic reticulum and decreased sarcolemmal calcium
123 tudies uncovered progressive dilation of the sarcoplasmic reticulum and ectopic and misaligned transv
124 the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of C
125 the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of
126 hat can prolong the AP duration and load the sarcoplasmic reticulum and likely contributes to the alt
127 e underwent extensive remodeling of both the sarcoplasmic reticulum and mitochondria, including alter
129 ultrastructural abnormalities of junctional sarcoplasmic reticulum and transverse tubules, and (4) a
130 consisting of ryanodine receptors (RyRs) at sarcoplasmic reticulum apposing CaV1.2 channels at t-tub
131 similar to those present in the lumen of the sarcoplasmic reticulum at rest, whereas Ca(2+) concentra
132 cell shortening, Ca transient amplitude and sarcoplasmic reticulum Ca content compared with sham car
133 cell shortening, Ca transient amplitude, and sarcoplasmic reticulum Ca content in colon ascendens ste
134 ak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum Ca content, Ca transient amplitud
137 mined the subcellular mechanisms involved in sarcoplasmic reticulum Ca loss that mediate altered Ca h
138 sim) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca release, by simultaneous live
139 mic reticular calcium ATPase 2 abundance and sarcoplasmic reticulum Ca uptake are depressed in both s
141 Sarcolipin (SLN) is a novel regulator of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) in muscle.
142 fects and that murine PDE3A1 associates with sarcoplasmic reticulum Ca(2+) ATPase 2 (SERCA2), phospho
143 e-type versus Fork-type; P<0.01), because of sarcoplasmic reticulum Ca(2+) ATPase pump potentiation c
144 o changes in expression of phospholamban and sarcoplasmic reticulum Ca(2+) ATPase, increased levels o
146 dling proteins, intracellular [Ca(2+)]i, and sarcoplasmic reticulum Ca(2+) content and increases in p
147 crease in amplitude of Ca(2+) transients and sarcoplasmic reticulum Ca(2+) content in LQT2 myocytes.
148 n of transient outward potassium current and sarcoplasmic reticulum Ca(2+) content via rescue of cont
149 , reduced Ca(2+) spark dimensions, increased sarcoplasmic reticulum Ca(2+) content, and augmented the
150 arcoplasmic reticulum Ca(2+) leak, augmented sarcoplasmic reticulum Ca(2+) content, increased the mag
152 , sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic reticulum Ca(2+) handling proteins in post-
153 vation of neuronal nitric oxide synthase and sarcoplasmic reticulum Ca(2+) handling proteins, and ide
154 osphorylated neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) handling proteins, intrace
158 )]Bulk=100 nmol/L) is dictated mainly by the sarcoplasmic reticulum Ca(2+) leak rather than sarcolemm
160 loss without marked changes in cytosolic and sarcoplasmic reticulum Ca(2+) levels, likely owing to al
161 Ca(2+)-dependent mechanism without altering sarcoplasmic reticulum Ca(2+) load and by increasing uns
162 Ca(2+) concentration transients and a lesser sarcoplasmic reticulum Ca(2+) load due to a down-regulat
164 f mutant ryanodine receptor type 2 channels, sarcoplasmic reticulum Ca(2+) load, measured by caffeine
166 otoxin (but not ranolazine), suggesting that sarcoplasmic reticulum Ca(2+) release and Na(+) current
168 L-type Ca(2+) current (ICaL) reactivation or sarcoplasmic reticulum Ca(2+) release and Na(+)/Ca(2+) e
170 hese models: one relies mainly on fractional sarcoplasmic reticulum Ca(2+) release and uptake, and th
172 ure for synchronization and stabilization of sarcoplasmic reticulum Ca(2+) release in healthy cardiom
173 enge slowed late repolarization, potentiated sarcoplasmic reticulum Ca(2+) release, and initiated EAD
174 orylation of neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and sarcoplasmic
175 pterin, the dimers of nitric oxide synthase, sarcoplasmic reticulum Ca(2+) release, and the expressio
178 (fl/fl) mice post HF revealed both increased sarcoplasmic reticulum Ca(2+) spark frequency and disrup
179 crease Ca(2+) influx to enhance refilling of sarcoplasmic reticulum Ca(2+) stores, slow muscle fatigu
180 Ca(2+) load due to a down-regulation of the sarcoplasmic reticulum Ca(2+)-adenosine triphosphatase p
181 h there is some evidence that suppression of sarcoplasmic reticulum Ca(2+)-ATP-ase (SERCA2) contribut
183 namics (MD) simulations of the calcium pump (sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)) in complex
185 merization of phospholamban, which activates sarcoplasmic reticulum Ca(2+)-ATPase and increases cytos
186 ed myocardial oxidative stress and decreased sarcoplasmic reticulum Ca(2+)-ATPase protein expression
193 embrane proteins, such as bacteriorhodopsin, sarcoplasmic reticulum Ca(2+)ATPase (SERCA1a), and its a
195 Patients with mutations in RyR2 or in the sarcoplasmic reticulum Ca-binding protein calsequestrin
196 sine formation in lymphocytes as an index of sarcoplasmic reticulum Ca-release-induced adenosine 5'-t
197 vidence has suggested a role for spontaneous sarcoplasmic reticulum Ca2+ -release events in long-stan
198 ent AF, but the occurrence and mechanisms of sarcoplasmic reticulum Ca2+ -release events in paroxysma
199 creased sarcoplasmic reticulum Ca2+ leak and sarcoplasmic reticulum Ca2+ -release events, causing del
200 However, mRNA and protein levels of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory pr
201 een linked to Ca2+ cycling proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in
202 D amplitude and timing include cytosolic and sarcoplasmic reticulum Ca2+ concentrations, inwardly rec
203 sed, activation of X-ROS signaling increases sarcoplasmic reticulum Ca2+ leak and contributes to glob
205 enhanced SERCA2a activity promote increased sarcoplasmic reticulum Ca2+ leak and sarcoplasmic reticu
207 d stretching does not significantly increase sarcoplasmic reticulum Ca2+ leak; and 4) when the chemic
209 studies point to a combination of increased sarcoplasmic reticulum Ca2+ load related to phospholamba
210 role in the normal sympathetic regulation of sarcoplasmic reticulum Ca2+ release or cardiac contracti
212 state contractions and increased spontaneous sarcoplasmic reticulum Ca2+ sparks mediated by enhanced
214 eased activity and expression of the cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a), a criti
215 virus serotype 1 (AAV1) vector carrying the sarcoplasmic reticulum calcium ATPase gene (AAV1/SERCA2a
216 eticulum stress, as well as an activation of sarcoplasmic reticulum calcium ATPase isoform 2 and citr
217 e activity in Runx1-deficient mice increased sarcoplasmic reticulum calcium content and sarcoplasmic
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
222 Calcium transient amplitude and fractional sarcoplasmic reticulum calcium release were larger and a
224 interacting with messenger RNA encoding the sarcoplasmic reticulum calcium uptake pump SERCA2a (also
225 are strongly correlated with fluctuations in sarcoplasmic reticulum calcium, because of strong releas
226 as associated with altered protein levels of sarcoplasmic reticulum calcium-regulatory proteins parti
227 effect on the mechanisms responsible for the sarcoplasmic reticulum charge-compensating counter curre
230 -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 VT VMs and PCs than respective controls, and sarcoplasmic reticulum fractional release was greater in
237 rastructural alterations of mitochondria and sarcoplasmic reticulum in muscle and abnormal collagen f
238 l role of abnormal calcium releases from the sarcoplasmic reticulum in producing repetitive electrica
240 Orai1 channels in complex with STIM1 in the sarcoplasmic reticulum is one such potential disease mec
241 efine a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junctions as unexpected but major
243 nm) pore connects the transport sites to the sarcoplasmic reticulum lumen through a chain of water mo
245 nd nearly fully opened at 2 mum cytosolic or sarcoplasmic reticulum luminal Ca(2+), and Ca(2+)- and v
246 ated that sAnk1 and SLN can associate in the sarcoplasmic reticulum membrane and after exogenous expr
247 g sites (ECC couplons) comprising plasma and sarcoplasmic reticulum membrane calcium channels are imp
254 dantrolene inhibits Ca(2+) release from the sarcoplasmic reticulum of skeletal and cardiac muscle pr
256 A2a, the protein that pumps calcium into the sarcoplasmic reticulum of the cardiomyocyte, seems promi
257 increased distance between mitochondria and sarcoplasmic reticulum on electron microscopy, and 3) ni
258 Immunostaining showed mislocalization of the sarcoplasmic reticulum proteins Serca1 and Ryr1 in a pat
262 urce of reactive oxygen species (ROS) in the sarcoplasmic reticulum that may reduce SERCA2a function.
263 le are essential for Ca(2+) release from the sarcoplasmic reticulum that mediates excitation-contract
264 of the calcium release channel (RyR1) in the sarcoplasmic reticulum that supplies the calcium signal
266 ne receptors (RyR1s) release Ca(2+) from the sarcoplasmic reticulum to initiate skeletal muscle contr
267 ptor (RyR1) mediates Ca(2+) release from the sarcoplasmic reticulum to initiate skeletal muscle contr
269 on RyR1 channel activity after incorporating sarcoplasmic reticulum vesicles into lipid bilayers.
270 sAnk1 interacts specifically with SERCA1 in sarcoplasmic reticulum vesicles isolated from rabbit ske
274 bules), the intracellular calcium store (the sarcoplasmic reticulum), and the co-localisation of thes
275 KCNQ1 mainly resides in the jSR (junctional sarcoplasmic reticulum), whereas KCNE1 resides on the ce
276 are caused by cyclic Ca(2+) release from the sarcoplasmic reticulum, although Ca(2+) influx via plasm
277 r in the regulation of calcium uptake in the sarcoplasmic reticulum, and by probing its dynamical act
278 channels (ryanodine receptors, RyR2) in the sarcoplasmic reticulum, and the frequency of Ca(2+) spar
279 tructural bridge between the plasmalemma and sarcoplasmic reticulum, is essential for precise Ca(2+)-
281 nger function, reduction of Ca(2+) uptake to sarcoplasmic reticulum, reduced K(+) currents, and incre
282 dine receptor would lead to Ca leak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum
283 o RyR1 that triggers Ca(2+) release from the sarcoplasmic reticulum, retrograde signaling from RyR1 t
285 d sarcoplasmic reticulum calcium content and sarcoplasmic reticulum-mediated calcium release, preserv
300 accumulated and co-localized with DNAJB6 at sarcoplasmic stress granules suggesting that these prote
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