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1 SERCA [sarco(endo)plasmic reticulum calcium ATPase] is r
2 SERCA activity in muscle can be regulated by phospholamb
3 SERCA activity is regulated by a variety of small transm
4 SERCA block likely produces mild SR depletion in normal
5 SERCA function remains constant during compensated hyper
6 SERCA function remains constant in CH but decreases (tau
7 SERCA inhibition was maximally relieved by P16-PLB (the
8 SERCA resides in an environment made up largely by the l
9 SERCA uses separate proton and metal ion pathways during
10 SERCA-mediated Ca(2+) uptake was measured with the ER-ta
11 SERCAs (sarco-endoplasmic reticulum Ca(2+)-ATPases) pump
13 that mitochondria supply ATP to the ER and a SERCA-dependent Ca(2+) gradient across the ER membrane i
16 ) in ICC, and blocking Ca(2+) release with a SERCA inhibitor (thapsigargin) or a store-operated Ca(2+
22 TBBPA activated RyR1 and inhibited DHPR and SERCA, inducing a net efflux of Ca(2+) from loaded micro
25 e energy transfer (FRET) from PLB to PLB and SERCA to PLB, suggesting a change in quaternary conforma
26 e, molecular dynamics simulations of SLN and SERCA interaction showed a rearrangement of SERCA residu
27 strated a novel interaction between WFS1 and SERCA by co-immunoprecipitation in Cos7 cells and with e
28 The sarcoplasmic reticulum Ca(2+)-ATPase SERCA promotes muscle relaxation by pumping calcium ions
29 tory membrane proteins of the calcium ATPase SERCA, namely sarcolipin and phospholamban, in explicit
34 co/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally elevated in the muscle of Duche
36 a sarcoendoplasmic reticulum Ca(2+) ATPase (SERCA) inhibitor, on a panel of unselected patient-deriv
37 ion of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) pump is one of the key determinants of the phenot
38 sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA) pump, could contribute to heat production in skel
39 d sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA)-mediated reuptake rather than changes in Ca(2+) i
43 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) activity, (2) CAMKII modulation of SERCA, L-type
44 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) as the principal regulators of systolic and diast
45 sarco-endoplasmic reticulum Ca(2+) -ATPase (SERCA) at the propagation front elevates local [Ca(2+) ]
46 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) pump and blockers of inositol triphosphate recept
47 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) pump is necessary for maintenance of spontaneity.
51 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) and are implicated in breast cancer and Hailey-Ha
53 Sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA) and phospholamban (PLB) are essential for intrace
54 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) complex regulates heart r
55 a sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) Ca(2+) pump inhibitor, reproducibly displayed sig
56 m pump sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) counter-transports Ca(2+) and H(+) at the expense
57 e sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) has emerged as a major contributor to ER stress.
58 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) is a P-type ATPase that transports Ca(2+) from th
59 he sarcoendoplasmic reticulum Ca(2+)-ATPase (SERCA) is responsible for intracellular Ca(2+) homeostas
60 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) protein expression or activity was not altered, i
61 irectly binds to the sarco/ER Ca(2+)-ATPase (SERCA) pump at the ER, changing its oxidative state and
63 e sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) pump is a major regulatory axis in cardiac muscle
64 The sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) transports two Ca(2+) ions from the cytoplasm to
67 Sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), a member of the P-type ATPases family, transport
68 , sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA), and decreases levels of the pro-apoptotic protei
69 co/endoplasmic reticulum (ER) Ca(2+)-ATPase (SERCA), disrupts Ca(2+) homeostasis, and causes cell dea
70 he sarcoendoplasmic reticulum Ca(2+)-ATPase (SERCA), which plays a lead role in muscle contractility.
73 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA)2a signalling and decreased myocardial energy meta
74 rcoendoplasmic reticulum Ca(2+)alpha ATPase (SERCA) expression is downregulated and mitochondrial fun
77 the sarco-/endoplasmic reticulum Ca-ATPase (SERCA) pump, inositol-1,4,5-triphosphate receptor (IP3R)
79 coplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) activity was reduced and western blot analysis sh
80 s of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory protein sarcolipin, which is predomina
81 ncreased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake, modulated by increased phospholamb
82 sarco/endoplasmic reticulum calcium ATPase (SERCA) establishes the intracellular calcium gradient ac
83 sarco(endo)plasmic reticulum calcium ATPase (SERCA) in cardiac myocytes is modulated by an inhibitory
85 sarco/endoplasmic reticulum calcium ATPase (SERCA), which plays a key role in the maintenance of Ca(
88 butions of RyRs and sarco/ER calcium-ATPase (SERCA) pumps that we predict using a computational model
90 ed that sarco(endo)plasmic reticulum ATPase (SERCA) expression was elevated in several WFS1-depleted
92 doplasmic reticulum calcium trasport ATPase (SERCA) pump activity with thapsigargin prolonged NMDAR-D
93 doplasmic reticulum calcium trasport ATPase (SERCA) pump prolonged NMDAR-DeltaCa(2+) responses in sha
94 In myocytes from SERCA knock-in mice, basal SERCA activity and SR calcium content were decreased.
96 noted multiple modes of interaction between SERCA and phospholamban and observed that once a particu
97 ormational memory in the interaction between SERCA and phospholamban, thus providing insights into th
100 om Ca(2+)-bound SERCA, SLN continues to bind SERCA throughout its kinetic cycle and promotes uncoupli
101 lthough PLB gets dislodged from Ca(2+)-bound SERCA, SLN continues to bind SERCA throughout its kineti
102 found that the transport sites of PLB-bound SERCA are completely exposed to the cytosol and that K(+
103 to determine structural changes of PLB-bound SERCA in response to binding of a single Ca(2+) ion.
104 pal component analysis showed that PLB-bound SERCA lies exclusively along the structural ensemble of
105 normal intracellular pH (7.1-7.2), PLB-bound SERCA populates an E1 state that is deprotonated at resi
106 calcium translocation and ATP hydrolysis by SERCA under conditions that mimic environments in sarcop
108 and that dimer formation is not modulated by SERCA conformational poise, PLB binding, or PLB phosphor
109 tered ATP-dependent calcium translocation by SERCA within the first transport cycle, whereas sarcolip
112 is accelerated by depletion of the cellular SERCA-like Pmr1 ATPase-driven Ca(2+)/Mn(2+) pump, regula
113 ny with its distinct role as a PLB-competing SERCA activator, in contrast to the inhibitory function
114 ent measurements, proteoliposomes containing SERCA and phospholamban or sarcolipin were adsorbed to a
116 conclude that R9C mutation of PLB decreases SERCA inhibition by decreasing the amount of the regulat
120 alizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phosp
124 increase in binding affinity of V49A-PLB for SERCA, and a gain of inhibitory function as quantified b
125 emains constant in CH but decreases (tau for SERCA-mediated Ca(2+) removal changed from 6.3 to 3.0 s(
128 n for decades as an assembly of calcium-free SERCA molecules induced by the addition of decavanadate.
130 g membrane repolarization and alterations in SERCA activity that reduce cardiomyocyte contractility.
131 Hence, we hypothesized that a decrease in SERCA pump expression and/or activity in lymphatic muscl
134 xistence of a transient water-filled pore in SERCA that connects the Ca(2+) binding sites with the lu
138 an (PLN) and sarcolipin (SLN), which inhibit SERCA, the membrane pump that controls muscle relaxation
140 i and colleagues demonstrate that inhibiting SERCA calcium pumps preferentially impairs the maturatio
141 ally occurring p53 missense mutants inhibits SERCA pump activity at the ER, leading to a reduction of
142 n that unphosphorylated PLB (U-PLB) inhibits SERCA and that phosphorylation of PLB at Ser-16 or Thr-1
143 ies alone have led to a greater insight into SERCA-PLB regulation, the structural mechanisms for Ca(2
146 t phosphorylation may lead to longer-lasting SERCA stimulation and may sustain maladaptive Ca(2+) han
148 graphy studies have suggested that PLB locks SERCA in a low-Ca(2+)-affinity E2 state that is incompat
151 structural mechanisms by which SLN modulates SERCA-dependent contractility and thermogenesis remain u
152 lish an inhibitory interaction with multiple SERCA conformational states with distinct effects on SER
162 y of SLN to decrease the maximal activity of SERCA, which is distinct from the ability of PLN to incr
163 pling skeletal muscle tissue for analyses of SERCA activity as well as gene expression of SERCA1a and
166 ext, we analyzed two-dimensional crystals of SERCA in the presence of wild-type SLN by electron cryom
168 on details of the structural determinants of SERCA regulation have been elusive because of the dynami
170 tions to evaluate the structural dynamics of SERCA-PLB in a solution containing 100 mM K(+) and 3 mM
175 ailability attenuated S-glutathionylation of SERCA, resulting in an increase in cytosolic calcium, en
176 ling model involves reversible inhibition of SERCA by monomeric PLN and storage of PLN as an inactive
178 d PLN strongly and relieve PLN inhibition of SERCA to a greater extent than a similar length random s
179 of the headpiece underlie PLB inhibition of SERCA, and binding of a single Ca(2+) ion is sufficient
180 201 displayed Ca(2+)-dependent inhibition of SERCA-dependent ATPase activity, which was measured in m
182 rstand the significance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynami
184 phosphomimetic R9C-PLB oxidation and loss of SERCA inhibition, leading to impaired calcium regulation
185 interacts with transmembrane segments M3 of SERCA and participates in a crystal contact that bridges
186 pentameric form of PLN interacts with M3 of SERCA and that it plays a distinct structural and functi
187 to interact with transmembrane segment M3 of SERCA, although the interaction appeared to be indirect
188 omeric form of PLN also interacts with M3 of SERCA, though the PLN oligomer straddles a SERCA-SERCA c
189 approaches to develop a structural model of SERCA-PLB interactions to gain a mechanistic understandi
190 mportance to guide therapeutic modulation of SERCA and other evolutionarily related ion-motive ATPase
191 reveal a major role for CAMKII modulation of SERCA in the peak Ca(2+) -frequency response, driven mos
192 e (SERCA) activity, (2) CAMKII modulation of SERCA, L-type channel and transient outward K(+) current
193 y discovered compounds with the potential of SERCA inhibition, discusses their mechanism of action, a
196 SERCA interaction showed a rearrangement of SERCA residues that is altered when the SLN N terminus i
197 We conclude that PLB-mediated regulation of SERCA activity in the heart results from biochemical and
198 role for WFS1 in the negative regulation of SERCA and provide further insights into the function of
199 anner similar to that of known regulators of SERCA activity, phospholamban (PLB) and sarcolipin (SLN)
202 e crystals are antiparallel dimer ribbons of SERCA, known for decades as an assembly of calcium-free
204 romoting particular conformational states of SERCA, we found that the effect of phospholamban on SERC
206 slow (millisecond) structural transitions of SERCA, the existence of simultaneous metal and proton pa
207 al regions of SLN that mediate uncoupling of SERCA, we employed mutagenesis and generated chimeras of
208 VF was not observed with an upregulation of SERCA, a potential drug therapy, using the same protocol
215 to the effects of annular and bulk lipids on SERCA activation, but the role of a nonannular lipid sit
216 we found that the effect of phospholamban on SERCA depends on substrate preincubation conditions.
217 interacts with a specific inhibitory site on SERCA, and low-resolution structural evidence suggests t
224 ge effects on PLB pentamer structure and PLB-SERCA regulatory complex conformation, increasing and de
228 ghly charged transport site, thus preserving SERCA's structural stability during active Ca(2+) transp
229 c-stimulated cardiomyocytes led to prolonged SERCA activation, presumably because 14-3-3 protected PL
230 In addition, the ER transmembrane proteins SERCA and calnexin were not detected in viroplasm-associ
233 as adenylate kinase, ATP-driven calcium pump SERCA, leucine transporter and glutamate transporter sho
236 The sarcoplasmic reticulum calcium pump (SERCA) is regulated by the small integral membrane prote
242 d PLB without losing the ability to regulate SERCA activity; however, the resulting chimeras acquire
244 SLN gene normalizes SLN expression, restores SERCA function, mitigates skeletal muscle and cardiac pa
245 ractive partner of the endoplasmic reticulum SERCA pumps and treatment with the SERCA-inhibitor Thaps
247 We modeled the binding of PLB to several SERCA conformations, representing different enzymatic st
248 phospholamban, the other well studied small SERCA-regulatory proteins, oligomerize either alone or t
250 eactive oxygen species, we hypothesized that SERCA oxidation at C674 would modulate the effects of re
252 zation of this isoform (zfPLN) revealed that SERCA inhibition and reversal by phosphorylation were co
259 nly endogenous peptide known to activate the SERCA pump by physical interaction and provides a means
260 it enhances SERCA activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregu
264 apsigargin, an irreversible inhibitor of the SERCA pump, exhibited anxiogenic-like behaviors and incr
266 ers formed in the absence or presence of the SERCA regulatory partner, phospholamban (PLB) and were u
267 Agonist-stimulated phosphorylation of the SERCA regulatory protein phospholamban was increased in
269 iation is engaged it persists throughout the SERCA transport cycle and multiple turnover events.
270 er-regulin (ALN) are reported to bind to the SERCA calcium pump in a manner similar to that of known
272 reticulum SERCA pumps and treatment with the SERCA-inhibitor Thapsigargin halted intracellular MRSA s
274 a(2+) to LCC density and diastolic Ca(2+) to SERCA density decreased by 16-fold and increased by 23%,
275 availability of the micropeptide to bind to SERCA in a regulatory complex, we used co-immunoprecipit
277 optosis and autophagy by directly binding to SERCA and causing endoplasmic reticulum (ER) stress and
282 ine (non-sensitising) had similar effects to SERCA inhibition: decreased systolic [Ca(2+)]i , increas
284 c reticulum Ca(2+) adenosine triphosphatase (SERCA)2a, a critical regulator of calcium homeostasis, i
285 at ventricular myocytes expressing wild-type SERCA, H(2)O(2) caused a 25% increase in mitochondrial c
286 fect of C674 oxidation on apoptosis in vivo, SERCA knock-in mice were subjected to chronic ascending
289 reduces its contractibility and explain why SERCA gene therapy, a change in calcium handling to trea
290 monstrating that PLN remains associated with SERCA and that the PLN pentamer is required for the regu
295 eptide species still showed robust FRET with SERCA, and there was a surprising positive correlation b
300 etic peptides in phospholipid membranes with SERCA and measured calcium-dependent ATPase activity.