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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
12          In addition to transporting Ca(2+), SERCA facilitates bidirectional proton transport across
13 that mitochondria supply ATP to the ER and a SERCA-dependent Ca(2+) gradient across the ER membrane i
14 f SERCA, though the PLN oligomer straddles a SERCA-SERCA crystal contact.
15 e with a model in which PLB interacts with a SERCA homodimer in a stoichiometry of 1:2.
16 ) in ICC, and blocking Ca(2+) release with a SERCA inhibitor (thapsigargin) or a store-operated Ca(2+
17                               MetS abolished SERCA activation by GLP-1 receptor agonists.
18 e GLP-1 receptor agonist exenatide activated SERCA but did not alter other Ca(2+) transporters.
19            Glucose metabolism also activates SERCA pumps, which fills the endoplasmic reticulum and h
20 PLN inhibition is length-dependent, allowing SERCA activity to be restored incrementally.
21 elation between oligomerization affinity and SERCA-binding.
22  TBBPA activated RyR1 and inhibited DHPR and SERCA, inducing a net efflux of Ca(2+) from loaded micro
23 to quantify micropeptide oligomerization and SERCA-binding.
24  quaternary conformation of PLB pentamer and SERCA-PLB regulatory complex.
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
30 (3)H]ryanodine binding and SR Ca(2+) ATPase (SERCA) activity were also tested.
31 d sarco-endoplasmic reticulum Ca(2+) ATPase (SERCA) activity.
32 nd sarcoendoplasmic reticulum Ca(2+) ATPase (SERCA) activity.
33      THADA binds the sarco/ER Ca(2+) ATPase (SERCA) and acts on it as an uncoupler.
34 co/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally elevated in the muscle of Duche
35 tor of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) in muscle.
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
40 plasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA).
41  sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA).
42 er sarcoendoplasmic reticulum Ca(2+) ATPase (SERCA).
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.
48  sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA).
49 rcoendoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA) activity.
50 ctions by repressing sarco/ER Ca(2+)-ATPase (SERCA) activity.
51  sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) and are implicated in breast cancer and Hailey-Ha
52 plasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) and Na(+), K(+)-ATPase.
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
62 e sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) pump during Ca(2+) refilling of the ER.
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
65 f sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) was tissue-specifically knocked down.
66  pump (sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)) in complex with phospholamban (PLB).
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.
71  sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA).
72 ed back into the SR by the SR Ca(2+)-ATPase (SERCA).
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
75   The sarco/endoplasmic reticulum Ca ATPase (SERCA) pump then refills SR Ca stores.
76 d/or decreased activity of the SR Ca ATPase (SERCA).
77  the sarco-/endoplasmic reticulum Ca-ATPase (SERCA) pump, inositol-1,4,5-triphosphate receptor (IP3R)
78 ity of the sarcoplasmic reticulum Ca-ATPase (SERCA).
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
84 tor of the endo/sarcoplasmic calcium ATPase (SERCA), is presented.
85  sarco/endoplasmic reticulum calcium ATPase (SERCA), which plays a key role in the maintenance of Ca(
86  sarco/endoplasmic reticulum calcium ATPase (SERCA).
87 lasmic/endoplasmic reticulum calcium ATPase (SERCA).
88 butions of RyRs and sarco/ER calcium-ATPase (SERCA) pumps that we predict using a computational model
89  sarco/endoplasmic reticulum calcium-ATPase (SERCA).
90 ed that sarco(endo)plasmic reticulum ATPase (SERCA) expression was elevated in several WFS1-depleted
91 dulation of the SR Ca(2+)-stimulated ATPase (SERCA) and RyRs by K201.
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.
95 N pentamer and the novel interaction between SERCA and an SLN monomer.
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
98  microscopy to study the interaction between SERCA and PLN.
99 d peptide can target and constitutively bind SERCA.
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
107 ying the active transport of calcium ions by SERCA.
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
110 ole in optimizing active Ca(2+) transport by SERCA.
111  results from the leak opposing Ca uptake by SERCA.
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
115                   However, despite decreased SERCA-PLB binding, intermolecular FRET for Val(49)-stop
116  conclude that R9C mutation of PLB decreases SERCA inhibition by decreasing the amount of the regulat
117 k and junctional SR, cytosolic Ca diffusion, SERCA uptake activity, and RyR open probability.
118 ed intermediate of the pump populated during SERCA regulation.
119  no therapeutics that directly target either SERCA or PLN.
120 alizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phosp
121                Aside from clinical features, SERCA activity measurement and SERCA1 western blot can a
122 ing the leaked SR Ca(2+) more accessible for SERCA.
123 in the binding affinity of truncated PLB for SERCA and loss of inhibitory potency.
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(
126 roximately 0.5 muM) was much larger than for SERCA (IC50 > 285 muM).
127                       In both crystal forms, SERCA molecules are organized into identical antiparalle
128 n for decades as an assembly of calcium-free SERCA molecules induced by the addition of decavanadate.
129                             In myocytes from SERCA knock-in mice, basal SERCA activity and SR calcium
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
132 ng but explained by the observed increase in SERCA activity.
133 olic failure, all of which were inhibited in SERCA knock-in mice.
134 xistence of a transient water-filled pore in SERCA that connects the Ca(2+) binding sites with the lu
135 a distinct structural and functional role in SERCA regulation.
136                   Large-scale transitions in SERCA occur at time-scales beyond the current reach of u
137 traction even when it successfully increases SERCA expression.
138 an (PLN) and sarcolipin (SLN), which inhibit SERCA, the membrane pump that controls muscle relaxation
139 some Pen derivatives significantly inhibited SERCA at concentrations required to modulate RyRs.
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
144                              We investigated SERCA dimerization in rabbit left ventricular myocytes u
145  impaired cellular signaling steps involving SERCA.
146 t phosphorylation may lead to longer-lasting SERCA stimulation and may sustain maladaptive Ca(2+) han
147             Western blotting of cross-linked SERCA revealed higher-molecular-weight species consisten
148 graphy studies have suggested that PLB locks SERCA in a low-Ca(2+)-affinity E2 state that is incompat
149                                     Lowering SERCA level will enable intracellular calcium oscillatio
150  a mechanistic understanding of PLB-mediated SERCA transport regulation.
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
153 n a crystal contact that bridges neighboring SERCA dimer ribbons.
154 d by phospholamban removal, which normalized SERCA function.
155 lation domain and the cytosolic ends of 5 of SERCA's 10 transmembrane helices.
156 or MG132 resulted in reduced accumulation of SERCA levels compared with wild-type cells.
157                          Redox activation of SERCA C674 regulates basal SR calcium content, thereby m
158                      Moreover, activation of SERCA promotes fusion in a BafilomycinA1-sensitive manne
159               Ca(2+)-dependent activation of SERCA-PLB provides a control function that regulates cyt
160 necessary for Ca(2+)-dependent activation of SERCA.
161                              The activity of SERCA is regulated by small membrane protein subunits, t
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
164                The multiscale correlation of SERCA group (scaling exponent: 0.77 +/- 0.07), on the ot
165 ll helical crystals and large 2D crystals of SERCA in the absence and presence of PLN.
166 ext, we analyzed two-dimensional crystals of SERCA in the presence of wild-type SLN by electron cryom
167 echanism, SLN promotes the futile cycling of SERCA, contributing to muscle heat production.
168 on details of the structural determinants of SERCA regulation have been elusive because of the dynami
169                           Diversification of SERCA regulators was much less extensive, indicating the
170 tions to evaluate the structural dynamics of SERCA-PLB in a solution containing 100 mM K(+) and 3 mM
171 mitochondrial function and the efficiency of SERCA in HF.
172 hat oligomerization occurs at the expense of SERCA-binding.
173 face proximal to the calcium entry funnel of SERCA.
174 uptake, likely due to S-glutathionylation of SERCA pumps.
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
177 h strong affinity and relieves inhibition of SERCA in a length-dependent manner.
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
181 rongly (Kd <10 nm) and relieve inhibition of SERCA.
182 rstand the significance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynami
183 cs can be modified by changing the levels of SERCA, IP3R, and/or RyR.
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
194 LN using co-reconstituted proteoliposomes of SERCA and SLN.
195 echanism for increasing the turnover rate of SERCA.
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)
200                      FXYDs and regulators of SERCA are present in fishes, as well as terrestrial vert
201                  We propose that reversal of SERCA-PLB inhibition is achieved by stringing together i
202 e crystals are antiparallel dimer ribbons of SERCA, known for decades as an assembly of calcium-free
203 y and structural dynamics of the E2 state of SERCA.
204 romoting particular conformational states of SERCA, we found that the effect of phospholamban on SERC
205 n calcium cycling and compared with those of SERCA inhibition.
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
209                 Platelets exhibit 2 types of SERCAs, SERCA2b and SERCA3 (SERCA3 deficient mice), whic
210         Moreover, the unique oligomerization/SERCA-binding profile of DWORF is in harmony with its di
211  domain to human PLN had a minimal effect on SERCA inhibition.
212 f phospholamban and its regulatory effect on SERCA transport activity.
213 diac tissue, and their functional effects on SERCA have not been determined directly.
214 nformational states with distinct effects on SERCA's kinetic properties.
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
218 ive affinities of PLB for candidate sites on SERCA.
219 interacts with distinct alternative sites on SERCA.
220 specificity became more ambivalent for other SERCA conformers.
221 rast to the inhibitory function of the other SERCA-binding micropeptides.
222 ant flies rescues their obesity, pinpointing SERCA as a key effector of THADA function.
223 effect of R9C on PLB oligomerization and PLB-SERCA binding.
224 ge effects on PLB pentamer structure and PLB-SERCA regulatory complex conformation, increasing and de
225 o SERCA and altered the structure of the PLB-SERCA regulatory complex.
226 tem studies may relate to potentially potent SERCA block under resting Ca(2+) conditions.
227 e of SR Ca(2+) loading, suggesting potential SERCA block and/or RyR agonism.
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
231  phenocopied by depletion of the Ca(2+) pump SERCA, a secondary target of this drug.
232                             The calcium pump SERCA is a transmembrane protein that is critical for ca
233 as adenylate kinase, ATP-driven calcium pump SERCA, leucine transporter and glutamate transporter sho
234 ks the sarco/endoplasmic Ca(2+) ATPase pump (SERCA 2), depleting the SER of calcium.
235 ate the sarcoplasmic reticulum calcium pump (SERCA) by relieving its inhibition by PLN.
236     The sarcoplasmic reticulum calcium pump (SERCA) is regulated by the small integral membrane prote
237                                      Reduced SERCA activity underlies dysregulation of Ca(2+) homeost
238  Ca(2+) clearance and relaxation and reduced SERCA activity.
239          This research suggests that reduced SERCA level is the main factor responsible for the reduc
240                                     Reducing SERCA activity in THADA mutant flies rescues their obesi
241 r, how phospholamban and sarcolipin regulate SERCA is not fully understood.
242 d PLB without losing the ability to regulate SERCA activity; however, the resulting chimeras acquire
243  structural changes and motions that relieve SERCA inhibition by PLB.
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
246                             To date, several SERCA inhibitors have been thoroughly studied and the mo
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
249                    Results demonstrated that SERCA inhibitor, thapsigargin, significantly reduced lym
250 eactive oxygen species, we hypothesized that SERCA oxidation at C674 would modulate the effects of re
251                    It has been proposed that SERCA forms homooligomers that increase the catalytic ra
252 zation of this isoform (zfPLN) revealed that SERCA inhibition and reversal by phosphorylation were co
253  fluorescently labeled SERCA2a revealed that SERCA readily forms homodimers.
254                        The data suggest that SERCA calcium binding induces the pump to undergo a tran
255         Together, these results suggest that SERCA forms constitutive homodimers in live cells and th
256                                          The SERCA (sarco-endoplasmic reticulum Ca(2+) ATPase) inhibi
257                                          The SERCA activator, CDN 1163 partially restored lymphatic c
258                                          The SERCA group shows longer heart beat intervals (Mean +/-
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
261       Mice with heterozygous knock-in of the SERCA C674S mutation were subjected to chronic ascending
262 ovel sites on M3 and with the outside of the SERCA helix M9.
263 e structure and functional properties of the SERCA mutant E340A.
264 apsigargin, an irreversible inhibitor of the SERCA pump, exhibited anxiogenic-like behaviors and incr
265 terminant of the quaternary structure of the SERCA regulatory complex.
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
268                      A projection map of the SERCA-SLN complex was determined to a resolution of 8.5
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
271 ection was abolished by cotreatment with the SERCA inhibitor cyclopiazonic acid.
272 reticulum SERCA pumps and treatment with the SERCA-inhibitor Thapsigargin halted intracellular MRSA s
273                                         This SERCA-SLN complex correlated with the ability of SLN to
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
276        The R9C also decreased PLB binding to SERCA and altered the structure of the PLB-SERCA regulat
277 optosis and autophagy by directly binding to SERCA and causing endoplasmic reticulum (ER) stress and
278               We propose that PLB binding to SERCA populates a novel (to our knowledge) E1 intermedia
279                               SLN binding to SERCA uncouples Ca(2+) transport from ATP hydrolysis.
280 merization are also important for binding to SERCA.
281 de that the luminal extension contributes to SERCA inhibition but only in the context of zfPLN.
282 ine (non-sensitising) had similar effects to SERCA inhibition: decreased systolic [Ca(2+)]i , increas
283 uptake by the Ca(2+)adenosine triphosphatase SERCA.
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
287        However, the exact mechanisms whereby SERCA inhibition induces cell death are incompletely und
288  Ca transient in the majority of cells while SERCA inhibition produced monophasic decay.
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
291 at during rest NCX effectively competes with SERCA for cytosolic Ca(2+) that leaks from the SR.
292                Meanwhile, new compounds with SERCA-inhibiting properties of natural, synthetic, or se
293 her-molecular-weight species consistent with SERCA oligomerization.
294                  MLN interacts directly with SERCA and impedes Ca(2+) uptake into the SR.
295 eptide species still showed robust FRET with SERCA, and there was a surprising positive correlation b
296 rm of all micropeptides that interacted with SERCA.
297 ccess to potential sites of interaction with SERCA.
298                SLN physically interacts with SERCA and differentially regulates contractility in skel
299 , we show that a PLN oligomer interacts with SERCA in a similar manner in both crystal forms.
300 etic peptides in phospholipid membranes with SERCA and measured calcium-dependent ATPase activity.

 
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