ライフサイエンスコーパス: SERCA

1 SERCA activity in muscle can be regulated by phospholamb

2 SERCA activity is regulated by a variety of small transm

3 SERCA block likely produces mild SR depletion in normal

4 SERCA E-P formation is rate-limited by enzyme activation

5 SERCA inhibition preferentially impairs the maturation a

6 SERCA inhibition was maximally relieved by P16-PLB (the

7 SERCA undergoes conformational changes as it harnesses t

8 SERCA uses separate proton and metal ion pathways during

9 calcium burst is suppressed by G1 venom in a SERCA-dependent manner, leading to the failure of plasma

10 Here, we report expression of PfATP6 (a SERCA pump) in yeast and demonstrate its inhibition by a

11 e with a model in which PLB interacts with a SERCA homodimer in a stoichiometry of 1:2.

12 MetS abolished SERCA activation by GLP-1 receptor agonists.

13 e GLP-1 receptor agonist exenatide activated SERCA but did not alter other Ca(2+) transporters.

14 Glucose metabolism also activates SERCA pumps, which fills the endoplasmic reticulum and h

15 PLN inhibition is length-dependent, allowing SERCA activity to be restored incrementally.

16 TBBPA activated RyR1 and inhibited DHPR and SERCA, inducing a net efflux of Ca(2+) from loaded micro

17 quaternary conformation of PLB pentamer and SERCA-PLB regulatory complex.

18 e energy transfer (FRET) from PLB to PLB and SERCA to PLB, suggesting a change in quaternary conforma

19 , Orai1, STIM1, IP(3) and RyR receptors, and SERCA following BDNF exposure, effects inhibited by inhi

20 (2-APB), ryanodine receptors (Ryanodine) and SERCA pump (cyclopiazonic acid and thapsigargin) abolish

21 e, molecular dynamics simulations of SLN and SERCA interaction showed a rearrangement of SERCA residu

22 strated a novel interaction between WFS1 and SERCA by co-immunoprecipitation in Cos7 cells and with e

23 hat interacts more strongly with the anionic SERCA cytoplasmic domain.

24 The sarcoplasmic reticulum Ca(2+)-ATPase SERCA promotes muscle relaxation by pumping calcium ions

25 tory membrane proteins of the calcium ATPase SERCA, namely sarcolipin and phospholamban, in explicit

26 holamban, which regulates the related ATPase SERCA, PLM is reported to oligomerize.

27 (3)H]ryanodine binding and SR Ca(2+) ATPase (SERCA) activity were also tested.

28 d sarco-endoplasmic reticulum Ca(2+) ATPase (SERCA) activity.

29 THADA binds the sarco/ER Ca(2+) ATPase (SERCA) and acts on it as an uncoupler.

30 co/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally elevated in the muscle of Duche

31 tor of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) in muscle.

32 sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA) pump, could contribute to heat production in skel

33 (sarco-endoplasmic reticulum Ca(2+) ATPase (SERCA)) and Cu(+) (ATP7A/B) ATPases utilize ATP through

34 d sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA)-mediated reuptake rather than changes in Ca(2+) i

35 sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA).

36 er sarcoendoplasmic reticulum Ca(2+) ATPase (SERCA).

37 plasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA).

38 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) activity, (2) CAMKII modulation of SERCA, L-type

39 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) as the principal regulators of systolic and diast

40 sarco-endoplasmic reticulum Ca(2+) -ATPase (SERCA) at the propagation front elevates local [Ca(2+) ]

41 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) pump and blockers of inositol triphosphate recept

42 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) pump is necessary for maintenance of spontaneity.

43 sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA).

44 Sarco(endo)plasmic reticulum Ca(2+)ATPase (SERCA) pump activity is modulated by phospholamban (PLB)

45 ctions by repressing sarco/ER Ca(2+)-ATPase (SERCA) activity.

46 plasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) and Na(+), K(+)-ATPase.

47 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) complex regulates heart r

48 en the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) controls Ca(2+) transport

49 a sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) Ca(2+) pump inhibitor, reproducibly displayed sig

50 m pump sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) counter-transports Ca(2+) and H(+) at the expense

51 e sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) has emerged as a major contributor to ER stress.

52 e sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) is a transmembrane ion transporter belonging to t

53 he sarcoendoplasmic reticulum Ca(2+)-ATPase (SERCA) is responsible for intracellular Ca(2+) homeostas

54 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) protein expression or activity was not altered, i

55 irectly binds to the sarco/ER Ca(2+)-ATPase (SERCA) pump at the ER, changing its oxidative state and

56 Sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) transports two Ca(2+) ions across the membrane of

57 f sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) was tissue-specifically knocked down.

58 pump (sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)) in complex with phospholamban (PLB).

59 Sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), a member of the P-type ATPases family, transport

60 , sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA), and decreases levels of the pro-apoptotic protei

61 co/endoplasmic reticulum (ER) Ca(2+)-ATPase (SERCA), disrupts Ca(2+) homeostasis, and causes cell dea

62 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA).

63 ed back into the SR by the SR Ca(2+)-ATPase (SERCA).

64 r or sarcoplasmic/endoplasmic Ca(2+)-ATPase (SERCA).

65 sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA)2a signalling and decreased myocardial energy meta

66 rcoendoplasmic reticulum Ca(2+)alpha ATPase (SERCA) expression is downregulated and mitochondrial fun

67 The sarco/endoplasmic reticulum Ca ATPase (SERCA) pump then refills SR Ca stores.

68 d/or decreased activity of the SR Ca ATPase (SERCA).

69 onstituted sarcoplasmic reticulum Ca-ATPase (SERCA) and its regulator phospholamban (PLB).

70 the sarco-/endoplasmic reticulum Ca-ATPase (SERCA) pump, inositol-1,4,5-triphosphate receptor (IP3R)

71 ity of the sarcoplasmic reticulum Ca-ATPase (SERCA).

72 ion of the sarcoplasmic reticulum Ca-ATPase (SERCA).

73 s of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory protein sarcolipin, which is predomina

74 sarco/endoplasmic reticulum calcium ATPase (SERCA) activity due to altered phospholipid composition

75 Sarco/endoplasmic reticulum calcium ATPase (SERCA) channels emerged at the intersection of these com

76 sarco/endoplasmic reticulum calcium ATPase (SERCA) establishes the intracellular calcium gradient ac

77 sarco(endo)plasmic reticulum calcium ATPase (SERCA) is regulated in a tissue-dependent manner via int

78 e sarcoendoplasmic reticulum calcium ATPase (SERCA) plays a key role in cardiac calcium handling and

79 sarco/endoplasmic reticulum calcium ATPase (SERCA) pump.

80 sarco/endoplasmic reticulum calcium ATPase (SERCA).

81 sarco/endoplasmic reticulum calcium ATPase (SERCA).

82 sarco/endoplasmic reticulum calcium-ATPase (SERCA).

83 ed that sarco(endo)plasmic reticulum ATPase (SERCA) expression was elevated in several WFS1-depleted

84 ion and sarco(endo)plasmic reticulum ATPase (SERCA) inhibitor-induced apoptosis, and both are attenua

85 dulation of the SR Ca(2+)-stimulated ATPase (SERCA) and RyRs by K201.

86 doplasmic reticulum calcium trasport ATPase (SERCA) pump activity with thapsigargin prolonged NMDAR-D

87 doplasmic reticulum calcium trasport ATPase (SERCA) pump prolonged NMDAR-DeltaCa(2+) responses in sha

88 triated muscle, the archetype P-type ATPase, SERCA (sarco(endo)plasmic reticulum Ca(2+)-ATPase), pump

89 noted multiple modes of interaction between SERCA and phospholamban and observed that once a particu

90 ormational memory in the interaction between SERCA and phospholamban, thus providing insights into th

91 we mapped the physical interactions between SERCA and both unphosphorylated and phosphorylated PLN i

92 The relationship between SERCA activity and LV function in the rabbit is highly n

93 d peptide can target and constitutively bind SERCA.

94 om Ca(2+)-bound SERCA, SLN continues to bind SERCA throughout its kinetic cycle and promotes uncoupli

95 such as cysteine and leucine eliminate both SERCA inhibition and phospholamban phosphorylation, wher

96 lthough PLB gets dislodged from Ca(2+)-bound SERCA, SLN continues to bind SERCA throughout its kineti

97 found that the transport sites of PLB-bound SERCA are completely exposed to the cytosol and that K(+

98 pal component analysis showed that PLB-bound SERCA lies exclusively along the structural ensemble of

99 normal intracellular pH (7.1-7.2), PLB-bound SERCA populates an E1 state that is deprotonated at resi

100 calcium translocation and ATP hydrolysis by SERCA under conditions that mimic environments in sarcop

101 ying the active transport of calcium ions by SERCA.

102 and that dimer formation is not modulated by SERCA conformational poise, PLB binding, or PLB phosphor

103 tered ATP-dependent calcium translocation by SERCA within the first transport cycle, whereas sarcolip

104 ole in optimizing active Ca(2+) transport by SERCA.

105 n from the ER when the cells were treated by SERCA inhibitor, and (2) significant downregulation of S

106 imental evidence that local Ca(2+) uptake by SERCA into the SR facilitates the propagation of cytosol

107 results from the leak opposing Ca uptake by SERCA.

108 permeablized myocytes, ageing did not change SERCA activity and spark frequency but decreased spark a

109 cellular Ca(2+) and Na(+) following complete SERCA inhibition eventually limit contractile function a

110 phosphorylation and results in constitutive SERCA inhibition.

111 ent measurements, proteoliposomes containing SERCA and phospholamban or sarcolipin were adsorbed to a

112 These studies "credential" SERCA as a therapeutic target in cancers associated with

113 pliced X box-binding protein 1 and decreased SERCA, which were accompanied by reduced levels of intra

114 However, despite decreased SERCA-PLB binding, intermolecular FRET for Val(49)-stop

115 conclude that R9C mutation of PLB decreases SERCA inhibition by decreasing the amount of the regulat

116 A comparison of different SERCA conformations reveals that this C-terminal pathway

117 k and junctional SR, cytosolic Ca diffusion, SERCA uptake activity, and RyR open probability.

118 7)RSYQY), which may contribute to a distinct SERCA regulatory mechanism.

119 ed intermediate of the pump populated during SERCA regulation.

120 no therapeutics that directly target either SERCA or PLN.

121 ed phosphorylation of PLN at Ser-16 enhances SERCA activity via an unknown mechanism.

122 alizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phosp

123 ytoplasmic headpiece, thereby assigning FITC-SERCA as a nucleotide-free enzyme.

124 cterize FMP-SERCA (ATP.E2 state) versus FITC-SERCA in Ca(2+)-free, Ca(2+)-bound, and actively cycling

125 eased probe accessibility compared with FITC-SERCA, indicating that ATP exhibits enhanced dynamics wi

126 , and quenching was used to characterize FMP-SERCA (ATP.E2 state) versus FITC-SERCA in Ca(2+)-free, C

127 Time-resolved spectroscopy revealed that FMP-SERCA exhibits increased probe dynamics but decreased pr

128 ing the leaked SR Ca(2+) more accessible for SERCA.

129 in the binding affinity of truncated PLB for SERCA and loss of inhibitory potency.

130 increase in binding affinity of V49A-PLB for SERCA, and a gain of inhibitory function as quantified b

131 icative of an open, disordered structure for SERCA in the E2 (Ca-free) enzymatic substate.

132 ected four discrete structural substates for SERCA expressed in cardiac muscle cells.

133 roximately 0.5 muM) was much larger than for SERCA (IC50 > 285 muM).

134 -type) phosphoenzyme intermediate formation, SERCA and ATP7A/B possess distinctive features of cataly

135 fluorescence resonance energy transfer from SERCA to PLB, thus probing directly the SERCA-PLB comple

136 s and able to compensate for the decrease in SERCA.

137 Although defects in SERCA activity are known to cause heart failure, the reg

138 rylation is tuned to maintain homeostasis in SERCA regulation.

139 ches further established that an increase in SERCA expression also resulted in subsequent inhibition

140 orientation of the thapsigargin molecule in SERCA is crucially dependent on these interactions.

141 despite almost complete (>95%) reduction in SERCA activity.

142 Large-scale transitions in SERCA occur at time-scales beyond the current reach of u

143 Increased SERCA activity (beta-adrenergic stimulation with 1 muM i

144 e populations toward the B state, increasing SERCA activity.

145 the L-type Ca(2+) channels (Ca(2+) influx), SERCA pumps (sarcoplasmic reticulum (SR) Ca(2+) uptake),

146 n of PLN and tested their ability to inhibit SERCA.

147 an (PLN) and sarcolipin (SLN), which inhibit SERCA, the membrane pump that controls muscle relaxation

148 s, the HIV drugs plus alcohol also inhibited SERCA expression and increased expression of glucose-reg

149 some Pen derivatives significantly inhibited SERCA at concentrations required to modulate RyRs.

150 i and colleagues demonstrate that inhibiting SERCA calcium pumps preferentially impairs the maturatio

151 ally occurring p53 missense mutants inhibits SERCA pump activity at the ER, leading to a reduction of

152 n that unphosphorylated PLB (U-PLB) inhibits SERCA and that phosphorylation of PLB at Ser-16 or Thr-1

153 Unphosphorylated PLB (uPLB) inhibits SERCA at low [Ca(2+)] but phosphorylated PLB (pPLB) is l

154 ay crystallography has provided insight into SERCA structural substates, but it is not known how well

155 We investigated SERCA dimerization in rabbit left ventricular myocytes u

156 impaired cellular signaling steps involving SERCA.

157 Complementary measurements with labeled SERCA showed no change in mobility after co-reconstituti

158 Western blotting of cross-linked SERCA revealed higher-molecular-weight species consisten

159 graphy studies have suggested that PLB locks SERCA in a low-Ca(2+)-affinity E2 state that is incompat

160 Lowering SERCA level will enable intracellular calcium oscillatio

161 rmational equilibrium is central to maintain SERCA's apparent Ca(2+) affinity within a physiological

162 A small-molecule SERCA inhibitor has on-target activity in two mouse mode

163 lish an inhibitory interaction with multiple SERCA conformational states with distinct effects on SER

164 In cardiac muscle, SERCA is regulated by phospholamban (PLB), a small inhib

165 ron paramagnetic resonance in the absence of SERCA but also by time-resolved fluorescence resonance e

166 or MG132 resulted in reduced accumulation of SERCA levels compared with wild-type cells.

167 Moreover, activation of SERCA promotes fusion in a BafilomycinA1-sensitive manne

168 necessary for Ca(2+)-dependent activation of SERCA.

169 rotein that decreases the Ca(2+) affinity of SERCA and attenuates contractile strength.

170 ork between thapsigargin and the backbone of SERCA.

171 to a previously undescribed conformation of SERCA in which the Ca(2+) binding sites are collapsed an

172 holamban stabilizes a unique conformation of SERCA that is characterized by a compact architecture.

173 The multiscale correlation of SERCA group (scaling exponent: 0.77 +/- 0.07), on the ot

174 echanism, SLN promotes the futile cycling of SERCA, contributing to muscle heat production.

175 on and ER stress response, and a decrease of SERCA.

176 , and to identify structural determinants of SERCA regulation by phospholamban.

177 Diversification of SERCA regulators was much less extensive, indicating the

178 tions to evaluate the structural dynamics of SERCA-PLB in a solution containing 100 mM K(+) and 3 mM

179 mitochondrial function and the efficiency of SERCA in HF.

180 ation of [Ca(2+)](SR), whereas inhibition of SERCA (3 muM cyclopiazonic acid) had the opposite effect

181 despite no detectable further inhibition of SERCA activity.

182 h strong affinity and relieves inhibition of SERCA in a length-dependent manner.

183 d PLN strongly and relieve PLN inhibition of SERCA to a greater extent than a similar length random s

184 Rapid and complete (>95%) inhibition of SERCA was associated with a moderate decrease in cardiac

185 tifaceted: it is important for inhibition of SERCA, it increases the efficiency of phosphorylation, a

186 201 displayed Ca(2+)-dependent inhibition of SERCA-dependent ATPase activity, which was measured in m

187 rongly (Kd <10 nm) and relieve inhibition of SERCA.

188 Dephosphorylated PLN is an inhibitor of SERCA and phosphorylation of PLN relieves this inhibitio

189 rstand the significance of altered levels of SERCA, IP3R, and RyR on the intracellular calcium dynami

190 cs can be modified by changing the levels of SERCA, IP3R, and/or RyR.

191 phosphomimetic R9C-PLB oxidation and loss of SERCA inhibition, leading to impaired calcium regulation

192 e to quantify the direction and magnitude of SERCA motions as the pump performs work in live cardiac

193 d ER stress and injury through modulation of SERCA and maintaining calcium homeostasis could be a the

194 reveal a major role for CAMKII modulation of SERCA in the peak Ca(2+) -frequency response, driven mos

195 e (SERCA) activity, (2) CAMKII modulation of SERCA, L-type channel and transient outward K(+) current

196 LN using co-reconstituted proteoliposomes of SERCA and SLN.

197 SERCA interaction showed a rearrangement of SERCA residues that is altered when the SLN N terminus i

198 We conclude that PLB-mediated regulation of SERCA activity in the heart results from biochemical and

199 role for WFS1 in the negative regulation of SERCA and provide further insights into the function of

200 tinct, essential domain in the regulation of SERCA and that the functional properties of the SLN tail

201 We found that the allosteric regulation of SERCA depends on the conformational equilibrium of PLN,

202 Much like phospholamban regulation of SERCA, phospholemman exists as both a sodium pump inhibi

203 s, and Arg(14) deletion, alter regulation of SERCA.

204 rophobic balance in proper PLN regulation of SERCA.

205 FXYDs and regulators of SERCA are present in fishes, as well as terrestrial vert

206 The ion-binding sites of SERCA are accessible from either the cytoplasm or the sa

207 lations performed on a Ca(2+)-bound state of SERCA reveal a water-filled pathway that may be used by

208 of the key unsolved conformational states of SERCA and provides a structural explanation for how deph

209 romoting particular conformational states of SERCA, we found that the effect of phospholamban on SERC

210 n calcium cycling and compared with those of SERCA inhibition.

211 slow (millisecond) structural transitions of SERCA, the existence of simultaneous metal and proton pa

212 nding of SLN to SERCA promotes uncoupling of SERCA, we compared SLN and SERCA1 interaction with that

213 al regions of SLN that mediate uncoupling of SERCA, we employed mutagenesis and generated chimeras of

214 nts a paradigm shift in our understanding of SERCA regulation by posttranslational phosphorylation an

215 VF was not observed with an upregulation of SERCA, a potential drug therapy, using the same protocol

216 om PLB: 1) SLN primarily affects the Vmax of SERCA-mediated Ca(2+) uptake but not the pump affinity f

217 domain to human PLN had a minimal effect on SERCA inhibition.

218 f phospholamban and its regulatory effect on SERCA transport activity.

219 diac tissue, and their functional effects on SERCA have not been determined directly.

220 nformational states with distinct effects on SERCA's kinetic properties.

221 de to synthesize FITC monophosphate (FMP) on SERCA, producing a phosphorylated pseudosubstrate tether

222 we found that the effect of phospholamban on SERCA depends on substrate preincubation conditions.

223 interact with a different set of residues on SERCA.

224 An inability to knockout parasite SERCA pumps provides genetic evidence that they are esse

225 ant flies rescues their obesity, pinpointing SERCA as a key effector of THADA function.

226 effect of R9C on PLB oligomerization and PLB-SERCA binding.

227 ge effects on PLB pentamer structure and PLB-SERCA regulatory complex conformation, increasing and de

228 the long sought crystal structure of the PLB-SERCA complex at 2.8-A resolution.

229 o SERCA and altered the structure of the PLB-SERCA regulatory complex.

230 tem studies may relate to potentially potent SERCA block under resting Ca(2+) conditions.

231 e of SR Ca(2+) loading, suggesting potential SERCA block and/or RyR agonism.

232 ghly charged transport site, thus preserving SERCA's structural stability during active Ca(2+) transp

233 phenocopied by depletion of the Ca(2+) pump SERCA, a secondary target of this drug.

234 as adenylate kinase, ATP-driven calcium pump SERCA, leucine transporter and glutamate transporter sho

235 ks the sarco/endoplasmic Ca(2+) ATPase pump (SERCA 2), depleting the SER of calcium.

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 ng Ca(2+) back into the SR during a release, SERCA is able to prolong a Ca(2+) spark, and this may co

244 on of PLB increases the R state and relieves SERCA inhibition, suggesting that R is less inhibitory.

245 SLN gene normalizes SLN expression, restores SERCA function, mitigates skeletal muscle and cardiac pa

246 phospholamban, the other well studied small SERCA-regulatory proteins, oligomerize either alone or t

247 It has been proposed that SERCA forms homooligomers that increase the catalytic ra

248 zation of this isoform (zfPLN) revealed that SERCA inhibition and reversal by phosphorylation were co

249 fluorescently labeled SERCA2a revealed that SERCA readily forms homodimers.

250 The data suggest that SERCA calcium binding induces the pump to undergo a tran

251 Together, these results suggest that SERCA forms constitutive homodimers in live cells and th

252 The SERCA (sarco-endoplasmic reticulum Ca(2+) ATPase) inhibi

253 The SERCA group shows longer heart beat intervals (Mean +/-

254 nly endogenous peptide known to activate the SERCA pump by physical interaction and provides a means

255 , evoked by ER depletion, was removed by the SERCA and depended on the mitochondrial membrane potenti

256 from SERCA to PLB, thus probing directly the SERCA-PLB complex.

257 it enhances SERCA activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregu

258 etect dynamic protein interaction during the SERCA cycle.

259 presence of Ca(2+) causes uncoupling of the SERCA pump and increased heat production.

260 thermogenesis by promoting uncoupling of the SERCA pump, but the mechanistic details are unknown.

261 apsigargin, an irreversible inhibitor of the SERCA pump, exhibited anxiogenic-like behaviors and incr

262 kinetic cycle and promotes uncoupling of the SERCA pump.

263 terminant of the quaternary structure of the SERCA regulatory complex.

264 ers formed in the absence or presence of the SERCA regulatory partner, phospholamban (PLB) and were u

265 Agonist-stimulated phosphorylation of the SERCA regulatory protein phospholamban was increased in

266 iation is engaged it persists throughout the SERCA transport cycle and multiple turnover events.

267 these parts and their interactions with the SERCA environment were examined by transient kinetic ana

268 ection was abolished by cotreatment with the SERCA inhibitor cyclopiazonic acid.

269 d H(+) ions across the lipid bilayer through SERCA.

270 a(2+) to LCC density and diastolic Ca(2+) to SERCA density decreased by 16-fold and increased by 23%,

271 strated by the addition of ATP and Ca(2+) to SERCA deprived of Ca(2+) (E2) as compared with ATP to Ca

272 pump affinity for Ca(2+); 2) SLN can bind to SERCA in the presence of high Ca(2+), but PLB can only i

273 The R9C also decreased PLB binding to SERCA and altered the structure of the PLB-SERCA regulat

274 optosis and autophagy by directly binding to SERCA and causing endoplasmic reticulum (ER) stress and

275 We propose that PLB binding to SERCA populates a novel (to our knowledge) E1 intermedia

276 SLN binding to SERCA uncouples Ca(2+) transport from ATP hydrolysis.

277 ons, suggesting a similar mode of binding to SERCA.

278 We conclude that PLB binds to SERCA in two distinct structural states of the cytoplasm

279 Contrary to SERCA, ATP7B phosphoenzyme cleavage shows much lower tem

280 g a Ca(2+) spark, and this may contribute to SERCA-dependent changes in Ca(2+) wave speed.

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 (FRET) between fluorescent proteins fused to SERCA cytoplasmic domains.

284 As opposed to SERCA after Ca(2+) chelation, ATP7A/B does not undergo r

285 To better define how binding of SLN to SERCA promotes uncoupling of SERCA, we compared SLN and

286 uptake by the Ca(2+)adenosine triphosphatase SERCA.

287 c reticulum Ca(2+) adenosine triphosphatase (SERCA)2a, a critical regulator of calcium homeostasis, i

288 lized after co-reconstitution with unlabeled SERCA, reflecting their association to form the regulato

289 ariation in the ratios of X(p)/tPLB and uPLB/SERCA, suggesting that PLB phosphorylation is tuned to m

290 Using SERCA transmembrane mutants, we additionally show that P

291 vo for several weeks after knockout, whereas SERCA protein levels decrease and calcium dynamics are s

292 However, the exact mechanisms whereby SERCA inhibition induces cell death are incompletely und

293 Ca transient in the majority of cells while SERCA inhibition produced monophasic decay.

294 at during rest NCX effectively competes with SERCA for cytosolic Ca(2+) that leaks from the SR.

295 her-molecular-weight species consistent with SERCA oligomerization.

296 MLN interacts directly with SERCA and impedes Ca(2+) uptake into the SR.

297 tinct from PLB; its ability to interact with SERCA in the presence of Ca(2+) causes uncoupling of the

298 of function and persistent interaction with SERCA.

299 state; and 3) unlike PLB, SLN interacts with SERCA throughout the kinetic cycle and promotes uncoupli

300 etic peptides in phospholipid membranes with SERCA and measured calcium-dependent ATPase activity.