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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
16 TBBPA activated RyR1 and inhibited DHPR and SERCA, inducing a net efflux of Ca(2+) from loaded micro
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
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
30 co/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally elevated in the muscle of Duche
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
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.
44 Sarco(endo)plasmic reticulum Ca(2+)ATPase (SERCA) pump activity is modulated by phospholamban (PLB)
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
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
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
70 the sarco-/endoplasmic reticulum Ca-ATPase (SERCA) pump, inositol-1,4,5-triphosphate receptor (IP3R)
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
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
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
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
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
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
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
111 ent measurements, proteoliposomes containing SERCA and phospholamban or sarcolipin were adsorbed to a
113 pliced X box-binding protein 1 and decreased SERCA, which were accompanied by reduced levels of intra
115 conclude that R9C mutation of PLB decreases SERCA inhibition by decreasing the amount of the regulat
122 alizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phosp
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
130 increase in binding affinity of V49A-PLB for SERCA, and a gain of inhibitory function as quantified b
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
139 ches further established that an increase in SERCA expression also resulted in subsequent inhibition
145 the L-type Ca(2+) channels (Ca(2+) influx), SERCA pumps (sarcoplasmic reticulum (SR) Ca(2+) uptake),
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
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
154 ay crystallography has provided insight into SERCA structural substates, but it is not known how well
157 Complementary measurements with labeled SERCA showed no change in mobility after co-reconstituti
159 graphy studies have suggested that PLB locks SERCA in a low-Ca(2+)-affinity E2 state that is incompat
161 rmational equilibrium is central to maintain SERCA's apparent Ca(2+) affinity within a physiological
163 lish an inhibitory interaction with multiple SERCA conformational states with distinct effects on SER
165 ron paramagnetic resonance in the absence of SERCA but also by time-resolved fluorescence resonance e
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.
178 tions to evaluate the structural dynamics of SERCA-PLB in a solution containing 100 mM K(+) and 3 mM
180 ation of [Ca(2+)](SR), whereas inhibition of SERCA (3 muM cyclopiazonic acid) had the opposite effect
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
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
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
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,
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
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
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.
227 ge effects on PLB pentamer structure and PLB-SERCA regulatory complex conformation, increasing and de
232 ghly charged transport site, thus preserving SERCA's structural stability during active Ca(2+) transp
234 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
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
248 zation of this isoform (zfPLN) revealed that SERCA inhibition and reversal by phosphorylation were co
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
257 it enhances SERCA activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregu
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
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
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
274 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
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
291 vo for several weeks after knockout, whereas SERCA protein levels decrease and calcium dynamics are s
297 tinct from PLB; its ability to interact with SERCA in the presence of Ca(2+) causes uncoupling of the
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.
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