ライフサイエンスコーパス: Ca2 ATPase

1 r cyclopiazonic acid (an inhibitor of the SR Ca2+-ATPase).

2 nnin with the nucleotide binding site of the Ca2+ATPase.

3 ut may involve reversal or inhibition of the Ca2+ ATPase.

4 ionophore or an inhibitor of the microsomal Ca2+ ATPase.

5 imulation of the sarcoplasmic reticulum (SR) Ca2+ ATPase.

6 and inhibition of endoplasmic reticulum (ER) Ca2+ ATPase.

7 and secondarily, the sarcoplasmic reticulum Ca2+ ATPase.

8 yosin heavy chain and sarcoplasmic reticulum Ca2+ ATPase.

9 ayers, which is unchanged in the presence of Ca2+-ATPase.

10 the structures of the sarcoplasmic reticulum Ca2+-ATPase.

11 effect on Ca2+ extrusion by the plasmalemmal Ca2+-ATPase.

12 2 structure of rabbit sarcoplasmic reticulum Ca2+-ATPase.

13 ine-5'-triphosphate-driven calcium pump, the Ca2+-ATPase.

14 ional change accompanying calcium binding to Ca2+-ATPase.

15 itor of the endoplasmic reticulum-associated Ca2+-ATPase.

16 g which encodes a putative secretory pathway Ca2+-ATPase.

17 erefore represents a new and distinct P-type Ca2+-ATPase.

18 similar to the nucleotide-bound forms of the Ca2+-ATPase.

19 ractions between CaM and the plasma-membrane Ca2+-ATPase.

20 e relief of PLB inhibition of the cardiac SR Ca2+-ATPase.

21 r, phospholamban, and sarcoplasmic reticulum Ca2+-ATPase.

22 ctivation of the sarcoplasmic reticulum (SR) Ca2+/ATPase.

23 They are closely related to mammalian Ca2+-ATPases.

24 ent inhibitor of sarco/endoplasmic reticulum Ca2+-ATPases.

25 acid, an inhibitor of endoplasmic reticulum Ca2+-ATPases.

26 +-ATPases to six in H+-, Na+,K+-, Mg2+-, and Ca2+-ATPases.

27 hat encodes the sarco(endo)plasmic reticulum Ca2+-ATPase 1 (SERCA1), a Ca2+ pump found in the muscle

28 and the Golgi Ca2+-ATPase, secretory pathway Ca2+-ATPase 1, in the trans-Golgi.

29 myocyte expression of sarcoplasmic reticulum Ca2+ ATPase 2 (SERCA-2) and left ventricular SERCA-2 pro

30 or myosin 1c, myosin 7a, and plasma membrane Ca2+ ATPase 2 was studied to determine the developmental

31 ed by the human sarco(endo)plasmic reticulum Ca2+-ATPase 2 (SERCA2) isoforms, SERCA2a and SERCA2b, an

32 mobility, and trafficking of plasma membrane Ca2+ATPase-2 (PMCA2), a protein enriched in the hair cel

33 regulator of cardiac sarcoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) and is expressed abundantly in

34 Sarcoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) protein levels were increased (

35 s and the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a)/phospholamban complex contribut

36 ously that deficiency of the plasma membrane Ca2+ ATPase 4 (PMCA4) in L929 cells impaired tumor necro

37 reas Ca2+ reuptake by the sarco(endo)plasmic Ca2+ ATPase (72+/-5%) dominates in further differentiate

38 However, in the sarcoplasmic reticulum Ca2+-ATPase, a structurally characterized P-type ATPase,

39 n ER membrane marker and a typical "ER-type" Ca2+-ATPase, ACA3p/ECA1p.

40 before maximal binding of CaM to MLCK or SR Ca2+/ATPase activation occurred and binding and enzyme a

41 The Mg2+- and Ca2+-ATPase activities of CF1 respond differently in the

42 However, when Ca2+ -ATPase activity was irreversibly inhibited with th

43 a valid and reliable method for examining SR Ca2+ ATPase activity and for investigating its interacti

44 ical regulator of the sarcoplasmic reticulum Ca2+-ATPase activity and myocardial contractility.

45 myocyte hypertrophy, sarcoplasmic reticulum Ca2+-ATPase activity and uptake, and mRNA gene expressio

46 es Mg2+-ATPase activity although it inhibits Ca2+-ATPase activity can be reconciled by assuming that

47 Although basal Ca2+-ATPase activity of the full-length protein was low,

48 pholamban phosphorylation and jasmone on the Ca2+-ATPase activity paralleled their effects on Ca2+ up

49 en proposed that halothane inhibition of the Ca2+-ATPase activity results from conformational changes

50 as reduced (P=0.015), sarcoplasmic reticulum Ca2+-ATPase activity was impaired (P<0.0001), and cardia

51 sociation of the VA-impaired PMCA, while the Ca2+-ATPase activity was not recovered.

52 mban (PLB), decreased sarcoplasmic reticulum Ca2+-ATPase activity, and a decrease in L-type Ca2+ curr

53 ic approximately half-maximally inhibits the Ca2+-ATPase activity.

54 ecrease in Km(Ca) with comparable changes in Ca2+-ATPase activity.

55 horylated PLB on sarco/endoplasmic reticulum Ca2+-ATPase, Ad-PLB transduction significantly attenuate

56 of [Ca2+]i was abolished showing that the SR Ca2+-ATPase alone cannot produce decay of [Ca2+]i.

57 including the cardiac sarcoplasmic reticulum Ca2+-ATPase, alpha-ketoglutarate dehydrogenase, and the

58 up-regulation of the PMCA2bw plasma membrane Ca2+-ATPase also occurs during lactation and is more str

59 croM; an inhibitor of sarcoplasmic reticulum Ca2+-ATPase) also activated the nifedipine-sensitive sus

60 nk), a 30% decline in sarcoplasmic reticulum Ca2+-ATPase, an 80% reduction in phospholamban, and a 60

61 TG concentration required for inhibition of Ca2+ ATPase and coupled Ca2+ transport.

62 NOS1-/- had increased SR Ca2+ ATPase and decreased phospholamban protein abundanc

63 ected changes in the S3 stalk segment of the Ca2+ ATPase and found that mutation of five amino acids

64 in these failing hearts reveal that both SR Ca2+ ATPase and phospholamban are decreased on average b

65 Additionally, disruptions of a putative Ca2+-ATPase and a gene cluster encoding a putative Na+-A

66 oscopy, with helical crystals in the case of Ca2+-ATPase and as isolated tetramers in the case of rya

67 B), Ca2+-ATPases (endoplasmic reticulum-type Ca2+-ATPase and autoinhibited Ca2+-ATPase, P2A and P2B),

68 The tomato LCA1 gene encodes a Ca2+-ATPase and gives rise to two major mRNA transcripts

69 Altered sarcoplasmic reticulum (SR) Ca2+-ATPase and Na+-Ca2+ exchange (NCX) function have be

70 rus cell expression system for investigating Ca2+-ATPase and phospholamban regulatory interactions wa

71 downregulated, whereas Ca2+-uptake proteins (Ca2+-ATPase and phospholamban) were unchanged or slightl

72 eduction in both sarco/endoplasmic reticulum Ca2+-ATPase and skeletal muscle ryanodine receptor prote

73 tion transport by the sarcoplasmic reticulum Ca2+-ATPase and the Na+, K+-ATPase of animal cells.

74 eversible inhibitory interaction between the Ca2+-ATPase and the small transmembrane protein phosphol

75 ich inhibits endoplasmic reticulum-dependent Ca2+-ATPase and thereby increases cytosolic Ca2+, to ind

76 ong connection with nucleotide activation of Ca2+ATPase and phospholamban inhibition has been found.

77 on forward flux and backflux through the SR Ca2+ ATPase) and (2) diastolic SR Ca2+ leak (ryanodine r

78 phosphorylation, sarco/endoplasmic reticulum Ca2+ -ATPase, and cAMP-responsive element binding activi

79 ssion of Ca2+ cycling proteins (increased SR Ca2+-ATPase, and depressed phosphorylated phospholamban)

80 ve impact of alterations in SR Ca2+ leak, SR Ca2+-ATPase, and Na+-Ca2+ exchange on SR Ca2+ load in HF

81 rize CG2165, which encodes a plasma membrane Ca2+-ATPase, and show that it plays an important role in

82 , cytosolic diffusion, resequestration by SR Ca2+-ATPases, and the association and dissociation of Ca

83 Plasma membrane Ca2+ ATPases are P-type pumps important for intracellula

84 ects on the kinetics of fast skeletal muscle Ca2+-ATPase are largely known.

85 The SR Ca2+ ATPase assay was run for various time periods and u

86 uggest that the sarco-/endoplasmic reticular Ca2+ ATPases associated with the KCl-/caffeine- and carb

87 Structures of Ca2+-ATPase at 8-A resolution reveal the packing of tran

88 mutations in the endoplasmic reticulum (ER) Ca2+ ATPase ATP2A2 (protein SERCA2).

89 kin disease, resulting from mutations in the Ca2+ ATPase ATP2C1, which controls Ca2+ concentrations i

90 ring skin disease caused by mutations in the Ca2+ ATPase ATP2C1.

91 ing skin disease caused by a mutation in the Ca2+-ATPase ATP2C1 (protein SPCA1), responsible for cont

92 is most similar to a "plasma membrane-type" Ca2+-ATPase, but is smaller (110 kDa), contains a unique

93 These data show that, although the SR Ca2+-ATPase contributes to the decay of [Ca2+]i, it cann

94 suggest that this endoplasmic reticulum-type Ca2+-ATPase could support cell growth in plants as in ye

95 d bityrosine accounts for the intermolecular Ca2+-ATPase cross-links, as well as intramolecular cross

96 wild-type, pentameric phospholamban with the Ca2+-ATPase decreased the apparent affinity of the ATPas

97 ete densities that most likely correspond to Ca2+-ATPase dimers, unlike previous maps of untilted cry

98 hibition of the sarco(endo)plasmic reticulum Ca2+-ATPase, disruption of mitochondrial Ca2+ uptake, or

99 s, ACA2 encodes a novel calmodulin-regulated Ca2+-ATPase distinguished by a unique N-terminal regulat

100 ansients and that the thapsigargin-sensitive Ca2+ ATPases do not contribute significantly to the rise

101 reticulum is the ryanodine receptor, whereas Ca2+-ATPase effects reuptake in an ATP-dependent manner.

102 f P-type ATPases: heavy-metal ATPases (P1B), Ca2+-ATPases (endoplasmic reticulum-type Ca2+-ATPase and

103 rteries, I-1 and sarco/endoplasmic reticulum Ca2+ -ATPase expression is specific to contractile vascu

104 stolic SR Ca2+ leak (via sparks), reduced SR Ca2+-ATPase expression, and increased Na+-Ca2+ exchanger

105 However, the apparent affinity of the SR Ca2+-ATPase for Ca2+ remains unchanged in transgenic hea

106 bsence and presence of the SERCA1 isoform of Ca2+-ATPase for structural investigation by cross-polari

107 on to the study of rat brain microsomal Mg2+/Ca2+ ATPase from a membrane fraction.

108 +, we isolated a full-length cDNA encoding a Ca2+-ATPase from a model plant, Arabidopsis, and named i

109 Sarco-endoplasmic reticulum Ca2+-ATPase from fast skeletal (SERCA1) or cardiac muscl

110 ently been solved at 8 A resolution for both Ca2+-ATPase from rabbit sarcoplasmic reticulum and H+-AT

111 this method to thin, monoclinic crystals of Ca2+-ATPase from sarcoplasmic reticulum, thus characteri

112 Both compounds appear to relieve the Ca2+ATPase from phospholamban inhibition, thereby increa

113 gesting that the sarcoplasmic reticulum (SR) Ca2+-ATPase function is not altered by overexpression of

114 Sacro (endo)plasmic reticulum Ca2+-ATPase function was evaluated by 45Ca uptake.

115 Model estimates of average SR Ca2+ ATPase functional downregulation obtained using the

116 thapsigargin, an inhibitor of the microsomal Ca2+ATPase, gave a similar result.

117 ce transporter gene (pfcrt) and P falciparum Ca2+ ATPase gene (pfATP6) were assessed by PCR-restricti

118 diac/slow twitch sarcoplasmic reticulum (SR) Ca2+-ATPase gene (SERCA2 ) encodes a calcium transport p

119 ory effect of mutations in secretory pathway Ca2+-ATPase genes on the secretion of rice alpha-amylase

120 bic inhibitor of endoplasmic reticulum (ER) (Ca2+)-ATPase, greatly reduced cell growth in the capsula

121 the Na+/Ca2+exchanger or the plasma membrane Ca2+ ATPase had no influence on the ability of NO to dec

122 These results suggest that Ca2+-ATPase has a long-range effect on the structure of

123 iazonic acid (CPA), a nanomolar inhibitor of Ca2+-ATPase, has a pentacyclic indole tetramic acid scaf

124 gene encoding an endoplasmic reticulum-type Ca2+-ATPase homolog in the yeast (Saccharomyces cerevisi

125 responding to the following sequences of the Ca2+-ATPase: (i) Glu121 to Lys128, (ii) His190 to Lys218

126 lar modeling studies of 2-APB binding to the Ca2+ ATPase identified two potential binding sites close

127 pregulation and downregulation of NCX and SR Ca2+ ATPase in heart failure using data obtained from 2

128 k was to investigate the role of sarcolemmal Ca2+-ATPase in rat ventricular myocytes.

129 nstrate the role of a carboxyeosin-sensitive Ca2+-ATPase in the control of resting [Ca2+]i and the re

130 We have investigated the roles of the store Ca2+-ATPases in regulating both the upstroke and downstr

131 rom rat and other organisms, we suggest that Ca2+-ATPases in the Golgi will form a discrete subgroup

132 Ca2+-ATPase inactivation can occur through SERCA2a nitra

133 of animal sarcoplasmic/endoplasmic reticulum Ca2+-ATPase, inhibited Ca2+ transport (50% inhibition do

134 ning increase was blocked by the sarcolemmal Ca2+ ATPase inhibitor carboxyeosin.

135 to ER stress induced by thapsigargin, an ER Ca2+ ATPase inhibitor, the response of ATF6 was markedly

136 observed if the sarco/endoplasmic reticulum Ca2+-ATPase inhibitor cyclopiazonic acid (30 mum) was al

137 increased whole-cell currents evoked by the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA) by about

138 The endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin (100 nM) caused a tra

139 n in WEHI7.2 lymphoma cells treated with the Ca2+-ATPase inhibitor thapsigargin (TG) but does not pre

140 The SR Ca2+-ATPase inhibitor thapsigargin abolished the phasic

141 ar Ca2+ concentration and treatment with the Ca2+-ATPase inhibitor thapsigargin or the muscarinic rec

142 is increased in dose-dependent manner by the Ca2+-ATPase inhibitor thapsigargin, a treatment that doe

143 of a sarcoplasmic-endoplasmic reticulum (ER) Ca2+-ATPase inhibitor thapsigargin.

144 ot significantly affected by thapsigargin, a Ca2+-ATPase inhibitor that depletes intracellular Ca2+ s

145 CIF was extracted with thapsigargin, a Ca2+-ATPase inhibitor, from isolated neutrophils and CIF

146 icroM), a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase inhibitor, rescued the surface expression of

147 on of [Ca2+](i) by the endoplasmic reticulum Ca2+-ATPase inhibitor, thapsigargin, was abolished 15 mi

148 sphate via the patch pipette, or through the Ca2+ATPase inhibitor thapsigargin.

149 the endoplasmic reticulum Ca2+ release with Ca2+-ATPase inhibitors cyclopiazonic acid (5 microM) or

150 Other sarcoplasmic/endoplasmic reticulum Ca2+-ATPase inhibitors did not rescue G601S or F805C.

151 uptake of Ca2+ by the sarcoplasmic reticulum Ca2+-ATPase into a ryanodine-sensitive store limits the

152 Although the inhibition of Ca2+-ATPase involves PLN monomers, in a lipid bilayer me

153 gen phosphorylase and sarcoplasmic reticular Ca2+ ATPase is examined.

154 -M3 (stalk and membrane-bound) region of the Ca2+ ATPase is involved in TG binding.

155 The Ca2+-ATPase is also more potently inhibited at lower pH

156 ld by increasing concentrations of LDAO, the Ca2+-ATPase is inhibited in a biphasic manner by increas

157 The activity of the SR Ca2+-ATPase is not only dependent on the energy state of

158 e data suggest that nucleotide activation of Ca2+ATPase is functionally coupled to the phospholamban

159 he calcium pump from sarcoplasmic reticulum (Ca2+-ATPase) is typical of the large family of P-type ca

160 We investigated how loss of plasma membrane Ca2+ ATPase isoform 2 (PMCA2), the calcium transporter i

161 Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase isoform 2 (SERCA2) is an intracellular Ca2+

162 Sarco(endo)plasmic reticulum Ca2+ ATPase isoform 3 (SERCA3) is one of two Ca2+ pumps

163 monstrated that sarco(endo)plasmic reticulum Ca2+-ATPase isoform (SERCA2a) mRNA levels were increased

164 eading to the degradation of plasma membrane Ca2+-ATPase isoform 1 and fodrin; the degradation is att

165 Plasma membrane Ca2+-ATPase isoform 2 (PMCA2) exhibits a highly restrict

166 The sarco(endo)plasmic reticulum Ca2+-ATPase isoform 2 (SERCA2) gene encodes both SERCA2a

167 gene, encoding sarco(endo)plasmic reticulum Ca2+-ATPase isoform 2 (SERCA2), leads to squamous cell t

168 sory neurons mediated by the plasma membrane Ca2+-ATPase isoform 4 (PMCA4).

169 r localization of isoform ACA2p (Arabidopsis Ca2+-ATPase, isoform 2 protein) in Arabidopsis.

170 Arabidopsis, and named it ACA2 (Arabidopsis Ca2+-ATPase, isoform 2).

171 by increasing the calcium sensitivity of the Ca2+ATPase like that observed with phosphorylation of ph

172 phosphorylase and the sarcoplasmic reticular Ca2+ ATPase may couple to form a three-enzyme complex.

173 These steps in the catalytic cycle of the Ca2+-ATPase may contribute to or account for phospholamb

174 lated pumps in animals, plasma membrane-type Ca2+-ATPases, members of this new subfamily are distingu

175 ype 2 deiodinase, sarcoendoplasmic reticulum Ca2+-ATPase, mitochondrial glycerol 3-phosphate dehydrog

176 s include Ca2+ extrusion via plasma membrane Ca2+-ATPase, mitochondrial uptake, myoplasmic Ca2+-bindi

177 Sarcoplasmic reticulum Ca2+-ATPase mRNA levels were depressed in male LVH but n

178 Clearly, this portion of Ca2+ATPase needs further study to elucidate its role in

179 een determined, although a 14-A structure of Ca2+-ATPase, obtained by electron microscopy of frozen-h

180 ibitor (maximal inhibition is 85-90%) of the Ca2+-ATPase of CF1 activated by heat, dithiothreitol, or

181 ve examined the oxidative sensitivity of the Ca2+-ATPase of skeletal muscle sarcoplasmic reticulum (S

182 nd exhibits 34 to 38% identity with vacuolar Ca2+-ATPases of Saccharomyces cerevisiae and Dictyosteli

183 phospholamban, PLB(1-20), interacts with the Ca2+ATPase of the sarcoplasmic reticulum, SERCA1a, docki

184 inhibitor of the sarcoplasmic reticulum (SR) Ca2+-ATPase on excitation-contraction (EC) coupling in g

185 eceptors, calsequestrin, junctin, triadin 1, Ca2+-ATPase, or phospholamban.

186 yosin heavy chain and sarcoplasmic reticulum Ca2+-ATPase (P>0.1).

187 reticulum-type Ca2+-ATPase and autoinhibited Ca2+-ATPase, P2A and P2B), H+-ATPases (autoinhibited H+-

188 there were increases in protein levels of SR Ca2+-ATPase, phospholamban, and calreticulin and decreas

189 ble to Ca2+ extrusion by the plasma membrane Ca2+ ATPase (PMCA).

190 The relative importance of plasma membrane Ca2+-ATPase (PMCA) 1 and PMCA4 was assessed in mice carr

191 d the potential roles of the plasma membrane Ca2+-ATPase (PMCA) at the blood-CSF and blood-brain barr

192 contrast, inhibition of the plasma membrane Ca2+-ATPase (PMCA) by increasing the pH slowed the decay

193 Cardiomyocyte plasma membrane Ca2+-ATPase (PMCA) extrudes Ca2+ but has little effect o

194 an (Trp) fluorescence of the plasma membrane Ca2+-ATPase (PMCA) is significantly quenched by halothan

195 xpression of TRPV6/ECaC2 and plasma membrane Ca2+-ATPase (PMCA) isoforms 1 and 4 were unaltered.

196 localized and quantified the plasma membrane Ca2+-ATPase (PMCA) of the bundle.

197 enzyme belongs to a group of plasma membrane Ca2+-ATPase (PMCA) that lack a calmodulin-binding domain

198 abolism in the platelet, the plasma membrane Ca2+-ATPase (PMCA) was assessed for cAMP-dependent and t

199 ns whereas inhibition of the plasma membrane Ca2+-ATPase (PMCA) with La3+ had little effect.

200 interaction of CaM with the plasma membrane Ca2+-ATPase (PMCA), a Ca2+ pump regulated by binding of

201 n near the C-terminus of the plasma membrane Ca2+-ATPase (PMCA), causing the release of this domain a

202 le anesthetics (VAs) and the plasma membrane Ca2+-ATPase (PMCA).

203 Isoform 2 of the plasma-membrane Ca2+-ATPase (PMCA2), required for hearing and balance, i

204 resence of inhibitors of the plasma membrane Ca2+ ATPases (PMCAs) and mitochondrial Ca2+ sequestratio

205 sarcoplasmic reticulum, the plasma membrane Ca2+-ATPases (PMCAs), which extrude Ca2+ from the cell,

206 ined the contribution of the Golgi-localized Ca2+ ATPase Pmr1p in the maintenance of cellular Ca2+ ho

207 ivity correlating with the loss of monomeric Ca2+-ATPase polypeptides, and the concomitant appearance

208 2-to-E1 conformational change postulated for Ca2+-ATPase probably applies to Na+,K+-ATPase as well as

209 e cardiac sarcoplasmic/endoplasmic reticulum Ca2+ ATPase pump (SERCA2a) has the potential to open a n

210 We inquired whether sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2a) overexpression could reduce i

211 sociated with a lower sarcoplasmic reticulum Ca2+ ATPase pump to phospholamban protein ratio in SAN t

212 inhibitor of the sarco/endoplasmic reticulum Ca2+ ATPase pump.

213 coding the canine cardiac sarco(endo)plasmic Ca2+-ATPase pump (SERCA2a) was cloned for the first time

214 e known to be associated with a reduction in Ca2+-ATPase pump levels of the sarcoplasmic reticulum (S

215 2 gene, encoding sarco/endoplasmic reticulum Ca2+-ATPase pump type 2b isoform (SERCA2b).

216 ion factor 1 and sarco-endoplasmic reticulum Ca2+ ATPase, respectively, result in persistent (>4 hr)

217 confirming the presence of a third class of Ca2+-ATPase (secretory pathway Ca2+-ATPase, SPCA).

218 C gamma1, IP3 receptor (IP3R), and the Golgi Ca2+-ATPase, secretory pathway Ca2+-ATPase 1, in the tra

219 This suggests that the SR Ca2+-ATPase sequesters a significant amount of Ca2+ into

220 port function and enzymatic properties of SR Ca2+ ATPase (SERCA) in individual mouse hearts.

221 The sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) is specifically inhibited by thapsig

222 ted muscle, the sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA) plays an important role in terminati

223 protein levels of the sarcoplasmic reticulum Ca2+ ATPase (SERCA) regulatory protein sarcolipin, which

224 activity of the sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA).

225 ion behavior to the crystal structure of the Ca2+ ATPase (SERCA).

226 oding the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA)2 has been identified as the defectiv

227 Expression of sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA)2 small interfering RNA (siRNA) in Ha

228 a dynamic membrane protein complex formed by Ca2+-ATPase (SERCA) and phospholamban (PLN), which in hu

229 an inhibitor of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ pumps, and additionally increas

230 X) activity (with only modest decrease in SR Ca2+-ATPase (SERCA) function), similar to many end-stage

231 in (alphaMHC) and the sarcoplasmic reticulum Ca2+-ATPase (SERCA) genes was repressed.

232 The sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor cyclopiazonic acid (CPA) d

233 ene encodes the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) isoform 2 pump, which transports Ca2

234 smic reticulum (SR) Ca2+ by inhibition of SR Ca2+-ATPase (SERCA) led to sustained elevation of [Ca2+]

235 ialysis with the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump blocker thapsigargin was able t

236 Treatment with sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump blockers dramatically altered t

237 holamban (PLB) or the sarcoplasmic reticulum Ca2+-ATPase (SERCA) were fused to cyan fluorescent prote

238 bition of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) with 30 micromol/L 2,5-di-(tert-buty

239 single-pass membrane proteins that regulate Ca2+-ATPase (SERCA), an ATP-driven pump that translocate

240 However, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA)-2 mRNA levels were reduced within 4

241 ession of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA)-2a and alpha-myosin heavy chain were

242 ere we show that sarco-endoplasmic reticulum Ca2+-ATPase (SERCA)-mediated Ca2+ uptake into intracellu

243 es a sarcoplasmic/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA)-type calcium pump.

244 mpair the function of sarcoplasmic reticulum Ca2+-ATPase (SERCA).

245 inhibitor of the sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA).

246 nhibitor of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA).

247 d isoforms of the sarcoendoplasmic reticulum Ca2+-ATPase (SERCA)2 gene display differential Ca2+ wave

248 , an inhibitor of sarcoendoplasmic reticulum Ca2+-ATPases (SERCA), caused a time- and concentration-d

249 Protection of the Ca2+ATPase (SERCA) from proteinase K digestion has been

250 Ca2+ affinity of sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2).

251 onship, and decreased sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) activity.

252 wall demonstrate that sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) expression was significantly less

253 of a muscle-specific sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) inhibitor, phospholamban, rescued

254 Ca(2+) handling, the sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), induces functional improvement in

255 ing proteins, such as sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), located in the sarcoplasmic retic

256 s the activity of the sarcoplasmic reticulum Ca2+ ATPase (SERCA2a).

257 Reduced sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a isoform) activity is a major determ

258 d with diminished sarcoendoplasmic reticular Ca2+-ATPase (SERCA2a) activity, findings in insulin-resi

259 orylation (P < 0.04), sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) affinity for calcium (P < 0.015),

260 he relative amount of sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) and its crucial inhibitor phosphol

261 ion of cardiac muscle sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) by beta1-agonists involves cAMP- a

262 an tissues: the sarco(endo)plasmic reticulum Ca2+-ATPases (SERCAs), which sequester Ca2+ within the e

263 Activity studies performed using mutant Ca2+-ATPases show that Tyr837 is critical for the inhibi

264 the cell, and the putative secretory pathway Ca2+-ATPase (SPCA), the function of which is poorly unde

265 hird class of Ca2+-ATPase (secretory pathway Ca2+-ATPase, SPCA).

266 heart, we have overexpressed the cardiac SR Ca2+-ATPase specifically in the mouse heart using the al

267 Ca2+-ATPase specifically maintains the low cytoplasmic c

268 I-1 and sarco/endoplasmic reticulum Ca2+ -ATPase synergistically induce the vascular smooth

269 tagonist of the sarco(endo)plasmic reticulum Ca2+ ATPase (thapsigargin), or by ryanodine.

270 is an inhibitor of the endoplasmic reticulum Ca2+-ATPase that induces caspase 3 activation and apopto

271 no effect), activation of a plasma membrane Ca2+-ATPase (two inhibitors, vanadate (30 mM) and lantha

272 hich encodes the sarco/endoplasmic reticulum Ca2(+)-ATPase type 2 isoform (SERCA2) and is highly expr

273 ort that the gene encoding a plasma membrane Ca2+-ATPase type 2 pump (Atp2b2, also known as Pmca2) is

274 the assay, we were able to confirm that the Ca2+ ATPase uses ATP that is synthesized locally from PC

275 l (SR Ca2+ gradient) is maintained by the SR Ca2+-ATPase using the free energy available from hydroly

276 Sarcoplasmic reticulum (SR) Ca2+ ATPase was derivatized with 4,4'-diisothiocyanatost

277 lial expression of the endoplasmic reticulum Ca2+ ATPase was not altered in fistulas compared with sh

278 The gene encoding an organelle-type Ca2+-ATPase was cloned and sequenced and found overexpre

279 A unique subfamily of calmodulin-dependent Ca2+-ATPases was recently identified in plants.

280 Stimulation of Ca2+ATPase was followed by pronounced inhibiton at only

281 Maximal stimulation of Ca2+ATPase was identical to that observed with the anti-

282 lice variant of the sarcoplasmic-endoplasmic Ca2+ ATPase, was found mostly in photoreceptors, whereas

283 uptake by cardiac SR vesicles, catalyzed by Ca2+-ATPase, was inhibited by NO. produced endogenously

284 solution X-ray structures determined for the Ca2+-ATPase, we have generated two homology models of th

285 these two structures, atomic coordinates for Ca2+-ATPase were fit to Na+,K+-ATPase, and several flexi

286 r, if the sarcolemmal Na+-Ca2+ exchanger and Ca2+-ATPase were inhibited then recovery of [Ca2+]i was

287 when the Na+-Ca2+ exchanger and sarcolemmal Ca2+-ATPase were inhibited.

288 red expression of the sarcoplasmic reticulum Ca2+-ATPase, when interpreted through the use of a compu

289 ty of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase, which allows the SR Ca2+ gradient to move c

290 nsistent with the observation that the SPCA1 Ca2+-ATPase, which is expressed in the Golgi, is induced

291 by inhibiting the sarcoendoplasmic reticulum Ca2+-ATPase, which subsequently reduced the effect of ac

292 ovel biological role for the plasma membrane Ca2+-ATPases, which are generally regarded as premier re

293 Ca2+ removal was confirmed by inhibiting SR Ca2+ ATPase with cyclopiazonic acid, which slowed Ca2+ r

294 ors and inhibition of endoplasmic reticulum (Ca2+)ATPase with thapsigargin.

295 nhibition of the sarcoplasmic reticulum (SR) Ca2+-ATPase with cyclopiazonic acid (CPA).

296 Inhibition of the SR Ca2+-ATPase with thapsigargin abolished the oscillations

297 hibition of the oocyte endoplasmic reticular Ca2+-ATPase with thapsigargin produced a transient incre

298 r, depletion of SR Ca2+ by inhibiting the SR Ca2+-ATPase (with cyclopiazonic acid (CPA), 20 microM) r

299 holamban decreases the number of activatable Ca2+ATPase without affecting substrate affinity or the a

300 Ca2+/H+ exchange mediated by plasma-membrane Ca2+-ATPase would rapidly acidify mechanically sensitive