ライフサイエンスコーパス: PMCA

1 PMCA internalization is representative of endocytosis of

2 PMCA involves incubating materials containing minute amo

3 PMCA is able to detect the equivalent of a single molecu

4 PMCA results from hamster and CWD agent-infected elk pri

5 PMCA using normal Tg(cerPrP)1536 brains as the PrP(C) su

6 PMCA-generated samples caused the same clinical disease

7 PMCAs comprise four isoforms and over 20 splice variants

8 We show that 140 PMCA cycles leads to a 6,600-fold increase in sensitivit

9 n large variation in plasma membrane Ca(2+) (PMCA) pump activity was correlated with RBC age.

10 d in the C-terminal segment and results in a PMCA of high maximal velocity of transport and high affi

11 e found that intracellular introduction of a PMCA pump inhibitor (carboxyeosin) allows for the induct

12 Since its invention 10 years ago, PMCA has helped to answer fundamental questions about th

13 med protein misfolding cyclic amplification (PMCA) and prion-infected cell lines.

14 ped protein misfolding cyclic amplification (PMCA) and scrapie cell assay (SCA) techniques to study t

15 the protein misfolding cyclic amplification (PMCA) assay for highly efficient detection of CWD prions

16 ing protein misfolding cyclic amplification (PMCA) confirmed a reduction of 2 log10 in PrP(263K) and

17 by protein misfolding cyclic amplification (PMCA) in a strain-specific fashion.

18 hat protein misfolding cyclic amplification (PMCA) of DY and HY TME maintains the strain-specific pro

19 ive protein misfolding cyclic amplification (PMCA) protocol to evaluate replication efficiency of soi

20 g a protein misfolding cyclic amplification (PMCA) reaction, infectivity and disease-associated prote

21 eed protein misfolding cyclic amplification (PMCA) reactions, enabling the rapid concentration of dil

22 the protein misfolding cyclic amplification (PMCA) technique can be used to form infectious prion mol

23 the protein misfolding cyclic amplification (PMCA) technique to amplify minute quantities of PrP(Sc),

24 the protein misfolding cyclic amplification (PMCA) technique with a preparation containing only nativ

25 the protein misfolding cyclic amplification (PMCA) technique, used for fast amplification of prion pr

26 the protein misfolding cyclic amplification (PMCA) technique, we were able to overcome the species ba

27 the protein misfolding cyclic amplification (PMCA) technology can be automated and optimized for high

28 the protein misfolding cyclic amplification (PMCA) technology to sustain the autocatalytic replicatio

29 by protein misfolding cyclic amplification (PMCA) technology.

30 and protein-misfolding cyclic amplification (PMCA) to amplify PrP(CWD) in vitro.

31 ro, protein misfolding cyclic amplification (PMCA) uses PrP(Sc) in prion-infected brain homogenates a

32 ing protein misfolding cyclic amplification (PMCA) with Teflon beads.

33 ay, protein misfolding cyclic amplification (PMCA), by using experimental scrapie and human prion str

34 Protein misfolding cyclic amplification (PMCA), described in detail in this protocol, is a simple

35 of protein misfolding cyclic amplification (PMCA), the topic of faithful propagation of prion strain

36 ing protein misfolding cyclic amplification (PMCA), we now report that the recombinant full-length hu

37 on, protein misfolding cyclic amplification (PMCA), which mimics PrP(C)-to-PrP(Sc) conversion with ac

38 ted protein misfolding cyclic amplification (PMCA)-competent prions within the female reproductive tr

39 hat protein misfolding cyclic amplification (PMCA)-generated hypertransmissible mink encephalopathy (

40 as protein misfolding cyclic amplification (PMCA)-which are based on sonication, the RT-QuIC techniq

41 by protein misfolding cyclic amplification (PMCA).

42 rPSc using cyclical sonicated amplification (PMCA) reactions and brain homogenate as a source of PrP-

43 prior chemotherapy treatment (P = .001), and PMCA histopathologic subtype (P < .001) were independent

44 were compared to those of brain-derived and PMCA material generated in the presence of RNA.

45 y eliminating the Na(+)/Ca(2+) exchanger and PMCA.

46 duces the association between GPER/GPR30 and PMCA.

47 influx was dominated by the mitochondria and PMCA, with no contribution from the Na(+)/Ca(2+) exchang

48 onal interaction between actin oligomers and PMCA represents a novel regulatory pathway by which the

49 the ubiquitous expression of both STIM1 and PMCA, these findings have wide-ranging implications for

50 f stromal interacting molecule 1 (STIM1) and PMCA-mediated Ca(2+) clearance.

51 d plasma membrane Ca(2+) ATPases (SERCAs and PMCAs, respectively), Na/K-ATPase, as well as to the nuc

52 nce in mouse parotid acinar cells and apical PMCA activity in Par-C10 cells.

53 howed Cas-PMCA clusters with other arthropod PMCA proteins.

54 [Ca(2+)]i clearance assay was used to assess PMCA activity.

55 lation of the plasma membrane Ca(2+) ATPase (PMCA) by tyrosine kinases.

56 The plasma membrane Ca(2+) ATPase (PMCA) has previously been identified as a critical playe

57 The plasma membrane Ca(2+) ATPase (PMCA) is completely internalized during maturation, and

58 ATP-dependent plasma membrane Ca(2+) ATPase (PMCA) is critical for maintaining low [Ca(2+)]i and thus

59 rm 4b of the plasma membrane Ca(2+) -ATPase (PMCA) pump is represented by peptide C28.

60 pended on the plasma membrane Ca(2+)-ATPase (PMCA) and mitochondria that accounted for approximately

61 usion via the plasma membrane Ca(2+)-ATPase (PMCA) and Na(+)/Ca(2+) exchanger, to the clearance of vo

62 CaM with the plasma membrane Ca(2+)-ATPase (PMCA) and other target proteins to downregulate cellular

63 he ATP-driven plasma membrane Ca(2+)-ATPase (PMCA) important for maintaining low resting [Ca(2+)]i.

64 horylates the plasma membrane Ca(2+)-ATPase (PMCA) in a Ca(2+)-dependent manner in parotid acinar cel

65 The plasma membrane Ca(2+)-ATPase (PMCA) is essential for removal of cytoplasmic Ca(2+) and

66 The plasma membrane Ca(2+)-ATPase (PMCA) is found near postsynaptic NMDARs.

67 yT2, neuronal plasma membrane Ca(2+)-ATPase (PMCA) isoforms 2 and 3, and Na(+)/Ca(2+)-exchanger 1 (NC

68 the two main plasma membrane Ca(2+)-ATPase (PMCA) isoforms in the cortex of the rat cerebellum.

69 Plasma membrane Ca(2+)-ATPase (PMCA) protein expression was confirmed in vitro in all c

70 The plasma membrane Ca(2+)-ATPase (PMCA) provides a final common path for cells to "defend"

71 domain of the plasma membrane Ca(2+)-ATPase (PMCA) pump isoform 4b.

72 or alpha, the plasma membrane Ca(2+)-ATPase (PMCA), and endothelial nitric-oxide synthase (eNOS).

73 animal cells: plasma membrane Ca(2+)-ATPase (PMCA), sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase

74 bilization of the plasma membrane Ca-ATPase (PMCA) in an inactive conformation upon oxidation of mult

75 brane Ca(2+) pump plasma membrane Ca-ATPase (PMCA), and the ER Ca(2+) pump sarco/ER Ca(2+)-ATPase (SE

76 xtrusion by the plasma membrane Ca2+ ATPase (PMCA).

77 hibition of the plasma membrane Ca2+-ATPase (PMCA) by increasing the pH slowed the decay of the Ca2+

78 Cardiomyocyte plasma membrane Ca2+-ATPase (PMCA) extrudes Ca2+ but has little effect on excitation-

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

80 s to a group of plasma membrane Ca2+-ATPase (PMCA) that lack a calmodulin-binding domain and have vac

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

82 terminus of the plasma membrane Ca2+-ATPase (PMCA), causing the release of this domain and relief of

83 y our group, plasma membrane calcium ATPase (PMCA) activity can be regulated by the actin cytoskeleto

84 e ubiquitous plasma membrane calcium ATPase (PMCA) has not been measured in any neurone.

85 ation of the plasma membrane calcium ATPase (PMCA).

86 membrane Ca(2+)/calmodulin-dependent ATPase (PMCA), and that its deletion leads to abnormal dystrophi

87 The plasma membrane Ca(2+)-ATPases (PMCA) represent the major high-affinity Ca(2+) extrusion

88 M)-activated plasma membrane Ca(2+) ATPases (PMCAs) that extrude Ca(2+) from the cell, play a key rol

89 Plasma membrane Ca(2+) ATPases (PMCAs), the Ca(2+) extrusion pumps, interact with an Mpp

90 Plasma membrane calcium ATPases (PMCAs) actively extrude Ca(2+) from the cell and are ess

91 ps includes plasma membrane calcium ATPases (PMCAs).

92 bundance of plasma membrane calcium ATPases (PMCAs).

93 e plasma membrane calcium-dependent ATPases (PMCAs) play an essential role in controlling intracellul

94 of Cas-PMCA is as expected for an authentic PMCA protein.

95 ntains all signature domains of an authentic PMCA, including ten transmembrane domains and a calmodul

96 bility state was attributed to autoinhibited PMCA-CaM complexes with a nondissociated autoinhibitory

97 ctionally isolate the apical and basolateral PMCA activity by applying La(3+) to the opposite side to

98 We found an inverse correlation between PMCA strength and Hb A1c content, indicating that PMCA a

99 e for a novel functional interaction between PMCA and calcineurin, suggesting a role for PMCA as a ne

100 We demonstrate a novel interaction between PMCA and the calcium/calmodulin-dependent phosphatase, c

101 lations analysis of the interactions between PMCA and the phospholipid bilayer in which it is embedde

102 This was confirmed by PMCA detection of HY PrP(Sc) in animals where DY TME had

103 trate alpha-synuclein aggregate formation by PMCA, and the strain imprint of the alpha-synuclein fibr

104 rain modifications of 263K prions induced by PMCA seem to have been partially reversed when PMCA prod

105 alpha-synuclein fibril formation induced by PMCA.

106 e biological properties of RML propagated by PMCA under RNA-depleted conditions were compared to thos

107 E2 increases CaM-PMCA association, but the expected stimulation of Ca(2+)

108 < .001), peritoneal mucinous carcinomatosis (PMCA) histopathologic subtype (P < .001), major postoper

109 e PCR revealed stage-specific changes in Cas-PMCA abundance during the molting cycle, with peak expre

110 The predicted membrane topography of Cas-PMCA is as expected for an authentic PMCA protein.

111 g frame encoding a 1170-residue protein (Cas-PMCA).

112 A proteins from different species showed Cas-PMCA clusters with other arthropod PMCA proteins.

113 tern consistent with the hypothesis that Cas-PMCA functions to maintain cellular Ca(2+) homeostasis i

114 ssment of tissue distribution showed the Cas-PMCA transcript to be broadly distributed in both neural

115 Compared to control PMCA conducted without plasminogen, addition of plasmino

116 However, we observed decreased PMCA expression in cancer cells compared with fibroblast

117 lial cells, GPER/GPR30 agonist G-1 decreases PMCA-mediated Ca(2+) extrusion by promoting PMCA tyrosin

118 GPER/GPR30 overexpression decreases PMCA activity, and G-1 further potentiates this effect.

119 c inhibition induced profound ATP depletion, PMCA inhibition, [Ca(2+)]i overload, and cell death in P

120 t functional properties may permit different PMCA splice variants to accommodate different kinds of l

121 The role of these different PMCA isoforms in the control of calcium-regulated cell d

122 During PMCA, labeled nucleic acids form nuclease-resistant comp

123 strain characteristics are preserved during PMCA when parent seeds are amplified in PrP(C) substrate

124 over, the striking distribution of inner-ear PMCA isoforms dictated by selective targeting suggests a

125 CaM binds to either PMCA or C28 by a mechanism in which the primary anchor r

126 ostasis through downregulation of endogenous PMCA.

127 We show that endogenous PMCA and NCX activities are necessary for GlyT2 activity

128 traffics in a similar fashion to endogenous PMCA.

129 -localizes with PMCA4b, the main endothelial PMCA isoform.

130 Enhanced proteolysis was observed for PMCA upon binding CaM or ATP.

131 dies define the mechanistic requirements for PMCA internalization during oocyte maturation.

132 PMCA and calcineurin, suggesting a role for PMCA as a negative modulator of calcineurin-mediated sig

133 Under sonication conditions used for PMCA, large RNA molecules were found to degrade into sma

134 There are four PMCA isoforms (PMCA1-4), and alternative splicing of the

135 uring oocyte maturation is required for full PMCA internalization.

136 of the extreme C-terminal segment of the h4 PMCA is disturbed by changes of negatively charged resid

137 fusion of GFP to the C terminus of the h4xb PMCA causes partial loss of autoinhibition by specifical

138 of the molecule brought the Vmax of the h4xb PMCA to near that of the calmodulin-activated enzyme wit

139 autoinhibitory sequence, which in the human PMCA is located in the C-terminal segment and results in

140 Collectively, this work identifies PMCA and mitochondria as the major regulators of presyna

141 PrP conversion in PMCA was substantially less efficient with plasminogen-d

142 oil yielded a greater-than-1-log decrease in PMCA replication efficiency with a corresponding 1.3-log

143 il over time corresponded with a decrease in PMCA replication efficiency.

144 a substantial portion of PrPres generated in PMCA might be noninfectious.

145 res (specific infectivity) was much lower in PMCA versus brain-derived samples, suggesting the possib

146 Furthermore, as observed in PMCA, plasminogen and kringles promoted PrP(Sc) propagat

147 nstrated that the presence of plasminogen in PMCA enhanced the PrP(Sc) production rate to approximate

148 hout plasminogen, addition of plasminogen in PMCA using wild-type brain material significantly increa

149 rt all of the available PrP(C) to PrP(Sc) in PMCA, suggesting the mechanism of prion strain interfere

150 o evidence for generation of a new strain in PMCA.

151 required for complete blockage of HY TME in PMCA compared to several previous in vivo studies, sugge

152 The emergence of HY TME in PMCA was controlled by the initial ratio of the TME agen

153 tate infectious prion formation in vitro.Ina PMCA reaction lacking PrPSc template seed, synthetic pol

154 a presynaptic protein complex that includes PMCAs and has a role in modulating Ca(2+) homeostasis an

155 GPER/GPR30 knockdown increases PMCA activity, whereas PMCA knockdown substantially redu

156 TEA, and TPA, respectively) did not inhibit PMCA.

157 st Ca(2+) overload, ATP depletion, inhibited PMCA activity, and consequently induced necrosis.

158 ent organic cation, ethyl diamine, inhibited PMCA but was not competitive with Ca(2+).

159 guanidine and tetramethylguanidine inhibited PMCA by competing with Ca(2+).

160 more potent than butyl diamine in inhibiting PMCA.

161 Activation of GPER/GPR30 further inhibits PMCA activity through tyrosine phosphorylation of the pu

162 Plasma membrane calcium ATPase isoforms (PMCAs) are expressed in a wide variety of tissues where

163 nteraction of purified G-actin with isolated PMCA and examine the effect of G-actin during the first

164 contrast, Ca2+ pumps in the plasma membrane (PMCA) and sarco-endoplasmic reticulum as well as buffers

165 tion of Ca(2+) pumps in the plasma membrane (PMCA) with caloxin 3A1 reduced Ca(2+) extrusion and incr

166 ng affinity of CaM with oxidatively modified PMCA (K(d) = 9.8 +/- 2.0 nM), indicating that the previo

167 stimulated activity for oxidatively modified PMCA is not a result of reduced CaM binding.

168 s partially blocked for oxidatively modified PMCA, even in the presence of ATP.

169 matrix to alter Ca(2+) signals by modulating PMCA-mediated Ca(2+) clearance.

170 In mice lacking Mpp4, PMCAs were lost from rod photoreceptor presynaptic membr

171 The current work introduced a new PMCA technique for amplification of atypical PrPres and

172 Here we employed the new PMCA format with beads (PMCAb) to gain insight into the

173 complexed with oxidized PMCA or nonoxidized PMCA.

174 in the presence of ATP, whereas nonoxidized PMCA-CaM complexes existed almost exclusively in a high-

175 g to the CaM-binding domain of isoform 1b of PMCA.

176 Previous assays of PMCA-CaM interactions were indirect, based on activity o

177 glycero-3-phosphocholine, the association of PMCA to actin produced a shift in the distribution of th

178 holoCaM to the full-length binding domain of PMCA.

179 he unprecedented amplification efficiency of PMCA leads to a several billion-fold increase of sensiti

180 was accomplished by studying the exposure of PMCA to surrounding phospholipids by measuring the incor

181 However, inhibition of PMCA activity did enhance the amplitude and slowed the r

182 Functionally, inhibition of PMCA activity is significantly reduced by truncation of

183 Competitive inhibition of PMCA activity was used to measure apparent dissociation

184 Pharmacological inhibition of PMCA increased the frequency but not the amplitude of mE

185 that PMCA2w/a is the hair-bundle isoform of PMCA in rat hair cells and that 2w targets PMCA2 to bund

186 ce of the expression of multiple isoforms of PMCA in the same cell type are not well understood.

187 Antisense knockdown of PMCA isoform 4 removed tonic inhibition of Ca(2+) cleara

188 Oxidative modification of PMCA is known to result in a loss of activity for the en

189 sults suggest that oxidative modification of PMCA reduced the propensity of the autoinhibitory domain

190 by E2-stimulated tyrosine phosphorylation of PMCA.

191 s for the different functional properties of PMCA isoforms.

192 This study reinforces the emerging role of PMCA as a molecular organizer and regulator of signaling

193 Successive rounds of PMCA amplification result in adaptation of the in vitro-

194 Two successive rounds of PMCA cycles resulted in a 10 million-fold increase in se

195 Here during four to eight rounds of PMCA, end-point dilution titrations detected a >320-fold

196 Indeed, after seven rounds of PMCA, we were able to generate large amounts of PrPSc st

197 t species, was subjected to serial rounds of PMCA.

198 ysis of nonredundant amino acid sequences of PMCA proteins from different species showed Cas-PMCA clu

199 The activity of PMCAs is controlled by autoinhibition.

200 tributable to Ca2+-dependent inactivation of PMCAs.

201 ad response but had no significant effect on PMCA activity.

202 undation to explain its functional effect on PMCA.

203 are similar for CaM complexed with oxidized PMCA or nonoxidized PMCA.

204 e structural analysis of parent and progeny (PMCA-derived) PrP seeds by an improved approach of sensi

205 PMCA-mediated Ca(2+) extrusion by promoting PMCA tyrosine phosphorylation.

206 heir effects on plasma membrane Ca(2+) pump (PMCA).

207 sma membrane calcium/calmodulin ATPase pump (PMCA), as a potential modulator of signal transduction p

208 e inhibition of the plasma membrane Ca pump (PMCA) were determined and compared to inhibition of the

209 aM) vary among plasma membrane calcium pump (PMCA) isoforms.

210 s to study the plasma membrane calcium pump (PMCA) reaction cycle by characterizing conformational ch

211 carried out by plasma membrane Ca(2+) pumps (PMCAs) is essential for maintaining low Ca(2+) concentra

212 dal neurons that plasma membrane Ca2+ pumps (PMCAs) and Na+/Ca2+ exchangers are the major Ca2+ extrus

213 lcium, ATP, and vanadate binding to purified PMCA.

214 linectes sapidus) a cDNA encoding a putative PMCA.

215 Here we describe a quantitative PMCA procedure to calculate the concentration of very lo

216 in urine calculated by means of quantitative PMCA was estimated at 1x10(-16) g per milliliter, or 3x1

217 More recently, PMCA techniques using bacterially derived recombinant Pr

218 Bcl-2 regulates PMCA function in pancreatic acinar cells and thereby inf

219 ere we investigate the mechanisms regulating PMCA internalization.

220 While the addition of RNA restored PMCA conversion efficiency, the effect of synthetic poly

221 ch faster seeded polymerization method (rPrP-PMCA) which detects >or=50 ag of hamster PrPSc (approxim

222 d (approximately 39%) when the PKC-sensitive PMCA isoform was knocked down by expression of an antise

223 Notably, serial PMCA enables detection of PrP(Sc) in blood samples of sc

224 A single PMCA assay takes little more than 3 d to replicate a lar

225 The targeting of some PMCA isoforms may enhance the effectiveness of therapies

226 Gradual increases in Sp-PMCA and Sp-SERCA mRNA begin at the 18 hour hatched blas

227 The primary structures of Sp-PMCA and Sp-SERCA in the sea urchin, Strongylocentrotus

228 d sea urchin genome reveals that Sp-SPCA, Sp-PMCA and Sp-SERCA have 23, 17 and 24 exons.

229 of Sp-SPCA are at low levels compared to Sp-PMCA and Sp-SERCA.

230 ocal [Ca(2+)] transients, but for a specific PMCA to play a unique role in local Ca(2+) handling it m

231 We show here that region-specific PMCA in part reproduces the specific brain targeting obs

232 These experiments showed that successful PMCA propagation of PrP(Sc) molecules in a purified syst

233 Our results show that alpha-synuclein PMCA is a fast and reproducible system that could be use

234 fibrils are able to seed new alpha-synuclein PMCA reactions and to enter and aggregate in cells in cu

235 A of Xenopus PMCA1, and show that GFP-tagged PMCA traffics in a similar fashion to endogenous PMCA.

236 gical and co-localization studies argue that PMCA is internalized through a lipid raft endocytic path

237 These data demonstrate that PMCA efficiently replicates the prion agent and provide

238 This is not to imply that PMCA is inherently selective against monovalent cations

239 Our results indicate that PMCA is a valuable tool for the investigation of cross-s

240 strength and Hb A1c content, indicating that PMCA activity declines monotonically with RBC age.

241 article of infectious PrPSc, indicating that PMCA may enable detection of as little as one oligomeric

242 Infrared microspectroscopy revealed that PMCA of native hamster 263K scrapie seeds in hamster PrP

243 Here, we show that PMCA and GPER/GPR30 physically interact and functionally

244 Here we show that PMCA enables the specific and reproducible amplification

245 These findings show that PMCA might be useful as a blood test for routine, live a

246 ut reducing the ER capacity, suggesting that PMCA and SERCA compete for Ca2+.

247 +) homeostasis and the previous finding that PMCAs act as digenic modulators in Ca(2+)-linked patholo

248 The PMCA (protein misfolding cyclic amplification) assay was

249 The PMCA efficiency of bound prions varied with soil type, w

250 t the inability of CaM to fully activate the PMCA after methionine oxidation originates in a reduced

251 ate that, following electrical activity, the PMCA is the predominant mechanism of Ca2+ clearance from

252 xtracellular alkaline shift generated by the PMCA.

253 In rat sensory neurons grown in culture, the PMCA was under tonic inhibition by a member of the Src f

254 uses a conformational study to describe the PMCA P-type ATPase reaction cycle, adding important feat

255 ndrial versus glycolytic ATP in fuelling the PMCA in human pancreatic cancer cells.

256 g La(3+) to the opposite side to inhibit the PMCA.

257 s a long lifetime (minutes) and may keep the PMCA primed for activation.

258 n CaM-L7 and the CaM-binding sequence of the PMCA (C28W) due to methionine oxidation.

259 rval muscle fibers showed high levels of the PMCA at the neuromuscular junction.

260 s (PMCA1-4), and alternative splicing of the PMCA genes creates a suite of calcium efflux pumps.

261 Targeting the glycolytic regulation of the PMCA may, therefore, be an effective strategy for select

262 The three-dimensional structure of the PMCA pump has not been solved, but its basic mechanistic

263 this ratio and the electroneutrality of the PMCA suggest that the Ca2+ : H+ ratio is 1 : 2, ensuring

264 To evaluate the sensitivity of the PMCA system as an alpha-synuclein anti-aggregating drug

265 Tonic inhibition of the PMCA was attenuated in cells expressing a dominant-negat

266 ) overload, ATP depletion, inhibition of the PMCA, and necrosis.

267 osolic Ca(2+) overload and inhibition of the PMCA.

268 s binding to the CaM-binding sequence of the PMCA.

269 l domain and the CaM-binding sequence of the PMCA.

270 on was prevented by dialysis of BAPTA or the PMCA inhibitor carboxyeosin.

271 SFKs did not appear to phosphorylate the PMCA directly but instead activated focal adhesion kinas

272 the CaM-binding sequence that stabilizes the PMCA in an inhibited conformation.

273 We tested whether the PMCA acts in an autocrine fashion to boost pH-sensitive,

274 To assess whether the PMCA-competent prions residing at the maternal-fetal int

275 ters the interaction of this domain with the PMCA.

276 The PMCAs use energy derived from ATP to extrude submicromol

277 n the CaM-binding domain of isoform 3 of the PMCAs in a family with X-linked congenital cerebellar at

278 Therefore, PMCA offers great promise for the development of highly

279 sufficient to maintain cellular ATP and thus PMCA activity, thereby preventing Ca(2+) overload, even

280 Thus, PMCA has been established as a valuable analytical tool

281 igated the Ca2+ dependence of CaM binding to PMCA.

282 Relative to PMCA, the amyloid fibril growth assay is less restrictiv

283 usly attributed such high-mobility states to PMCA-CaM complexes with a dissociated autoinhibitory/CaM

284 ngly, purified HaPrPC molecules subjected to PMCA selectively incorporate an approximately 1-2.5-kb s

285 cular hyaluronan from CD44, attenuated tonic PMCA inhibition.

286 To track PMCA trafficking in live cells we cloned a full-length c

287 asma membrane Ca2+-adenosine triphosphatase (PMCA) efflux pump.

288 rprisingly, we found that Ca2+ extrusion via PMCA and Na+/Ca2+ exchangers slows in an activity-depend

289 Transport fluxes via PMCA, SERCA, ER leakage, and Type II IP3 receptors are a

290 ansmission of PrP(Sc) misfolding by in vitro PMCA amplification.

291 Similar EPSC reduction occurred when PMCA activation was prevented by dialysis of BAPTA or th

292 CA seem to have been partially reversed when PMCA products were reinoculated into the original host s

293 We found that, when PMCA is reconstituted in mixed micelles, neutral phospho

294 0 knockdown increases PMCA activity, whereas PMCA knockdown substantially reduces GPER/GPR30-mediated

295 While PMCA reactions produce high levels of protease-resistant

296 with PMCA, yielding a K(d) value of CaM with PMCA (5.8 +/- 0.5 nM) consistent with previous indirect

297 coupling magnetic nanoparticle capture with PMCA could accelerate and improve prion detection.

298 GPER/GPR30 co-immunoprecipitates with PMCA with or without treatment with 17beta-estradiol, th

299 n resonance, G-actin directly interacts with PMCA with an apparent 1:1 stoichiometry in the presence

300 eled with Oregon Green 488 on titration with PMCA, yielding a K(d) value of CaM with PMCA (5.8 +/- 0.