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 was again nonreactive in all CON, and positive in a

7 PMCA-generated samples caused the same clinical disease

8 PMCAs comprise four isoforms and over 20 splice variants

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 alphaSyn-PMCA was nonreactive in all CON, whereas all MSA samples

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

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

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

17 the Protein Misfolding Cyclic Amplification (PMCA) assay.

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

19 by protein misfolding cyclic amplification (PMCA) demonstrated that low levels of the c-BSE agent we

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

21 by protein misfolding cyclic amplification (PMCA) in urine of patients affected with variant Creutzf

22 Protein misfolding cyclic amplification (PMCA) is a technique that has previously been used to de

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

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

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

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

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

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

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

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

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

32 the Protein Misfolding Cyclic Amplification (PMCA) technology as a screening tool for the presence of

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

34 by protein misfolding cyclic amplification (PMCA) technology.

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

36 and protein misfolding cyclic amplification (PMCA) to detect alphaSyn oligomers in CSF.

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

38 by protein misfolding cyclic amplification (PMCA) were studied.

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

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

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

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

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

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

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

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

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

48 by protein misfolding cyclic amplification (PMCA).

49 and protein misfolding cyclic amplification (PMCA).

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

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

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

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

54 duces the association between GPER/GPR30 and PMCA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 ps includes plasma membrane calcium ATPases (PMCAs).

98 bundance of plasma membrane calcium ATPases (PMCAs).

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

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

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

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

103 loped for therapeutic use and found it to be PMCA-negative for vCJD and BSE prions.

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

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

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

107 creted PrP(D) and following amplification by PMCA.

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

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

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

111 alpha-synuclein fibril formation induced by PMCA.

112 is a strain-specific feature, measurable by PMCA and mouse bioassay, and a great tool to distinguish

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 ostasis through downregulation of endogenous PMCA.

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

135 traffics in a similar fashion to endogenous PMCA.

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

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

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

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

140 uring oocyte maturation is required for full PMCA internalization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 more potent than butyl diamine in inhibiting PMCA.

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

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

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

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

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

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

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

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

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

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

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

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

178 of codon 96 polymorphisms and the ability of PMCA to detect CWD in the blood of pre-clinical WTD.

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

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

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

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

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

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

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

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

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

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

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

190 ine and are faithfully amplified by means of PMCA; moreover, they suggest that the PrP(D) urine test

191 by E2-stimulated tyrosine phosphorylation of PMCA.

192 s for the different functional properties of PMCA isoforms.

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

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

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

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

197 First, we demonstrated the sensitivity of PMCA to detect a single cell infected with prions.

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

199 e excretion along with the obligatory use of PMCA raise the issue of whether strain characteristics o

200 The activity of PMCAs is controlled by autoinhibition.

201 tributable to Ca2+-dependent inactivation of PMCAs.

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

203 undation to explain its functional effect on PMCA.

204 s all core Ca(2+) signaling proteins: Orai1, PMCA, STIM1, IP(3) receptors, and SERCA2 at the ER/PM ju

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

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

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

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

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

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

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

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

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

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

215 linectes sapidus) a cDNA encoding a putative PMCA.

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

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

218 More recently, PMCA techniques using bacterially derived recombinant Pr

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

220 ere we investigate the mechanisms regulating PMCA internalization.

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

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

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

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 Here we show that the alpha-synuclein-PMCA assay can discriminate between samples of cerebrosp

236 ds to analyse the product of alpha-synuclein-PMCA, and found that the characteristics of the alpha-sy

237 be amplified and detected by alpha-synuclein-PMCA.

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

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

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

241 Next, we determined that PMCA performance was robust and uncompromised by the spi

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

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

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

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

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

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

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

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

250 ions of an infected cell culture showed that PMCA enabled prion amplification from a sample comprised

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

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

253 The PMCA (protein misfolding cyclic amplification) assay was

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

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

256 xtracellular alkaline shift generated by the PMCA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 Our findings demonstrate that the PMCA technology has unparalleled sensitivity and specifi

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

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

277 The PMCAs use energy derived from ATP to extrude submicromol

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

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

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

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

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

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

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.