ライフサイエンスコーパス: MPR

1 MPR accumulation on the tumor cell surface during chemot

2 MPR index showed a stepwise reduction with increasing ex

3 MPR recycling requires Rab9 GTPase; Rab9 recruits the cy

4 MPR was calculated in the remaining 68 patients >151.7 p

5 MPR was greater in diastole than systole in all segment

6 MPR(CMR) and MPR(PET) for the 2 lowest scoring segments

7 MPR-R has no advantage over MPT-T concerning efficacy.

8 MPR-R significantly prolonged progression-free survival

9 The differences in mean errors between 2D MPR and 3D endoluminal measurements were significant (P

10 The largest of the three 2D MPR measurements was considered the "optimized" 2D proje

11 yps were measured at CT colonography with 2D MPR and 3D endoluminal displays and electronic calipers

12 Strikingly, 4-HPR but not 4-MPR restricted infection in peripheral blood mononuclear

13 4-HPR but not 4-MPR was found to specifically upregulate the protein kin

14 4-Oxo-N-(4-methoxyphenyl)retinamide (4-oxo-4-MPR) had minimal effects on DES activity.

15 N-(4-Methoxyphenyl)retinamide (4-MPR) and 4-Oxo-N-(4-methoxyphenyl)retinamide (4-oxo-4-MP

16 ly related N-(4-methoxyphenyl) retinamide (4-MPR) could reduce viral RNA levels and titers when appli

17 Overall, the percentage of patients with a MPR of 80% or greater at 12 months was 27.7%, while pers

18 P-1, and cells depleted of GCC185 accumulate MPRs in transport vesicles that are AP-1 decorated.

19 Suboptimal adherence (MPR<0.8) was recorded in 35 (51%).

20 no difference in outcome was detected among MPR, CPR, and Rd.

21 An MPR cutoff of 2.04 was 85.1% (95% CI 71.1 to 99.2) sensi

22 An MPR cutoff of 2.04 was 92.9% (95% CI 77.9 to 100.0) sens

23 An MPR(PET) </=1.44 predicted significant CAD with 82% sens

24 Nonadherence to HT was defined as an MPR less than 80% between the first and last prescriptio

25 Adequate adherence was characterized by an MPR >/=0.8 and ideal as MPR=1.0.

26 Subjects with an MPR >80% were considered adherent.

27 Patients with an MPR of at least 0.80 were classified as adherent.

28 -45.7]; fourth quarter 14.5 [2.51-83.6]) and MPR less than 95% (second quarter 9.44 [3.40-26.2]; four

29 MPR(CMR) and MPR(PET) for the 2 lowest scoring segments in each coron

30 ere is good correlation between MPR(CMR) and MPR(PET.) For the detection of significant CAD, MPR(PET)

31 as simulated with adenosine for both FFR and MPR.

32 Area under the ROC curve with stress MBF and MPR as the outcome measures, respectively, was 0.86 and

33 ial perfusion MR estimates of stress MBF and MPR were greater in diastole than systole in patients wi

34 between any of the models or between MBF and MPR, except that the Fermi model outperformed the one-co

35 the effects of eliminating the MR on MR- and MPR-mediated plasma clearance and tissue distribution of

36 e quantification of myocardial perfusion and MPR with PET have proven diagnostic and prognostic roles

37 e detection of significant CAD, MPR(PET) and MPR(CMR) seem comparable and very accurate.

38 0.7-2.6% of participants in any quarter and MPR of less than 95% for 3.3-11.1%.

39 Response rates were superior with MPR-R and MPR (77% and 68%, respectively, vs. 50% with MP; P<0.001

40 ith 82% sensitivity and 87% specificity, and MPR(CMR) </=1.45 predicted significant CAD with 82% sens

41 the remaining 141 patients by using CBRs and MPRs together, and the other half by using MPRs only.

42 for MPRs and 74% (520 of 698) when CBRs and MPRs were used together, which was significantly higher

43 characterized by an MPR >/=0.8 and ideal as MPR=1.0.

44 All images included axial, MPR, MIP, and VRT and were interpreted in one session.

45 There is good correlation between MPR(CMR) and MPR(PET.) For the detection of significant

46 attached to residue N325, and that it binds MPR, via mannose 6-phosphate, with a similar affinity to

47 (PET.) For the detection of significant CAD, MPR(PET) and MPR(CMR) seem comparable and very accurate.

48 In addition, CD-MPR binding affinities are modulated by divalent cations

49 mannose 6-phosphate receptors (CI-MPR and CD-MPR) for high mannose-type N-glycans of defined structur

50 A detailed comparison of the available CD-MPR structures reveals the positional invariability of s

51 ligands is pH-dependent; the homodimeric CD-MPR binds lysosomal enzymes optimally in the pH environm

52 MPR) and the 46 kDa cation-dependent MPR (CD-MPR) are key components of the lysosomal enzyme targetin

53 MPR) and the 46-kDa cation-dependent MPR (CD-MPR) are type I integral membrane glycoproteins that pla

54 n-dependent mannose 6-phosphate receptor (CD-MPR) is a key component of the lysosomal enzyme targetin

55 n-dependent mannose 6-phosphate receptor (CD-MPR) plays a key role in the delivery of lysosomal enzym

56 h different concentrations of recombinant CD-MPR or soluble CI-MPR.

57 d as essential for Man-6-P binding by the CD-MPR and domains 1-3 and 9 of the CI-MPR.

58 ntial for carbohydrate recognition by the CD-MPR and domains 3 and 9 of the CI-MPR, but lacks two cys

59 n(alpha1,2)Man-O-(CH(2))(8)COOMe), 2) the CD-MPR at pH 4.8 in an unbound state (i.e. endosome), and 3

60 unbound state (i.e. endosome), and 3) the CD-MPR at pH 7.4 (i.e. cell surface).

61 untered by the receptor including: 1) the CD-MPR bound at pH 6.5 (i.e. trans Golgi network) to a high

62 ic studies have shown that at pH 6.5, the CD-MPR bound to Man-6-P adopts a significantly different qu

63 The CD-MPR bound weakly or undetectably to the phosphodiester d

64 -MPR, residues 1-154) have shown that the CD-MPR exists as a homodimer and exhibits two distinct conf

65 ifferent quaternary conformation than the CD-MPR in a ligand-unbound state, a feature unique among kn

66 odified GAAs demonstrate that, unlike the CD-MPR or domain 9 of the CI-MPR, domain 5 exhibits a 14-18

67 pho-mono- or -diesters although, like the CD-MPR, it differentially recognized isomers of phosphoryla

68 s in the structure and functioning of the CD-MPR.

69 of phosphorylated glycans by the CI- and CD-MPRs has implications for understanding the biosynthesis

70 xpressing cells were fractionated using a CI-MPR affinity column, 35-45% of the total LIF molecules w

71 MPR interaction, suggesting that IncE and CI-MPR are dependent on the same binding surface on SNX5.

72 summary, beta2-agonist treatment enhanced CI-MPR-mediated uptake and trafficking of GAA in mice with

73 Finally, CI-MPR-KO/GAA-KO mice did not respond to combination therap

74 forming a multimeric complex required for CI-MPR sorting.

75 GGA3 phosphorylation, releasing GGA3 from CI-MPR and early endosomes.

76 proteins leads to a pronounced defect in CI-MPR endosome-to-TGN transport.

77 this study reappraise retromer's role in CI-MPR transport.

78 e quadriceps biopsies suggested increased CI-MPR at wk 12 (P=0.08), compared with baseline.

79 unctive beta2-agonist treatment increased CI-MPR expression and enhanced efficacy from gene therapy i

80 ated beta2-agonist drugs, which increased CI-MPR expression in GAA knockout (KO) mice.

81 sly demonstrated the benefit of increased CI-MPR-mediated uptake of recombinant human acid-alpha-gluc

82 om clenbuterol in GAA-KO mice that lacked CI-MPR in muscle, where it failed to reverse the high glyco

83 ade controlling PACS-1- and GGA3-mediated CI-MPR sorting.

84 retrieval of the cation-independent MPR (CI-MPR).

85 ivity, as measured by decreased levels of CI-MPR and lower activities of cellular lysosomal hydrolase

86 Cycling of CI-MPR between the TGN and early endosomes is mediated by G

87 that mediate the retrograde transport of CI-MPR from endosomes to the TGN independently of the core

88 lenbuterol, which increases expression of CI-MPR in muscle, was administered with the AAV vector.

89 The integral role of CI-MPR was demonstrated by the lack of effectiveness from c

90 IncE peptide inhibits the interaction of CI-MPR with SNX5.

91 addition of clenbuterol in the absence of CI-MPR, as was lysosomal vacuolation, which correlated with

92 ing that clenbuterol's effect depended on CI-MPR expression.

93 s, GGA3 and PACS-1 bind to an overlapping CI-MPR trafficking motif and their sorting activity is cont

94 or knockout of retromer does not perturb CI-MPR transport, the targeting of the retromer-linked sort

95 independent mannose-6-phosphate receptor (CI-MPR) and sortilin.

96 independent mannose 6-phosphate receptor (CI-MPR) and the 46 kDa cation-dependent MPR (CD-MPR) are ke

97 independent mannose 6-phosphate receptor (CI-MPR) and the 46-kDa cation-dependent MPR (CD-MPR) are ty

98 independent mannose-6-phosphate receptor (CI-MPR) follows a highly regulated sorting itinerary to del

99 independent mannose 6-phosphate receptor (CI-MPR) from endosomes to the trans-Golgi network (TGN), is

100 independent mannose-6-phosphate receptor (CI-MPR) in skeletal muscle.

101 independent mannose 6-phosphate receptor (CI-MPR) is a multifunctional protein that binds diverse int

102 independent mannose-6-phosphate receptor (CI-MPR) mediated uptake.

103 independent mannose 6-phosphate receptor (CI-MPR) plays a critical role in the trafficking of newly s

104 -kDa cation-independent Man-6-P receptor (CI-MPR) that transports newly synthesized acid hydrolases f

105 independent mannose-6-phosphate receptor (CI-MPR), a receptor for lysosomal hydrolases, and other end

106 independent mannose 6-phosphate receptor (CI-MPR), and we analyzed the effects of this modification o

107 independent mannose 6-phosphate receptor (CI-MPR), which contains multiple mannose 6-phosphate (Man-6

108 independent mannose 6-phosphate receptor (CI-MPR)-mediated endocytosis of the enzyme by the affected

109 independent mannose-6-phosphate receptor (CI-MPR)-mediated uptake and intracellular trafficking of GA

110 independent mannose 6-phosphate receptor (CI-MPR).

111 independent mannose-6-phosphate receptor (CI-MPR).

112 t for a high-affinity binding to receptor CI-MPR, while the presence of a M6P moiety at the alpha-1,6

113 -dependent mannose 6-phosphate receptors (CI-MPR and CD-MPR) for high mannose-type N-glycans of defin

114 ndependent mannose-6-phosphate receptors (CI-MPR) in the soma is disrupted in mutant hAPP neurons, ca

115 did regulate retromer-mediated retrograde CI-MPR trafficking, which required its association with end

116 omatis infection interferes with the SNX5:CI-MPR interaction, suggesting that IncE and CI-MPR are dep

117 trations of recombinant CD-MPR or soluble CI-MPR.

118 oding the N-terminal three domains of the CI-MPR (Dom1-3His) which contains both a mannose 6-phosphat

119 The CI-MPR also recognizes lysosomal enzymes that elude UCE mat

120 re performed using truncated forms of the CI-MPR and plasminogen.

121 e loop connecting domains 1 and 2) of the CI-MPR are key determinants for plasminogen binding but are

122 By contrast, the CI-MPR bound with high affinity to glycans containing eithe

123 ysis of LIF glycopeptides enriched on the CI-MPR column revealed that all six N-glycan sites could be

124 ts show that the N-terminal region of the CI-MPR containing domains 1 and 2, but not domain 1 alone,

125 From validating the CI-MPR dependency of SNX1/2-SNX5/6 tubular profile formatio

126 n to its role in lysosome biogenesis, the CI-MPR interacts with a number of different extracellular l

127 The CI-MPR is a receptor for plasminogen, and this interaction

128 The extracellular region of the CI-MPR is comprised of 15 repetitive domains and contains t

129 critical to achieve high affinity for the CI-MPR receptor.

130 The CI-MPR recognizes lysosomal enzymes bearing the Man-6-P mod

131 e results show the mechanism by which the CI-MPR recognizes Man-P-GlcNAc-containing ligands and provi

132 To determine how the CI-MPR recognizes phosphodiesters, the structure of domain

133 To identify the lysine residue(s) of the CI-MPR that serve(s) as an essential determinant for recogn

134 ish that SNX5 and SNX6 associate with the CI-MPR through recognition of a specific WLM endosome-to-TG

135 igh-affinity Man-6-P binding sites of the CI-MPR to domains 1-3 and 9 and one low-affinity site to do

136 que carbohydrate binding sites allows the CI-MPR to interact with the structurally diverse phosphoryl

137 This ability of the CI-MPR to target phosphodiester-containing enzymes ensures

138 e three carbohydrate binding sites of the CI-MPR, a phosphorylated glycan microarray was probed with

139 by the CD-MPR and domains 3 and 9 of the CI-MPR, but lacks two cysteine residues predicted to form a

140 hat, unlike the CD-MPR or domain 9 of the CI-MPR, domain 5 exhibits a 14-18-fold higher affinity for

141 ngles 1-4, but not kringles 1-3, bind the CI-MPR, indicating an essential role for the LBS in kringle

142 ay was probed with truncated forms of the CI-MPR.

143 y the CD-MPR and domains 1-3 and 9 of the CI-MPR.

144 1Ser(278), promoting binding of PACS-1 to CI-MPR to retrieve the receptor to the TGN.

145 However, during the clamp MPR was significantly lower in the HH group when compare

146 During clamp, MPR tended to decrease in the HH group (p < 0.1) but did

147 antly higher for oblique MPR than for curved MPR (P=.01), curved MIP (P=.03), and VRT (P<.001).

148 d 83% for curved MIP, 93% and 81% for curved MPR, and 91% and 73% for VRT).

149 han evaluation of prerendered images (curved MPR, curved MIP, or VRT images).

150 tions (MIPs, 5 mm thick), prerendered curved MPRs, prerendered curved MIPs, or prerendered three-dime

151 nd loss of either protein leads to defective MPR carrier biogenesis at the TGN and endosomes.

152 tor (CI-MPR) and the 46 kDa cation-dependent MPR (CD-MPR) are key components of the lysosomal enzyme

153 tor (CI-MPR) and the 46-kDa cation-dependent MPR (CD-MPR) are type I integral membrane glycoproteins

154 The CMR-derived MPR (MPR(CMR)) correlated well with PET-derived measurem

155 In case of difficulties MPR or MinIP projection was used.

156 Effective MPR-mediated delivery may be compromised by rapid cleara

157 % confidence interval: 0.73 to 0.94) and for MPR(CMR) was 0.83 (95% confidence interval: 0.74 to 0.92

158 receiver-operating characteristic curve for MPR(PET) to detect significant CAD was 0.83 (95% confide

159 s indicate that this domain is important for MPR recycling to the Golgi complex.

160 Thus, although IH is not necessary for MPR in this neuron type, it contributes indirectly by co

161 thin 4 wk, which served as the reference for MPR index assessment.

162 ins, is a Rab9 effector that is required for MPR recycling from endosomes to the TGN in living cells,

163 or all bone lesions was 35% (247 of 698) for MPRs and 74% (520 of 698) when CBRs and MPRs were used t

164 Global MPR correlated well with number of obstructed vessels (P

165 Global MPR index was higher in patients with normal MPI (n = 51

166 By multivariable regression analysis, global MPR index was associated with global stress TPD, age, an

167 ging-Raman imaging nanoparticle (termed here MPR nanoparticle) can accurately help delineate the marg

168 PRs) and subsequent capture of the hydrolase-MPR complexes into clathrin-coated vesicles or transport

169 el outperformed the one-compartment model if MPR was used as the outcome measure (P = .02).

170 cantly higher in the MPT-T arm: 16% vs 2% in MPR-R, resulting in a significant shorter duration of ma

171 grade >/=3 toxicity was neutropenia: 64% in MPR, 29% in CPR, and 25% in Rd patients (P < .0001).

172 on of maintenance therapy (5 vs 17 months in MPR-R), irrespective of age.

173 emulsification cataract surgery performed in MPRs of Kaiser Permanente Colorado from 2011 to 2014.

174 f office-based cataract surgery performed in MPRs.

175 In addition, cells showed increased MPR synthesis in conjunction with MPR missorting to the

176 fficient retrieval of the cation-independent MPR (CI-MPR).

177 capacity to interact with the beta3 integrin MPR (L325R) or NPLY sequence (W359A).

178 thalidomide being replaced by lenalidomide (MPR-R).

179 tion with melphalan-prednisone-lenalidomide (MPR) and compared lenalidomide maintenance therapy with

180 tion with melphalan-prednisone-lenalidomide (MPR) or cyclophosphamide-prednisone-lenalidomide (CPR) o

181 R-R) with melphalan-prednisone-lenalidomide (MPR) or melphalan-prednisone (MP) followed by placebo in

182 ved samples on a regular basis and had lower MPR than those who did not (P < 0.05).

183 l, 31 of 32 (97%) recipients accepted F-LR + MPR platelets; none developed antibodies to donor lympho

184 , platelet concentrates prepared from F-LR + MPR whole blood were also nonimmunogenic; that is, 10 of

185 uction followed by lenalidomide maintenance (MPR-R) with melphalan-prednisone-lenalidomide (MPR) or m

186 patients stop and restart medications makes MPR a robust measure of adherence over time that reflect

187 rrelated well with PET-derived measurements (MPR(PET)) (r = 0.75, p < 0.0001).

188 Median MPR was 0.79 (range, 0-1.3).

189 The CMR-derived MPR (MPR(CMR)) correlated well with PET-derived measurements

190 Measurements of the PD neuron MPR at more hyperpolarized voltages resulted in a reduct

191 The PD neuron MPR is sensitive to blockers of H- (IH) and calcium-curr

192 ulation and retention by the tumors, with no MPR accumulation in the surrounding healthy tissue, allo

193 ccuracy was significantly higher for oblique MPR than for curved MPR (P=.01), curved MIP (P=.03), and

194 88% for transverse, 99% and 91% for oblique MPR, 94% and 86% for oblique MIP, 94% and 83% for curved

195 play methods, especially interactive oblique MPRs, permits higher diagnostic accuracy than evaluation

196 ribute to the generation or amplification of MPR, but how the interaction of these currents with line

197 Unlike most cases of MPR, in these optimal models, the values of resonant- (f

198 tion to receive MPR-R (nine 4-week cycles of MPR followed by lenalidomide maintenance therapy until a

199 a mechanistic explanation the dependence of MPR on the ICa gating variable time constants.

200 tissues, thus enhancing the effectiveness of MPR-targeted ERT.

201 ombined treatment related to the kinetics of MPR upregulation and abrogation of this event abolished

202 Subsequently, a novel mechanism of MPR action was elucidated, with the development of novel

203 Multivariate linear regression models of MPR and proportional hazards models of persistence were

204 target of myb (TOM))-GFP led to retention of MPR, VAMP4, and syntaxin 6 in mature SGs (MSGs), suggest

205 OCRL1 with pacsin 2 and promotes scission of MPR-containing carriers.

206 Intravenous injection of MPRs into glioblastoma-bearing mice led to MPR accumulat

207 re, SKIP regulated retrograde trafficking of MPRs in noninfected cells.

208 ted Rab9-dependent retrograde trafficking of MPRs, thereby attenuating lysosome function.

209 lecular distinction between the transport of MPRs and TGN46 to the trans-Golgi.

210 osed role of AP-1 in retrograde transport of MPRs from late endosomes to the Golgi and indicates that

211 ifA-SKIP accounted for the effect of SifA on MPR transport and lysosome function.

212 melphalan plus stem-cell transplantation or MPR consolidation therapy after induction, and 251 patie

213 patients (10%) never took up a prescription (MPR=0).

214 %, 32%, and 8% of the patients in the MPR-R, MPR, and MP groups, respectively.

215 as defined as a medication possession ratio (MPR) less than 80%.

216 less than 95%, medication possession ratio (MPR) of less than 95%, and HIV viral load of 1000 copies

217 The mean medication possession ratio (MPR) was 0.64 (median 0.57) for the 13,956 subjects.

218 and calculating medication possession ratio (MPR), that is, the ratio of total days' supply of medica

219 lated using the medication possession ratio (MPR).

220 was defined as medication possession ratio (MPR): the proportion of the 365 followup days covered by

221 ch patient, the medication possession ratio (MPR: proportion of follow-up days patients were dispense

222 ment adherence (medication possession ratio [MPR]) and persistence were evaluated over a 1-year perio

223 ssion occurred [152 patients]) or to receive MPR (153 patients) or MP (154 patients) without maintena

224 re ineligible for transplantation to receive MPR-R (nine 4-week cycles of MPR followed by lenalidomid

225 assigned to receive MPT-T, and 319 received MPR-R.

226 a paradigm for mannose 6-phosphate receptor (MPR) independent lysosomal targeting, binding to beta-gl

227 ulation of the mannose-6-phosphate receptor (MPR) on the tumor cell surface.

228 7A localize to mannose 6-phosphate receptor (MPR)-containing trafficking intermediates, and loss of e

229 and tethering mannose 6-phosphate receptor (MPR)-containing transport vesicles en route to the Golgi

230 primarily the mannose 6-phosphate receptor (MPR).

231 by binding to mannose 6-phosphate receptors (MPRs) and subsequent capture of the hydrolase-MPR comple

232 Mannose 6-phosphate receptors (MPRs) are transported from endosomes to the Golgi after

233 Mannose 6-phosphate receptors (MPRs) deliver newly synthesized lysosomal enzymes to end

234 ransmembrane, mannose 6-phosphate receptors (MPRs) that cycle between the TGN and endosomes.

235 recycling of mannose 6-phosphate receptors (MPRs) to the Golgi and for microtubule nucleation at the

236 ransported by mannose-6-phosphate receptors (MPRs).

237 s, free oblique multiplanar reconstructions (MPRs), free oblique maximum intensity projections (MIPs,

238 cells results from accumulation of recycling MPRs in a population of light, small vesicles downstream

239 a-I; 0 of 5) nor Mirasol pathogen reduction (MPR; 1 of 7) treatment of donor platelets prevented allo

240 d more precisely in multiplanar reformatted (MPR) and volume rendered (VR) images.

241 s interpretation of multiplanar reformatted (MPR) images as the reference standard.

242 ween talin and the membrane-proximal region (MPR) in the beta-integrin cytoplasmic domain.

243 n with an integrin membrane-proximal region (MPR) that is critical for integrin activation.

244 Regional MPR index was associated with the same variables and wit

245 Regional MPR indices were significantly different in obstructed a

246 tigraphic estimations of global and regional MPR in multivessel patients using a cadmium zinc telluri

247 Global and regional MPR was assessed using flow difference (stress - rest) a

248 determination of Rhizomucor pusillus rennin (MPR) activity, in free and in immobilized form, along wi

249 Myocardial perfusion reserve (MPR) (MBFa/MBFr) was similar between the HE and HH group

250 Myocardial perfusion reserve (MPR) index was calculated as the ratio of the stress and

251 ntification of myocardial perfusion reserve (MPR) is an emerging topic in nuclear cardiology with an

252 perfusion and myocardial perfusion reserve (MPR) measurements in patients with coronary artery disea

253 stress MBF and myocardial perfusion reserve (MPR) serving as continuous measures.

254 e quantitative myocardial perfusion reserve (MPR) was calculated in 720 myocardial sectors (8 sectors

255 MBF and myocardial perfusion reserve (MPR) were calculated for each segment, and mean values i

256 Neuronal membrane potential resonance (MPR) is associated with subthreshold and network oscilla

257 f only the soluble extracellular region (sCD-MPR, residues 1-154) have shown that the CD-MPR exists a

258 nomer contacts in the functioning of the sCD-MPR, site-directed mutagenesis was used to generate a co

259 The mean +/- SD MPR was 0.52+/-0.31.

260 Cells displayed increased surface MPRs and lysosome-associated membrane protein 1.

261 The MPR assessments were compared to FFR (n = 44 coronary se

262 The MPR index was 1.11 (IQR, 1.01-1.21) versus 1.30 (IQR, 1.

263 The MPR was 1.54 +/- 0.36 in segments with FFR < or =0.75 (n

264 The MPR was 1.54 +/- 0.49 in coronary segments with > or =50

265 The MPR was calculated from the ratio between stress and res

266 The binding sites for beta-GCase and the MPR are functionally separate, so that a stable ternary

267 nce Resonance Energy Transfer (FRET) for the MPR by employing computational simulation techniques and

268 d in 35%, 32%, and 8% of the patients in the MPR-R, MPR, and MP groups, respectively.

269 Preliminary results show that the MPR index is lower in patients with perfusion defects an

270 The MPRs were detected by all three modalities with at least

271 The interaction between the MPRs and its ligands is pH-dependent; the homodimeric CD

272 Endogenous ligands for the MPRs that contain solely phosphomonoesters (Man-6-P) or

273 STX16, Vti1a, and VAMP3 is required for this MPR transport but not for the STX6-dependent transport o

274 or TIP47 and enhances its ability to bind to MPR cytoplasmic domains during transport vesicle formati

275 currents with linear currents contributes to MPR is not well understood.

276 oach delivers a larger fraction of enzyme to MPR-expressing tissues, thus enhancing the effectiveness

277 Depletion of STX10 leads to MPR missorting and hypersecretion of hexosaminidase.

278 f MPRs into glioblastoma-bearing mice led to MPR accumulation and retention by the tumors, with no MP

279 h doses of enzyme also improved targeting to MPR-containing tissues such as muscle, kidney, heart, an

280 progression-free survival (PFS) in triplet (MPR and CPR) vs doublet (Rd) lenalidomide-containing reg

281 opulation, the alkylator-containing triplets MPR and CPR were not superior to the alkylator-free doub

282 risingly, F-LR platelets that then underwent MPR were accepted by 21 of 22 (95%) recipients (P < .001

283 d MPRs together, and the other half by using MPRs only.

284 nd primary tumors was 7% with MPR-R, 7% with MPR, and 3% with MP.

285 ar rate of second primary tumors was 7% with MPR-R, 7% with MPR, and 3% with MP.

286 ession-free survival benefit associated with MPR-R was noted in patients 65 to 75 years of age but no

287 stem-cell transplantation, as compared with MPR, significantly prolonged progression-free and overal

288 MPR-R (hazard ratio for the comparison with MPR, 0.34; P<0.001) that was age-independent.

289 increased MPR synthesis in conjunction with MPR missorting to the lysosome.

290 also demonstrate that LIMP-2 interacts with MPR in living cells.

291 -free survival was significantly longer with MPR-R (31 months) than with MPR (14 months; hazard ratio

292 hs) vs 23 months (95% CI, 19-27 months) with MPR-R (hazard ratio, 0.87; 95% CI, 0.72-1.04; P = .12).

293 idomide maintenance vs myelosuppression with MPR.

294 6% reduction in the rate of progression with MPR-R (hazard ratio for the comparison with MPR, 0.34; P

295 ematologic toxicity was more pronounced with MPR-R, especially grades 3 and 4 neutropenia: 64% vs 27%

296 Response rates were superior with MPR-R and MPR (77% and 68%, respectively, vs. 50% with M

297 ntly longer with MPR-R (31 months) than with MPR (14 months; hazard ratio, 0.49; P<0.001) or MP (13 m

298 frequent with high-dose melphalan than with MPR (94.3% vs. 51.5%), as were gastrointestinal adverse

299 lan plus stem-cell transplantation than with MPR (median progression-free survival, 43.0 months vs. 2

300 horter with volume-rendered images than with MPR images (reader 1: 42 vs 78 seconds, P<.001; reader 2