ライフサイエンスコーパス: cathepsin D

1 mensional structure (i.e., pepsin, renin, or cathepsin D).

2 pepstatin A, a pharmacological inhibitor of cathepsin D.

3 phagolysosomes enriched with both lamp-1 and cathepsin D.

4 decreased activity of the lysosomal enzyme, cathepsin D.

5 d decreased activity of the lysosomal enzyme cathepsin D.

6 ting of the precursor of the acid hydrolase, cathepsin D.

7 , approaching the level obtained with intact cathepsin D.

8 ning for LAMPs but little or no staining for cathepsin D.

9 itment of MLKL protein and the activation of cathepsin D.

10 LAMPs) CD63 and LAMP1 and the acid hydrolase cathepsin D.

11 tyhelminth orthologue of mammalian lysosomal cathepsin D.

12 C12 cells and rodent embryonic cells lacking cathepsin D.

13 the receptor to endosomes, and missorting of cathepsin D.

14 plasma membranes by the lysosomal protease, cathepsin D.

15 espect to the highly homologous human enzyme cathepsin D.

16 oducts in human breast cancer cells: pS2 and cathepsin D.

17 somal markers, including LAMP-1, LAMP-2, and cathepsin D.

18 fluorescent when the latter were released by cathepsin D.

19 ase with some properties similar to those of cathepsin D.

20 olytic activation of the lysosomal hydrolase cathepsin D.

21 mutations in PGRN or CTSD, the gene encoding cathepsin D.

22 ation decreased access to the active site of cathepsin D.

23 t the structurally related aspartyl protease cathepsin D.

24 s to provide selectivity over memapsin 1 and cathepsin D.

25 enhancement of potency and selectivity over cathepsin D.

26 ctively, and with >200-fold selectivity over cathepsin D.

27 embrane protein 1 (LAMP-1) and 40% contained cathepsin D; 50% of the vacuoles could be labeled by end

28 e CCV were more frequently co-localized with Cathepsin D (a lysosomal marker) than the CCV in cells i

29 specifically by BACE1 and BACE2, but not by cathepsin D, a closely related aspartyl protease.

30 d amino acids 265-293 of the beta loop) from cathepsin D, a highly related lysosomal protease.

31 ctural data for pepstatin binding with human cathepsin D, a lysosomal aspartic protease that shares 3

32 what has been shown in Alzheimer's disease, cathepsin D, a lysosomal hydrolase, was redistributed to

33 cleavage products in density fractions with cathepsin D, a marker of lysosomes.

34 ion, we demonstrated increased expression of cathepsin D, a protein known to mediate autophagy.

35 diates suppression of VKORC1v2-cointeracting cathepsin D, a stress-released proapoptotic protein nega

36 Cells without cathepsin D accumulated more N-terminal htt fragments an

37 ophagic inhibitor that induces apoptosis via cathepsin D accumulation and enhances vorinostat-mediate

38 in the 5XFAD brains as indicated by reduced cathepsin D activity and decreased N-glycoyslation of th

39 nockdown of IrCD1 that decreased gut extract cathepsin D activity by >90%.

40 psin D activity, and suggests that decreased cathepsin D activity due to loss of PGRN contributes to

41 errupted cathepsin D processing, and reduced cathepsin D activity in retinal pigment epithelial cells

42 Therefore, cathepsin D activity significantly diminishes presentati

43 Cathepsin D activity varied among cultures and showed no

44 identifies PGRN as an activator of lysosomal cathepsin D activity, and suggests that decreased cathep

45 lysosomal proteolytic activity by increasing cathepsin D activity, levels of cathepsins B and D and t

46 e product of PGRN, is sufficient to increase cathepsin D activity.

47 d in type IV-V subjects, but due to enhanced cathepsin-D activity, SC thickness did not increase.

48 The endosomes of cancer cells are rich in cathepsin D, allowing on-site degradation of TH and faci

49 epitope is highly susceptible to cleavage by cathepsin D, an aspartic endopeptidase found almost excl

50 Cathepsin D: an Mvarphi-derived factor mediating increas

51 tioned approximately 34 A apart (34.06 A for cathepsin D and 33.80 A for cathepsin L).

52 hat in s-IBM, lysosomal enzyme activities of cathepsin D and B were decreased 60% (P < 0.01) and 40%

53 ression of estrogen-responsive genes such as cathepsin D and Bcl-2, which are involved in cell migrat

54 ria associated with the lysosomal hydrolases cathepsin D and beta-glucuronidase.

55 at Arg435 (Dom3(Ala)), were unable to target cathepsin D and beta-hexosaminidase to the lysosome.

56 In this study, the role of cathepsin D and calpain I in these processes was analyze

57 ced the processing of the precursor forms of cathepsin D and cathepsin L to their mature, lysosomal f

58 aled the multifocal epithelial expression of cathepsin D and coexpression with IL-1alpha in BPH tissu

59 Adjusted linear regression identified cathepsin D and confirmed six proteins (leptin, renin, i

60 cumulation of S1P also impairs maturation of cathepsin D and degradation of Lamp-2, indicating a gene

61 against fluorogenic substrates specific for cathepsin D and E and inactive against substrates specif

62 trate-specificity of the endosomal proteases Cathepsin D and E.

63 2-vIL-6 interaction-dependent suppression of cathepsin D and have found that this novel activity of v

64 ense double-membrane-limited AVs, containing cathepsin D and incompletely degraded LC3-II in perikary

65 proteases, including multiple forms of MMPs, cathepsin D and K, kallikrein 4 and proprotein convertas

66 creased lysosomal proteins including LAMP-2, cathepsin D and LC3.

67 ystatin C with the lysosomal marker proteins cathepsin D and legumain.

68 hanced the expression of the ER target genes cathepsin D and pS2, which are regulated by direct DNA b

69 onacidified phagosome with LAMPs but without cathepsin D and that the phagosomal membrane subsequentl

70 n-induced expression of ERalpha target genes cathepsin D and to a lesser extent pS2.

71 ated the expression of the catalytic enzymes cathepsin D and zinc-alpha(2)-glycoprotein in normal ker

72 We found cathepsin D and zinc-alpha(2)-glycoprotein, two catalyti

73 ohistochemical study with antibodies against cathepsin-D and beclin-1 showed numerous positive staine

74 bule-associated protein light chain-3 (LC3), cathepsin-D and beclin-1 were investigated by Western bl

75 uction significantly decreased activities of cathepsins D and B, increased levels of LC3-II, decrease

76 owed similar potency and selectivity against cathepsins D and E (IC(50)s of 7.27 nM and 354 pM, respe

77 Compound 1 selectively inhibited cathepsins D and E with IC(50)s of 26.5 nM and 886 pM, r

78 ect to BACE1 and related aspartic proteases, cathepsins D and E.

79 W7 and DDB1, as well as hypoxic induction of cathepsins D and S.

80 partment and rapidly matured into LAMP-1(+), cathepsin D(+), and acidic phagosomes.

81 . abortus 2308 BCP decreased while remaining cathepsin D(-) and LAMP-1(+).

82 ss of the progesterone receptor (PR), Bcl-2, cathepsin D, and cyclin D1 genes, but not the pS2 gene,

83 (matrix metalloproteinase 9, S100A8/S100A9, cathepsin D, and galectin-3-binding protein) improved ri

84 as documented by the acquisition of LAMP-2, cathepsin D, and lysosomal tracer Texas Red ovalbumin, a

85 1 over other key aspartyl proteases, notably cathepsin D, and profoundly lowers CSF and brain Abeta l

86 n-induced increase in the expression of pS2, cathepsin D, and progesterone receptor, three widely kno

87 d marked increases in the lysosomal protease cathepsin D, and reduces the expression of the cathepsin

88 urthermore, we find that PGRN interacts with cathepsin D, and that PGRN increases the activity of cat

89 osome in that they were devoid of LAMP-1 and cathepsin D, and they were colocalized with the endoplas

90 Proteolytic activities of aspartyl cathepsin D, and thiol cathepsins B and L were decreased

91 dditionally, protein levels of Aogen, renin, cathepsin D, angiotensin-converting enzyme, and AT(1) we

92 Phylogenetically, schistosome cathepsin D appeared to be more closely related to mamma

93 Elevated levels of the lysosomal enzyme cathepsin D are found in the early stages of Alzheimer's

94 d by using immunofluorescence microscopy and cathepsin D as a marker for lysosomes.

95 Using cathepsin D as a model target protease, we synthesized a

96 clusion, proteomic blood profiling indicated cathepsin D as a new IR biomarker and suggested a causal

97 Using the cDNA encoding S. mansoni cathepsin D as a probe, we isolated several positive bac

98 r the lysosomal proteins Lamp-1, Lamp-2, and cathepsin D as well as for G(M3) ganglioside.

99 (asp-1) and cDNA that encode a homologue of cathepsin D aspartic protease were cloned and characteri

100 g phoP mutant Y. pseudotuberculosis acquired cathepsin D at a higher rate than phagosomes containing

101 kers Rab7 and CD63, and the lysosomal marker cathepsin D at early (8 h) and late (72 h) time points p

102 s were studied for c-erbB-2, TGF-alpha, p53, cathepsin D, bcl-2, and estrogen and progesterone recept

103 ression of epidermal growth factor receptor, cathepsin D, bcl-2, p27, p53, or cyclin D.

104 By 2 h postinfection, however, the number of cathepsin D(+) BCP was significantly lower for live B. a

105 umbers, expression of lysosomal cathepsin B, cathepsin D, Beclin-1, and microtubule-associated protei

106 ically, we show that, in cells lacking WASH, cathepsin D becomes trapped in a late endosomal compartm

107 er, S100A6, as well as the aspartic protease cathepsin D, both of which are involved in cellular inva

108 n D, and that PGRN increases the activity of cathepsin D but not cathepsins B or L.

109 ed compounds inhibited the aspartyl protease cathepsin D but not the cysteine protease calpain, corro

110 ion increased levels of the lysosomal enzyme cathepsin D by an autophagy-dependent pathway.

111 Reduction of lysosomal aspartic protease cathepsin D by prior treatment with cathepsin D-specific

112 uppression of proapoptotic lysosomal protein cathepsin D by promotion of the ER-associated degradatio

113 suggest that increased release/activation of cathepsin D can trigger neurodegeneration and possibly d

114 pplied to related aspartyl proteases such as cathepsin D (Cat D) and BACE-2.

115 ion of vacuolar proton ATPase (v-ATPase) and cathepsin D (Cat D) using Western blot analysis and immu

116 a clickable photoaffinity probe to identify cathepsin D (CatD) as a principal off-target of BACE1 in

117 In an attempt to increase selectivity vs Cathepsin D (CatD) in our BACE1 program, a series of 1,3

118 iated partly via suppression of proapoptotic cathepsin D (CatD) via cocomplexing of the endoplasmic r

119 for a combinatorial library of inhibitors of cathepsin D (CatD), an aspartyl protease.

120 a reduction in the plasma lysosomal enzyme, cathepsin D (CatD), in children with NASH compared to ch

121 d high selectivity (>2000-fold) for BACE1 vs Cathepsin D (CatD).

122 y and gaining much improved selectivity over cathepsin-D (CatD).

123 were determined spectrophotometrically, and cathepsin D (CD) by liquid scintillation counting using

124 Cathepsin D (CD) is a major lysosomal protease, and muta

125 e have previously demonstrated the effect of cathepsin D (CD) on the mechanical disruption of retinal

126 cause INCL, those in the CLN10 gene encoding cathepsin D (CD) underlie CNCL.

127 liquid chromatography-mass spectrometry, and cathepsin D (CD) was identified as a major secreted prod

128 O), beta-N-acetyl-hexosaminidase (beta-NAH), cathepsin D (CD), and elastase-alpha-1-proteinase inhibi

129 Cathepsin D (CD), the major intracellular aspartyl prote

130 er, the main caspase-8 fragment generated by cathepsin D cleavage could be affinity-labeled with the

131 e H2A N-terminal sequence, intervened by the cathepsin D cleavage site.

132 agments as entire lysosomes, suggesting that cathepsin D cleavages are required to initiate alpha3(IV

133 flammatory or ischemic conditions, alongside cathepsin D-cleaved 20-kDa IL-1beta produced under acidi

134 Additionally, cathepsin D-cleaved 20-kDa IL-1beta was minimally active

135 athepsin D, resulting in lower intracellular cathepsin D content and impairment of prosaposin activat

136 y characterized as a unique hemoglobinolytic cathepsin D contributing to the complex intestinal prote

137 Our findings suggest that upregulation of cathepsin D could be an additional therapeutic strategy

138 3 (LGALS3), a pro-inflammatory molecule, and cathepsin D (CTSD), a lysosomal aspartic protease.

139 ological inhibitors of a lysosomal protease, cathepsin D (CTSD), abrogated pyocyanin-induced apoptosi

140 Within lysosomes, cathepsin D (CtsD), an aspartyl protease, is suggested t

141 Lysosomal proteases, particularly Cathepsin D (CtsD), play multiple roles in apoptosis how

142 B regulation by another lysosomal hydrolase, cathepsin D (CTSD), using mice with a complete (CTSD(-/-

143 radiol-responsive ER target genes, including cathepsin-D (CTSD).

144 In particular, the level of mature cathepsin D (CTSDmat) dramatically changed depending upo

145 lysis of nucleotide-free DnaK at pH 4.0 with cathepsin D cuts near the linker region, yielding both f

146 practice: DNA/ploidy by flow cytometry, p53, cathepsin D, cyclin E, proteomics, certain multiparamete

147 Third, murine cathepsin-D deficiencies fail to develop protective immu

148 of dendritic cells from wild-type as well as cathepsin D-deficient mice to present intact OVA, but no

149 were similar to those seen in three week-old cathepsin D-deficient mice.

150 cathepsin D or lysosomes, demonstrated that cathepsin D degraded alpha-synuclein very efficiently, a

151 er of the endocytic proteases cathepsin L or cathepsin D demonstrated that an isolated tyrosine-to-hi

152 t correlation between high susceptibility to Cathepsin D digestion and the capacity to stimulate prim

153 ld-type or increased sensitivity to in vitro cathepsin D digestion.

154 Finally, knockdown of cathepsin D diminishes the potency of this combination,

155 inished activity of the lysosomal hydrolase, cathepsin D, due to defective processing.

156 but was found to colocalize with LAMP-1 and cathepsin D during early stages of axonal spread.

157 h molecular weights and pI values typical of cathepsin D, E and pepsin.

158 This inhibitor was shown to block cathepsin D/E activity in cell-free assays and within de

159 ated by pepstatin A, a specific inhibitor of cathepsin D/E, even though lysosomal extracts contain a

160 B/L-like enzymes increased and activities of cathepsin D/E- and collagenase-like enzymes decreased wi

161 It could be partially inhibited by blocking cathepsin D enzyme activity and required the presence of

162 Hip1R silencing and actin poisons slowed cathepsin D exit from the TGN.

163 16 cells established that lucanthone induced cathepsin D expression and reduced cancer cell viability

164 as at least partially due to the increase in cathepsin D expression.

165 and down-regulating elevated lipocalin-2 and cathepsin D expression.

166 Cathepsin-D expression was also elevated at Day 1 (P<0.0

167 tion, and DNA fragmentation, but calpain and cathepsin D failed to initiate these events.

168 ctional diversity of multiple Ixodes ricinus cathepsin D forms (IrCDs).

169 on disrupts the CCV-dependent trafficking of cathepsin D from the trans-Golgi network to lysosomes an

170 We also showed that extracellular cathepsin D from U18666A-treated neurons or application

171 g these proteins, annexin A4, cyclophilin A, cathepsin D, galectin-1, 14-3-3zeta, alpha-enolase, pero

172 of a missense polymorphism in exon 2 of the cathepsin D gene (CTSD) and Alzheimer disease (AD).

173 e, structure and genomic organization of the cathepsin D gene locus of Schistosoma mansoni.

174 ncing of BAC clone 25-J-24 revealed that the cathepsin D gene locus was approximately 13 kb in length

175 egion of residues -145 to -119 (CD/L) of the cathepsin D gene promoter contains a GC-rich motif that

176 Purified cathepsin D generated the same major alpha3(IV)NC1 fragm

177 Cathepsin D generates an antiangiogenic cleavage product

178 igh selectivity over BACE 2 (>7000-fold) and cathepsin D (>250000-fold).

179 Although inhibition of parasite cathepsin D had a greater effect on primary cleavage of

180 Human cathepsin D (hCatD) is an aspartic peptidase with a low

181 binding to PfPM1 versus the homologous human cathepsin D (hcatD).

182 ochemical studies that demonstrated abundant cathepsin D immunoreactivity in the same population of t

183 Regional brain patterns of cathepsin D immunostaining were compared in dogs ages 0.

184 ptake of dead cells, and that proteolysis by cathepsin D in an acidic endosomal compartment is essent

185 ponse to the toxin, because the cells lacked cathepsin D in autophagosomes.

186 istant GAK restores the lysosomal sorting of cathepsin D in cells depleted of endogenous GAK, whereas

187 Knockdown of cathepsin D in cells overexpressing wild-type alpha-synu

188 Missorting of cathepsin D in GARP-depleted cells results from accumula

189 d in vitro internalized the lysosomal enzyme cathepsin D in proportion to the polyglutamine-length in

190 gosomes, it is not processed into the 46-kDa cathepsin D in the absence of SHP-1, suggesting a defect

191 Ang I) was generated from angiotensinogen by cathepsin D in the presence of normal glucose or HG.

192 ed neurons, we evaluated the significance of cathepsin D in toxicity induced by U18666A, a class II a

193 it appears that the connection of STAT-1 and cathepsin-D in a single compartment is relevant for prot

194 gen-responsive reporter genes/gene products (cathepsin D) in MCF-7 breast cancer cells.

195 sequence, structure and complexity to human cathepsin D, including to a greater or lesser extent the

196 e is evidence that the level and activity of cathepsin D increased markedly in vulnerable neurons in

197 ht stress activated caspases, calpain 2, and cathepsin D independently and led to the demise of the c

198 Immunoprecipitation of metabolically labeled cathepsin D indicated reduced intracellular retention an

199 The cathepsin D inhibitor pepstatin A suppressed in vitro cl

200 NLRP3 and caspase-1 but was inhibited by the cathepsin D inhibitor pepstatin A.

201 The cathepsin D inhibitor, pepstatin A, partially protected

202 membrane permeabilization and the release of cathepsin D into the cytosol, leading to TM cell death.

203 mal membrane, with the subsequent release of cathepsin D into the cytosol.

204 The cathepsin D intra-chain proteolysis greatly stabilized t

205 r, these features indicated that schistosome cathepsin D is a platyhelminth orthologue of mammalian l

206 Our data therefore indicate that cathepsin D is able to initiate the caspase cascade by d

207 Cathepsin D is an aspartyl protease that plays a crucial

208 sion and metastasis, and aspartyl proteinase cathepsin D is implicated as a major contributor to this

209 ynuclein degrading activity, indicating that cathepsin D is the main lysosomal enzyme involved in alp

210 As cathepsin D is ubiquitously expressed, this may represen

211 echniques for many of the markers, including cathepsin-D, Ki-67, HER2/neu, and p53, limited their cur

212 Of these, tumor size, tumor grade, cathepsin-D, Ki-67, S-phase fraction, mitotic index, and

213 follow-up periods, tumor size, tumor grade, cathepsin-D, Ki-67, S-phase fraction, mitotic index, and

214 Furthermore, lysosomes isolated from cathepsin D knockdown cells showed a marked reduction in

215 tes shown to contain denatured myelin within cathepsin-D-labeled endosomes, but NG2 progenitors born

216 B. abortus 2308 persisted within these cathepsin D(-), LAMP-1(+), and acidic vesicles; however,

217 Additionally, down-regulation of cathepsin D level prevented, whereas overexpression of t

218 Thus, targeting cathepsin D level/activity may provide a new therapeutic

219 regulation of LC3-I to LC3-II conversion and cathepsin D levels was reduced by a thrombin inhibitor,

220 bin increased conversion of LC3-I to LC3-II, cathepsin D levels, and formation of autophagic vacuoles

221 Inhibition of aspartic cathepsin D-like peptidases (APDs) has been often discus

222 lobin from ingested human blood, including a cathepsin D-like, aspartic protease that is overexpresse

223 1 regulates the expression of genes encoding cathepsin D; matrix metalloproteinase 2; urokinase plasm

224 In cells with reduced expression of ArfGAP3, Cathepsin D maturation was slowed and its secretion was

225 mitogenic secreted proenzyme (pCatD) form of cathepsin D (mature CatD), a proapoptotic lysosomal aspa

226 ction in STAT3 and a concomitant increase in cathepsin D may be a cause of this disease.

227 ed processing of mutant htt by autophagy and cathepsin D may contribute to HD pathogenesis.

228 This conditioned matrix was used to examine cathepsin D-mediated collagen degradation by human breas

229 cells and thus could play a critical role in cathepsin D-mediated matrix degradation and remodeling o

230 ific mutants of caspase-8, we show that both cathepsin D-mediated proteolysis and homodimerization of

231 I antigen-loading competent compartments for cathepsin-D-mediated LLO processing.

232 th mutations that enhance GGA binding sorted cathepsin D more efficiently than wild-type CD-MPR.

233 ed toxicity is accompanied by an increase in cathepsin D mRNA and enzyme activity but a decrease in t

234 Because cathepsin D mRNA was upregulated in NFT-bearing CA1 neur

235 ase in progesterone receptor (PgR), pS2, and cathepsin D mRNAs that were blocked by the antiestrogen

236 nd D and two proteins known to interact with cathepsin D, NPC1 and ABCA1.

237 ts, these findings indicated that changes in cathepsin D observed in AD, in particular in the tempora

238 Increases in cathepsin D occurred first in neurons and later in astro

239 tion, the susceptibilities to degradation by cathepsin D of MBP Cit6 and MBP-C1, both from normal and

240 The cytosolic level of cathepsin D, on the other hand, was increased along with

241 ny detectable reduction in the expression of cathepsin D or in acid protease activity.

242 s alpha-synuclein as substrates and purified cathepsin D or lysosomes, demonstrated that cathepsin D

243 membrane glycoproteins and does not acquire cathepsin D or markers of secondary lysosomes.

244 cathepsin B and beta-hexosaminidase but not cathepsins D or L.

245 the aspartyl proteases porcine pepsin, human cathepsin D, plasmepsin 2 from P. falciparum, HIV-1 prot

246 lysosomal pathway, in which cathepsin B and cathepsin D play redundant roles.

247 Cathepsin D plays a role in endothelial-pericyte interac

248 umulated phagosomes are frequently docked to cathepsin D-positive lysosomes, without mixing of phagos

249 llular growth, and appeared to be trapped in cathepsin D-positive phagolysosomes.

250 of intracellular killing and trafficking to cathepsin D-positive vacuoles were significantly higher.

251 decreased phagocytosis activity, interrupted cathepsin D processing, and reduced cathepsin D activity

252 by proteolytic enzymes, such as cathepsin B, cathepsin D, prolidase, and plasmin.

253 of Gibberellic Acid Insensitive (SlGAI) and Cathepsin D Proteinase Inhibitor (SlPI) differed signifi

254 y binding and by a reduction in the level of cathepsin D proteolysis of F42 and F43.

255 his functional relationship between PGRN and cathepsin D provides a possible explanation for overlapp

256 lial growth factor), and proteolysis (MMP26; cathepsin D; PRSS3 (protease serine 3)).

257 Accordingly, knockdown of cathepsin D reduced lucanthone-mediated apoptosis.

258 ibiting the vesicular trafficking pathway or cathepsin D release from the lysosome resulted in signif

259 ructurally related aspartyl proteases BACE2, cathepsin D, renin, and pepsin.

260 t of D-EA virions, but not T3D virions, with cathepsin D resulted in proteolysis of sigma3, a propert

261 d reduced binding capacity for extracellular cathepsin D, resulting in lower intracellular cathepsin

262 owing on collagen I gels or plastic, nor was cathepsin D secreted from these cells.

263 groups in order to optimize BACE1 affinity, cathepsin D selectivity, and blood-brain barrier (BBB) p

264 on protein, antithrombin III and a protease, cathepsin D, showcases how a comprehensive study followe

265 6-phosphate receptors to the TGN and impairs cathepsin D sorting.

266 protease cathepsin D by prior treatment with cathepsin D-specific antisense ON did not attenuate the

267 At acidic pH, cathepsin D specifically cleaved caspase-8 but not the i

268 thepsin D, and reduces the expression of the cathepsin-D substrate thioredoxin.

269 ared to be more closely related to mammalian cathepsin D than to other sub-families of eukaryotic asp

270 5-fold selectivity toward plasmepsin II over cathepsin D, the most closely related human protease, go

271 However, delivery of newly synthesized cathepsin D to lysosomes was slowed in cells expressing

272 y cooperates with the GGAs in the sorting of cathepsin D to lysosomes, probably by enabling the movem

273 rticipates in the transport of extracellular cathepsin D to the lysosome for prosaposin activation.

274 ion of a representative lysosomal hydrolase, cathepsin D, to early endosomal compartments.

275 ting of the precursor of the acid hydrolase, cathepsin D, to lysosomes and leads to its secretion int

276 i impairs the sorting of the acid hydrolase, cathepsin D, to lysosomes.

277 ss of 57 kDa, was purified 200-fold over the cathepsin D-treated plasma membranes.

278 Released proteases such as cathepsin D trigger the apoptotic program by activating

279 disulfide isomerase, heat shock protein 27, cathepsin D, triose-phosphate isomerase, peroxiredoxin 6

280 dy resisted protease treatment and contained cathepsin D, ubiquitin, and heat shock protein (HSP) 40.

281 Selectivity against BACE2 and cathepsin D was 14 and >1000-fold, respectively.

282 Expression of the proteases kallikrein 5 and cathepsin D was dramatically reduced in both HI epidermi

283 ysine residues in mannose phosphorylation of cathepsin D was explored by site-directed mutagenesis.

284 oteins, and the late endosomal processing of cathepsin D was impaired.

285 nd BiP, while colocalization with LAMP-1 and cathepsin D was not affected.

286 A direct and fast activation of caspase-8 by cathepsin D was shown to be crucial in the initial steps

287 The genomic organization of schistosome cathepsin D was similar in sequence, structure and compl

288 nant human caspase-8 protein, pre-cleaved by cathepsin D, was followed by caspase-3 activation.

289 ading proteases insulin-degrading enzyme and cathepsin D were impaired; hence insulin receptor activi

290 more N-terminal htt fragments and cells with cathepsin D were more efficient in degrading wt htt than

291 ein-2, and increased maturation of lysosomal cathepsin D were observed in cirrhotic livers.

292 Brain levels of lysosomal cathepsin D were significantly higher in mutant than in

293 chain 3(LC3) from the LC3-I form to LC3-II, cathepsin D Western blotting and monodansylcadaverine (M

294 secretory granules containing serotonin and cathepsin D, whereas regulated exocytosis of secretory g

295 were correlated with a marker of senescence (cathepsin D), which was also strongly correlated with pr

296 mal membrane permeabilization and release of cathepsin D, which contributes to cell death.

297 t lucanthone stimulated a large induction in cathepsin D, which correlated with cell death.

298 to higher density fractions containing more cathepsin D without any detectable reduction in the expr

299 he present study tested whether increases in cathepsin D would emerge during aging in another mammali

300 lysis of nucleotide-free DnaK at pH 4.5 with cathepsin D yields detectable fragments (masses > 20 kDa