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1 mensional structure (i.e., pepsin, renin, or cathepsin D).
2 enhancement of potency and selectivity over cathepsin D.
3 ctively, and with >200-fold selectivity over cathepsin D.
4 pepstatin A, a pharmacological inhibitor of cathepsin D.
5 phagolysosomes enriched with both lamp-1 and cathepsin D.
6 mutations in PGRN or CTSD, the gene encoding cathepsin D.
7 ting of the precursor of the acid hydrolase, cathepsin D.
8 , approaching the level obtained with intact cathepsin D.
9 ning for LAMPs but little or no staining for 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 decreased activity of the lysosomal enzyme, cathepsin D.
19 fluorescent when the latter were released by cathepsin D.
20 d decreased activity of the lysosomal enzyme cathepsin D.
21 ase with some properties similar to those of cathepsin D.
22 itment of MLKL protein and the activation of cathepsin D.
23 olytic activation of the lysosomal hydrolase cathepsin D.
24 ation decreased access to the active site of cathepsin D.
25 t the structurally related aspartyl protease cathepsin D.
26 s to provide selectivity over memapsin 1 and 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
31 what has been shown in Alzheimer's disease, cathepsin D, a lysosomal hydrolase, was redistributed to
34 diates suppression of VKORC1v2-cointeracting cathepsin D, a stress-released proapoptotic protein nega
36 ophagic inhibitor that induces apoptosis via cathepsin D accumulation and enhances vorinostat-mediate
37 in the 5XFAD brains as indicated by reduced cathepsin D activity and decreased N-glycoyslation of th
39 psin D activity, and suggests that decreased cathepsin D activity due to loss of PGRN contributes to
40 errupted cathepsin D processing, and reduced cathepsin D activity in retinal pigment epithelial cells
42 identifies PGRN as an activator of lysosomal cathepsin D activity, and suggests that decreased cathep
43 lysosomal proteolytic activity by increasing cathepsin D activity, levels of cathepsins B and D and t
45 d in type IV-V subjects, but due to enhanced cathepsin-D activity, SC thickness did not increase.
46 The endosomes of cancer cells are rich in cathepsin D, allowing on-site degradation of TH and faci
47 epitope is highly susceptible to cleavage by cathepsin D, an aspartic endopeptidase found almost excl
49 hat in s-IBM, lysosomal enzyme activities of cathepsin D and B were decreased 60% (P < 0.01) and 40%
50 ression of estrogen-responsive genes such as cathepsin D and Bcl-2, which are involved in cell migrat
53 proteins LC3B, ubiquitin, p62/sequestosome1, cathepsin D and cathepsin B were detected with co-locali
54 ced the processing of the precursor forms of cathepsin D and cathepsin L to their mature, lysosomal f
55 aled the multifocal epithelial expression of cathepsin D and coexpression with IL-1alpha in BPH tissu
57 cumulation of S1P also impairs maturation of cathepsin D and degradation of Lamp-2, indicating a gene
58 against fluorogenic substrates specific for cathepsin D and E and inactive against substrates specif
60 2-vIL-6 interaction-dependent suppression of cathepsin D and have found that this novel activity of v
61 ense double-membrane-limited AVs, containing cathepsin D and incompletely degraded LC3-II in perikary
62 ically interacts with the lysosomal protease cathepsin D and is required to maintain proper cathepsin
63 proteases, including multiple forms of MMPs, cathepsin D and K, kallikrein 4 and proprotein convertas
66 slowed LC3 turnover and the inactivation of cathepsin D and other lysosomal hydrolases known to be u
67 hanced the expression of the ER target genes cathepsin D and pS2, which are regulated by direct DNA b
68 onacidified phagosome with LAMPs but without cathepsin D and that the phagosomal membrane subsequentl
70 ated the expression of the catalytic enzymes cathepsin D and zinc-alpha(2)-glycoprotein in normal ker
72 ohistochemical study with antibodies against cathepsin-D and beclin-1 showed numerous positive staine
73 bule-associated protein light chain-3 (LC3), cathepsin-D and beclin-1 were investigated by Western bl
74 uction significantly decreased activities of cathepsins D and B, increased levels of LC3-II, decrease
75 owed similar potency and selectivity against cathepsins D and E (IC(50)s of 7.27 nM and 354 pM, respe
81 ss of the progesterone receptor (PR), Bcl-2, cathepsin D, and cyclin D1 genes, but not the pS2 gene,
82 (matrix metalloproteinase 9, S100A8/S100A9, cathepsin D, and galectin-3-binding protein) improved ri
83 as documented by the acquisition of LAMP-2, cathepsin D, and lysosomal tracer Texas Red ovalbumin, a
84 1 over other key aspartyl proteases, notably cathepsin D, and profoundly lowers CSF and brain Abeta l
85 n-induced increase in the expression of pS2, cathepsin D, and progesterone receptor, three widely kno
86 d marked increases in the lysosomal protease cathepsin D, and reduces the expression of the cathepsin
87 urthermore, we find that PGRN interacts with cathepsin D, and that PGRN increases the activity of cat
88 dditionally, protein levels of Aogen, renin, cathepsin D, angiotensin-converting enzyme, and AT(1) we
93 clusion, proteomic blood profiling indicated cathepsin D as a new IR biomarker and suggested a causal
95 ng activity from human saliva, we identified cathepsin D as a protease that can activate VEGF-C as we
97 (asp-1) and cDNA that encode a homologue of cathepsin D aspartic protease were cloned and characteri
98 g phoP mutant Y. pseudotuberculosis acquired cathepsin D at a higher rate than phagosomes containing
99 kers Rab7 and CD63, and the lysosomal marker cathepsin D at early (8 h) and late (72 h) time points p
100 s were studied for c-erbB-2, TGF-alpha, p53, cathepsin D, bcl-2, and estrogen and progesterone recept
101 By 2 h postinfection, however, the number of cathepsin D(+) BCP was significantly lower for live B. a
102 umbers, expression of lysosomal cathepsin B, cathepsin D, Beclin-1, and microtubule-associated protei
103 ically, we show that, in cells lacking WASH, cathepsin D becomes trapped in a late endosomal compartm
104 er, S100A6, as well as the aspartic protease cathepsin D, both of which are involved in cellular inva
106 ed compounds inhibited the aspartyl protease cathepsin D but not the cysteine protease calpain, corro
108 Reduction of lysosomal aspartic protease cathepsin D by prior treatment with cathepsin D-specific
109 uppression of proapoptotic lysosomal protein cathepsin D by promotion of the ER-associated degradatio
110 suggest that increased release/activation of cathepsin D can trigger neurodegeneration and possibly d
112 ion of vacuolar proton ATPase (v-ATPase) and cathepsin D (Cat D) using Western blot analysis and immu
113 a clickable photoaffinity probe to identify cathepsin D (CatD) as a principal off-target of BACE1 in
114 In an attempt to increase selectivity vs Cathepsin D (CatD) in our BACE1 program, a series of 1,3
115 iated partly via suppression of proapoptotic cathepsin D (CatD) via cocomplexing of the endoplasmic r
116 ojection neurons contain lysosomal hydrolase cathepsin D (CatD), a marker of neurons vulnerable to NF
119 a reduction in the plasma lysosomal enzyme, cathepsin D (CatD), in children with NASH compared to ch
122 were determined spectrophotometrically, and cathepsin D (CD) by liquid scintillation counting using
124 e have previously demonstrated the effect of cathepsin D (CD) on the mechanical disruption of retinal
126 liquid chromatography-mass spectrometry, and cathepsin D (CD) was identified as a major secreted prod
127 O), beta-N-acetyl-hexosaminidase (beta-NAH), cathepsin D (CD), and elastase-alpha-1-proteinase inhibi
128 er, the main caspase-8 fragment generated by cathepsin D cleavage could be affinity-labeled with the
130 agments as entire lysosomes, suggesting that cathepsin D cleavages are required to initiate alpha3(IV
131 flammatory or ischemic conditions, alongside cathepsin D-cleaved 20-kDa IL-1beta produced under acidi
133 athepsin D, resulting in lower intracellular cathepsin D content and impairment of prosaposin activat
134 y characterized as a unique hemoglobinolytic cathepsin D contributing to the complex intestinal prote
135 Our findings suggest that upregulation of cathepsin D could be an additional therapeutic strategy
137 ological inhibitors of a lysosomal protease, cathepsin D (CTSD), abrogated pyocyanin-induced apoptosi
140 B regulation by another lysosomal hydrolase, cathepsin D (CTSD), using mice with a complete (CTSD(-/-
141 uniting three major lysosomal proteins: (i) cathepsin D (CTSD), which plays a major role in alpha-sy
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
148 of dendritic cells from wild-type as well as cathepsin D-deficient mice to present intact OVA, but no
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
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
163 16 cells established that lucanthone induced cathepsin D expression and reduced cancer cell viability
169 on disrupts the CCV-dependent trafficking of cathepsin D from the trans-Golgi network to lysosomes an
171 g these proteins, annexin A4, cyclophilin A, cathepsin D, galectin-1, 14-3-3zeta, alpha-enolase, pero
172 ation with incident diabetes and 3 proteins (Cathepsin D, Galectin-4, Paraoxonase type 3) with a nove
175 ncing of BAC clone 25-J-24 revealed that the cathepsin D gene locus was approximately 13 kb in length
182 ochemical studies that demonstrated abundant cathepsin D immunoreactivity in the same population of t
184 ptake of dead cells, and that proteolysis by cathepsin D in an acidic endosomal compartment is essent
186 istant GAK restores the lysosomal sorting of cathepsin D in cells depleted of endogenous GAK, whereas
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
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
202 membrane permeabilization and the release of cathepsin D into the cytosol, leading to TM cell death.
205 r, these features indicated that schistosome cathepsin D is a platyhelminth orthologue of mammalian l
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
211 echniques for many of the markers, including cathepsin-D, Ki-67, HER2/neu, and p53, limited their cur
213 follow-up periods, tumor size, tumor grade, cathepsin-D, Ki-67, S-phase fraction, mitotic index, and
215 tes shown to contain denatured myelin within cathepsin-D-labeled endosomes, but NG2 progenitors born
220 regulation of LC3-I to LC3-II conversion and cathepsin D levels was reduced by a thrombin inhibitor,
222 bin increased conversion of LC3-I to LC3-II, cathepsin D levels, and formation of autophagic vacuoles
224 lobin from ingested human blood, including a cathepsin D-like, aspartic protease that is overexpresse
225 1 regulates the expression of genes encoding cathepsin D; matrix metalloproteinase 2; urokinase plasm
226 In cells with reduced expression of ArfGAP3, Cathepsin D maturation was slowed and its secretion was
227 mitogenic secreted proenzyme (pCatD) form of cathepsin D (mature CatD), a proapoptotic lysosomal aspa
230 This conditioned matrix was used to examine cathepsin D-mediated collagen degradation by human breas
231 cells and thus could play a critical role in cathepsin D-mediated matrix degradation and remodeling o
232 ific mutants of caspase-8, we show that both cathepsin D-mediated proteolysis and homodimerization of
234 Mechanistically the availability of active cathepsin D mediates the effect of VPS35 on pathological
235 th mutations that enhance GGA binding sorted cathepsin D more efficiently than wild-type CD-MPR.
236 ed toxicity is accompanied by an increase in cathepsin D mRNA and enzyme activity but a decrease in t
238 ase in progesterone receptor (PgR), pS2, and cathepsin D mRNAs that were blocked by the antiestrogen
240 ts, these findings indicated that changes in cathepsin D observed in AD, in particular in the tempora
242 tion, the susceptibilities to degradation by cathepsin D of MBP Cit6 and MBP-C1, both from normal and
245 s alpha-synuclein as substrates and purified cathepsin D or lysosomes, demonstrated that cathepsin D
248 associated degradation (ERAD) of nascent pro-cathepsin D (pCatD) and consequent suppression of lysoso
249 the aspartyl proteases porcine pepsin, human cathepsin D, plasmepsin 2 from P. falciparum, HIV-1 prot
252 umulated phagosomes are frequently docked to cathepsin D-positive lysosomes, without mixing of phagos
254 of intracellular killing and trafficking to cathepsin D-positive vacuoles were significantly higher.
255 decreased phagocytosis activity, interrupted cathepsin D processing, and reduced cathepsin D activity
257 Increased concentrations of caspase-3 and cathepsin-D proteases and components of the 26S proteaso
258 of Gibberellic Acid Insensitive (SlGAI) and Cathepsin D Proteinase Inhibitor (SlPI) differed signifi
260 his functional relationship between PGRN and cathepsin D provides a possible explanation for overlapp
263 ibiting the vesicular trafficking pathway or cathepsin D release from the lysosome resulted in signif
265 t of D-EA virions, but not T3D virions, with cathepsin D resulted in proteolysis of sigma3, a propert
266 d reduced binding capacity for extracellular cathepsin D, resulting in lower intracellular cathepsin
268 groups in order to optimize BACE1 affinity, cathepsin D selectivity, and blood-brain barrier (BBB) p
269 on protein, antithrombin III and a protease, cathepsin D, showcases how a comprehensive study followe
271 protease cathepsin D by prior treatment with cathepsin D-specific antisense ON did not attenuate the
274 ared to be more closely related to mammalian cathepsin D than to other sub-families of eukaryotic asp
275 y cooperates with the GGAs in the sorting of cathepsin D to lysosomes, probably by enabling the movem
276 rticipates in the transport of extracellular cathepsin D to the lysosome for prosaposin activation.
278 ting of the precursor of the acid hydrolase, cathepsin D, to lysosomes and leads to its secretion int
282 disulfide isomerase, heat shock protein 27, cathepsin D, triose-phosphate isomerase, peroxiredoxin 6
283 dy resisted protease treatment and contained cathepsin D, ubiquitin, and heat shock protein (HSP) 40.
285 Expression of the proteases kallikrein 5 and cathepsin D was dramatically reduced in both HI epidermi
287 A direct and fast activation of caspase-8 by cathepsin D was shown to be crucial in the initial steps
288 The genomic organization of schistosome cathepsin D was similar in sequence, structure and compl
290 ading proteases insulin-degrading enzyme and cathepsin D were impaired; hence insulin receptor activi
291 more N-terminal htt fragments and cells with cathepsin D were more efficient in degrading wt htt than
294 chain 3(LC3) from the LC3-I form to LC3-II, cathepsin D Western blotting and monodansylcadaverine (M
295 secretory granules containing serotonin and cathepsin D, whereas regulated exocytosis of secretory g
296 were correlated with a marker of senescence (cathepsin D), which was also strongly correlated with pr
299 to higher density fractions containing more cathepsin D without any detectable reduction in the expr
300 he present study tested whether increases in cathepsin D would emerge during aging in another mammali
301 lysis of nucleotide-free DnaK at pH 4.5 with cathepsin D yields detectable fragments (masses > 20 kDa