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1 tivity, including its processing by cysteine cathepsins.
6 h levels of ET-1 in the SVZ of patients with Cathepsin A-related arteriopathy with strokes and leukoe
7 st cytoplasm is sufficient to trigger active cathepsin accumulation in the host nucleus and cathepsin
10 ssion, thus revealing an unexpected role for cathepsin activity in non-canonical inflammasome regulat
13 rrowed down based on their ability to rescue cathepsin activity, a critical biochemical readout of ly
14 bolome, intracellular calcium, extracellular cathepsin activity, and cell migration and invasion anal
17 n aspartic protease in Alzheimer's disease), cathepsin B (a cysteine protease in cancer), and Alp2 (a
22 e intracellular activation of trypsinogen by cathepsin B (CTSB), which can be induced directly via G
26 as not altered in the cathepsin B mutant and cathepsin B activation was independent of vacuolar proce
28 suring conditions, the limit of detection of cathepsin B activity and concentration can reach 2.49 x
31 e-dependent increase in pH and a decrease in cathepsin B activity associated with bacterial survival.
32 rode array for rapid, multiplex detection of cathepsin B activity based on a simple electrochemical m
33 reactive oxygen species (ROS) production and cathepsin B activity, accompanied by an up-regulation of
39 ion were used to investigate the function of cathepsin B and PBA1 in ER-stress-induced PCD (ERSID).
40 lant proteases with caspase-3-like activity, cathepsin B and proteasome subunit PBA1, remains to be e
45 myelin build-up induces lysosomal damage and cathepsin B extracellular release by lysosomal exocytosi
46 uggest that activity-dependent exocytosis of Cathepsin B from lysosomes regulates the long-term struc
47 nterruption of either CCL2-CCR2 signaling or cathepsin B function significantly impaired PNI in vivo
52 ified the activity of the lysosomal protease cathepsin B in macrophages as a rate-limiting factor in
54 containing antimicrobial peptides linked to cathepsin B in the lysosomes (MACs) can be applied for t
55 ion of CTSB, as well as stronger staining of cathepsin B in the stratum granulosum of affected indivi
57 of these organelles resulting in leakage of cathepsin B into the cytosol leading to acinar cell deat
63 Tonoplast rupture was not altered in the cathepsin B mutant and cathepsin B activation was indepe
64 Simultaneous detection of the proteolysis of cathepsin B on the microelectrode array functionalized w
66 ategies for these ADCs involve cleavage with cathepsin B or papain to release and measure the antibod
71 tion of either lysosomal Ca(2+) signaling or Cathepsin B release prevented the maintenance of dendrit
73 Knock down of Beclin1, ATG16L1, Rubicon or cathepsin B significantly lowered the ability of neratin
74 CXCL13 solubilization requires the protease cathepsin B that cleaves CXCL13 into a stable product.
76 biquitin, p62/sequestosome1, cathepsin D and cathepsin B were detected with co-localizations of ubiqu
81 sponse of the formulation to the presence of cathepsin B, a proteolytic enzyme that is overexpressed
83 ike receptor protein 3 (NLRP3) inflammasome, cathepsin B, and caspase-1 and may play a role in the pa
84 ysteine protease CPR-4, a homologue of human cathepsin B, as the first RIBE factor in nematodes, to o
85 IHC showed that glomerular tuft staining for cathepsin B, cathepsin C, and annexin A3 in cFSGS was si
88 vealed an inflammatory infiltrate expressing cathepsin B, independent of the presence of pancreatic f
90 hepsin B, and IL-6 concentrations as well as cathepsin B, myeloperoxidase and trypsin activities were
91 rogrammed cell death through upregulation of cathepsin B, Tnf and Bid in a neutrophil-independent man
92 ppressed vesicle formation and knock down of cathepsin B-AIF significantly reduced neratinib lethalit
94 studies in human specimens demonstrated that cathepsin B-producing macrophages were enriched in invad
96 conjugated ex vivo to Cys34 of albumin via a cathepsin B-sensitive dipeptide linker to ensure that al
105 y increasing cathepsin D activity, levels of cathepsins B and D and two proteins known to interact wi
108 ated that it was a potent inhibitor of human cathepsins B, K, and L ( Ki = 6.87, 0.49, and 0.34 nM, r
109 derate to excellent selectivity versus human cathepsins B, L, and S and showed no apparent toxicity t
110 current study found that a cysteine protease Cathepsin B3 (CathB3), and the associated gene CathB3, w
113 at glomerular tuft staining for cathepsin B, cathepsin C, and annexin A3 in cFSGS was significantly g
115 Cysteine cathepsins are proteases capable of cathepsin cannibalism, where one cathepsin hydrolyzes an
116 ble inhibitors (E-64 derivative) of cysteine cathepsins (CCs) as trapping agents to increase the tumo
117 s with self-immolative hydrolytic linkers or cathepsin-cleavable valine-citrulline peptide linkers.
120 ojection neurons contain lysosomal hydrolase cathepsin D (CatD), a marker of neurons vulnerable to NF
122 e have previously demonstrated the effect of cathepsin D (CD) on the mechanical disruption of retinal
123 B regulation by another lysosomal hydrolase, cathepsin D (CTSD), using mice with a complete (CTSD(-/-
124 uniting three major lysosomal proteins: (i) cathepsin D (CTSD), which plays a major role in alpha-sy
127 associated degradation (ERAD) of nascent pro-cathepsin D (pCatD) and consequent suppression of lysoso
128 lysosomal proteolytic activity by increasing cathepsin D activity, levels of cathepsins B and D and t
130 proteins LC3B, ubiquitin, p62/sequestosome1, cathepsin D and cathepsin B were detected with co-locali
131 ically interacts with the lysosomal protease cathepsin D and is required to maintain proper cathepsin
132 proteases, including multiple forms of MMPs, cathepsin D and K, kallikrein 4 and proprotein convertas
134 slowed LC3 turnover and the inactivation of cathepsin D and other lysosomal hydrolases known to be u
135 ng activity from human saliva, we identified cathepsin D as a protease that can activate VEGF-C as we
137 uppression of proapoptotic lysosomal protein cathepsin D by promotion of the ER-associated degradatio
140 Mechanistically the availability of active cathepsin D mediates the effect of VPS35 on pathological
141 his functional relationship between PGRN and cathepsin D provides a possible explanation for overlapp
142 (matrix metalloproteinase 9, S100A8/S100A9, cathepsin D, and galectin-3-binding protein) improved ri
143 urthermore, we find that PGRN interacts with cathepsin D, and that PGRN increases the activity of cat
144 ation with incident diabetes and 3 proteins (Cathepsin D, Galectin-4, Paraoxonase type 3) with a nove
150 Increased concentrations of caspase-3 and cathepsin-D proteases and components of the 26S proteaso
151 sion with siRNA or BACE1 inhibition reversed cathepsin deficits in both fibroblasts and neurons.
153 c Atg5 knockout were similarly sensitized to cathepsin-dependent hepatocellular injury and death from
155 me through a reactive oxygen species- and/or cathepsin-dependent mechanism that was independent of ca
157 utrophil proteases such as elastase (NE) and cathepsin G (CG) attach to NETs and contribute to the di
159 mice lacking the neutrophil serine protease cathepsin G (CG)-induced hapten-reactive CD4 and CD8 T c
160 ted than in uninfected B cells, induction of cathepsin G activity by EBV led to total degradation of
162 1 interferon-associated genes, but increased cathepsin G and matrix metallopeptidase 9 expression.
165 a promising lead for further development of cathepsin G inhibitors targeting chronic inflammatory di
166 peptides MOG35-55 and MOG1-20 Inhibition of cathepsin G or citrullination of the arginine residue wi
169 vels of elastin degraded by proteinase 3 and cathepsin G were independently associated with mortality
171 rine protease activity in BALF (elastase and cathepsin G), plasma elastase footprint (Aalpha-Val(360)
172 ses polymorphonuclear (neutrophil) elastase, cathepsin G, and proteinase 3, but not neutrophil motili
173 ntified by mass spectroscopy, five proteins, cathepsin G, glutaredoxin-1, thioredoxin, GP1b, and fibr
174 ial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured u
175 ducts generated by the enzymes proteinase 3, cathepsin G, neutrophil elastase, MMP7 or MMP9/12 were p
177 rmolecular interactions formed by EapH1 with cathepsin-G differed considerably from that with neutrop
178 ealed a protease-binding mode for EapH1 with cathepsin-G that was globally similar to that seen in th
181 the physical basis for EapH1's inhibition of cathepsin-G, we crystallized EapH1 bound to this proteas
186 oncogene homolog 1 (AKT1), and the protease cathepsin H (CTSH), for which we establish a role in fil
187 capable of cathepsin cannibalism, where one cathepsin hydrolyzes another with substrate present, and
188 EBOV, the GP1 domain is cleaved by cellular cathepsins in acidic endosomes, removing the glycan cap
189 ripts increases the translation of lysosomal cathepsins in dendritic cells, and inhibition of catheps
192 ced macrophage cell death not rescued by pan-cathepsin inhibition, and 3) show that NSA inhibits infl
193 hibition and nuclear targeting of a cellular cathepsin inhibitor (stefin B) suppressed S. enterica Ty
196 even when its cleavage was prevented with a cathepsin inhibitor, indicating that it is endocytic F t
197 is, in part, mediated by the collagenolytic cathepsin K (catK) and cathepsin L (catL), with a tempor
199 n osteoclasts for bone resorption, including cathepsin K (Ctsk), and lactation elevates their express
200 id phosphatase 5, tartrate resistant (Acp5), cathepsin K (Ctsk), and TNF superfamily member 11 (Tnfsf
203 oblast co-cultures, acidification paralleled cathepsin K activity, and both were reduced by sodium bi
204 sion of osteoclast specific markers, such as cathepsin K and integrin beta3 at mRNA and protein level
205 gy, glutathione levels and protein levels of cathepsin K and those associated with Ca(2+) handling, c
206 o that esterase activity will liberate 5 and cathepsin K cleavage of the Leu-Arg-PABA element will li
207 results in lower expression and activity of cathepsin K compared with resting unpolarized macrophage
209 itively correlated with TNF-alpha, IL-6, and cathepsin K expression and negatively correlated with Ru
210 ear factor of activated T cells type c-1 and cathepsin K expression is defective in these macrophages
212 e expression profiling in whole lung tissue, cathepsin K gene expression was 40-fold overexpressed in
219 disease and the lysosomal cysteine protease cathepsin K plays a critical role in cardiac pathophysio
220 , we tested the hypothesis that, knockout of cathepsin K protects against diabetes-associated cardiac
222 Interestingly, AAV-sh-Ac45 impaired mature cathepsin K secretion more significantly than that by AA
224 d tartrate-resistant acid phosphatase (TRAP)/cathepsin K(+) OCs expressing phosphorylated Janus kinas
225 , FGF18 (fibroblast growth factor 18), CTSK (cathepsin K), and IL11 (interleukin 11), have therapeuti
226 ted T-cells cytoplasmic 1, NF-kappaB ligand, cathepsin K, and serum tartrate-resistant acid phosphata
227 levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cell-specific transmembrane prote
228 oclast-promoting genes, including Dickkopf1, Cathepsin K, Nf-kbeta,; and Calcr, suggesting a role for
229 9c2 myoblasts, pharmacological inhibition of cathepsin K, or treatment with calcineurin inhibitor res
230 ption volume and examined periodontal tissue cathepsin K, Runx2, TNF-alpha, and IL-6 expression.
231 ia-derived IFN-gamma exhibited low levels of Cathepsin K, TRAP, RANK, and tumor necrosis factor recep
234 potent gallinamide analog yet tested against cathepsin L (10, K(i) = 0.0937 +/- 0.01 nM and k(inact)/
236 by the collagenolytic cathepsin K (catK) and cathepsin L (catL), with a temporal component to their a
239 vel substituents for the apolar S2 pocket of cathepsin L and was conducted entirely in a prospective
240 pe inhibitor family likely regulate parasite cathepsin L proteases and/or impairs host immune cell ac
241 of IL-10, whereas tumor necrosis factor and cathepsin L release was reduced, further confirming pola
242 rier function through influencing macrophage cathepsin L secretion, thus reducing activation of the g
243 tion by three classes of proteases: plasmin, cathepsin L, and matrix metalloproteinases (MMP-2 and MM
245 ontrary, DPDG1s/G2s displayed an increase in Cathepsin L, but down-regulation of dynamin expressions
247 of parasite cathepsins L and host lysosomal cathepsin L, S and K cysteine proteases (inhibition cons
248 pite close sequence homology to the protease cathepsin L, the silicateins seem to exhibit no signific
252 teases but are potent inhibitors of parasite cathepsins L and host lysosomal cathepsin L, S and K cys
253 as intracellular cysteine proteases, such as cathepsin-L, might be involved in the degradation of gas
254 ESM [endothelial cell-specific molecule]-1, cathepsin L1, osteopontin, and MCSF-1) was also identifi
255 ess involves crystal phagocytosis, lysosomal cathepsin leakage, and increased release of reactive oxy
256 type II cystatin gene cluster, mucin 5, and cathepsin loci, via enhancer regulation of cancer-associ
257 epsins in dendritic cells, and inhibition of cathepsins markedly enhances cross-presentation of wild-
259 ntify cooperative and conflicting actions of cathepsin mediated collagen matrix degradation by consid
260 CD74, which inhibits viral entry by blocking cathepsin-mediated processing of the Ebola glycoprotein.
264 interface of the S1 and S1' subsites of the cathepsin protease, and (b) Arg(19) which forms cation-p
265 immune cell activation by blocking lysosomal cathepsin proteases involved in antigen processing and p
266 oteolytically cleaved, a process mediated by cathepsin proteases, liberating the N-terminal DID to fu
269 egradation by different proteases, including cathepsin S (CatS) and the intramembrane protease signal
271 MHC II, IFN-gamma, IL-1beta, TNF-alpha, and cathepsin S (Ctss) mRNA transcripts, and greater nitroty
272 1) repressed expression of the gene encoding cathepsin S (Ctss), a cysteine protease that cleaves inv
278 olecule inhibitors and siRNA gene silencing, cathepsin S was identified as the major IL-36gamma-activ
280 thermostability while inhibiting cleavage by cathepsin S, an endosomal protease essential for antigen
282 mma-Ser18, identified as the main product of cathepsin S-dependent IL-36gamma cleavage, induced psori
285 activation of IL-36gamma and highlight that cathepsin S-mediated activation of IL-36gamma may be imp
286 to Galpha(q), Galpha(s), and beta-arrestins, cathepsin-S (CS) and neutrophil elastase (NE) cleave PAR
287 impairs lysosomal calcium refilling, causes cathepsins translocation, inhibition of autophagic flux
288 These findings reveal a novel function for a cathepsin-type protease in aphid saliva that elicits eff
289 A class I antibodies significantly increased cathepsin-V (CTSV) expression and galectin-1 expression
290 rmal controls, and urinary excretion of both cathepsins was significantly greater in cFSGS compared w
292 ificant causal effects of type 2 diabetes on cathepsin Z and rennin, both known to have roles in the
293 The results show for the first time that cathepsin Z could be a future diagnostic biomarker for o
297 his study was to investigate whether altered cathepsin Z mRNA levels are associated with osteoporosis
300 ce these cell lineages produce the protease, cathepsin Z, the aim of this study was to investigate wh