ライフサイエンスコーパス: cathepsin

1 s is performed by pH-dependent endolysosomal cathepsins.

2 een implicated in cancer, including cysteine cathepsins.

3 ive against substrates specific for cysteine cathepsins.

4 has been reported about the role of cysteine cathepsins.

5 Cathepsin A (CatA) inhibitors attenuated L-ala,SP prodru

6 perone/transport protein, protective protein/cathepsin A.

7 escription drugs modifying the regulation of cathepsin activities and the MHC-peptidome may provide a

8 ed to HIV-infected persons variably modulate cathepsin activities in human APCs, dendritic cells and

9 ies production and pH, which led to enhanced cathepsin activities.

10 intensity of redness, but reduced muscle pH, cathepsin activity and fillet lightness.

11 imaging revealed a significant reduction in cathepsin activity in treated mice.

12 Modulation of cathepsin activity may prevent injury of organs exposed

13 f cystatin B in patient fibroblasts enhances cathepsin activity.

14 r entry and that they do so to access higher cathepsin activity.

15 mes add to the number of epitopes cleaved by cathepsins, altogether generating a wider peptide repert

16 U-Omp19 inhibits lysosome cathepsins and APC-derived microsome activity in vitro a

17 e nitric oxide synthase, annexins, galectin, cathepsins and heat shock proteins), whereas the anti-in

18 cathepsin hydrolytic activities: directly on cathepsins and indirectly on their regulators by inhibit

19 ion: the prolactins (two clusters), serpins, cathepsins, and the natural killer (NK)/C-type lectin (C

20 Cathepsins are most stable at acidic pH, although growin

21 Therefore, ABPs targeting the cysteine cathepsins are potentially valuable new reagents for rap

22 Cathepsin B (CatB) proteolytically degrades Abeta into n

23 dependent effects of simultaneously deleting cathepsin B (CtsB) and CtsS in a murine pancreatic neuro

24 Cathepsin B (CtsB) contributes to atherosclerosis and ca

25 The lysosomal hydrolase cathepsin B (CTSB) is a known activator of trypsinogen,

26 e intracellular activation of trypsinogen by cathepsin B (CTSB), which can be induced directly via G

27 as not altered in the cathepsin B mutant and cathepsin B activation was independent of vacuolar proce

28 ty of T-cytotoxic memory cells, which resist cathepsin B activation, may distinguish rejection-free a

29 Tc seemed resistant to cathepsin B activation; (3) with increasing rATG concent

30 e-dependent increase in pH and a decrease in cathepsin B activity associated with bacterial survival.

31 Mice and macrophages lacking cathepsin B activity had increased resistance to the cyt

32 on pathways was evaluated by studying pH and cathepsin B activity.

33 f inducible nitric oxide synthase (iNOS) and cathepsin B also reversed chlamydial killing.

34 Moreover, they are sensitive to proteases (cathepsin B and asparagine endopeptidase) that are over-

35 Co-expression of cathepsin B and cathepsin B-resistant mutant LFABP in Mc

36 phagic vacuoles and was blocked by lysosomal cathepsin B and L inhibition.

37 hese mice express greater amounts of hepatic cathepsin B and lower amounts of liver fatty acid-bindin

38 ERSID is regulated positively by cathepsin B and negatively by PBA1, revealing a complex

39 usion activity triggered by the host factors cathepsin B and Niemann-Pick C1.

40 ion were used to investigate the function of cathepsin B and PBA1 in ER-stress-induced PCD (ERSID).

41 lant proteases with caspase-3-like activity, cathepsin B and proteasome subunit PBA1, remains to be e

42 imal cerulein, and the cytosolic activity of cathepsin B and trypsin was evaluated.

43 cretion as compared with cells co-expressing cathepsin B and wildtype LFABP.

44 we identified a key cell-intrinsic role for cathepsin B as a negative feedback regulator of lysosoma

45 le of trypsin in AP and shows that cytosolic cathepsin B but not trypsin activates cell death pathway

46 Cytosolic cathepsin B but not trypsin activates the intrinsic path

47 Assembling a peptide-based Cathepsin B cleavable sensor over a large array of nano-

48 ic deletion or pharmacological inhibition of cathepsin B down-regulated mechanistic target of rapamyc

49 Cathepsin B downregulation reduced reactive oxygen speci

50 Surprisingly, suppression of cathepsin B expression via CRISPR-Cas9 gene deletion or

51 uggest that activity-dependent exocytosis of Cathepsin B from lysosomes regulates the long-term struc

52 nterruption of either CCL2-CCR2 signaling or cathepsin B function significantly impaired PNI in vivo

53 ediated knock-down of genes belonging to the cathepsin B gene family.

54 Knock-down of cathepsin B genes reduced aphid fitness, but only on the

55 Now, a chemiluminescent probe for cathepsin B has been developed that provides a 16,000-fo

56 ntial role of cytosolic trypsin vs cytosolic cathepsin B in activation of apoptosis.

57 ified the activity of the lysosomal protease cathepsin B in macrophages as a rate-limiting factor in

58 siRNA-mediated knockdown of cathepsin B in McA-RH7777 cells resulted in a 39% increa

59 f their possible target enzymes legumain and cathepsin B in MDA-MB-435S, A375, and C8161 melanoma cel

60 ntified a fundamental biological function of cathepsin B in providing a checkpoint for homeostatic ma

61 ion of CTSB, as well as stronger staining of cathepsin B in the stratum granulosum of affected indivi

62 Cathepsin B increased the activity of matrix metalloprot

63 escence, AlphaLISA, and enzymatic assays for cathepsin B inhibition.

64 Finally, excessive release of cathepsin B into the cytosol can lead to cell death thro

65 ite for AP only because it causes release of cathepsin B into the cytosol.

66 The cathepsin B knockdown and 24-h treatment with OA resulte

67 Cathepsin B knockdown was accompanied by a 74% increase

68 n vivo studies have suggested that during AP cathepsin B leaks into the cytosol from co-localized org

69 Cathepsin B may execute its function after tonoplast rup

70 Tonoplast rupture was not altered in the cathepsin B mutant and cathepsin B activation was indepe

71 Together, these data indicate that cathepsin B regulates VLDL secretion and free fatty acid

72 tion of either lysosomal Ca(2+) signaling or Cathepsin B release prevented the maintenance of dendrit

73 omal Zn, which activated lysosomal swelling, cathepsin B release, and LCD.

74 Overexpression of cathepsin B resulted in decreased OA uptake and VLDL sec

75 Co-localization of LFABP and cathepsin B was observed in a distinct Golgi apparatus-l

76 Transcript level and activity labelling of cathepsin B were used to assess activation.

77 ated with texture (r(2) = 0.4), as also were cathepsin B&L and sex.

78 cers were used in the design: a lysosomally (cathepsin B) cleavable tetrapeptide GFLG spacer conjugat

79 that multiple redundant cathepsins (not just cathepsin B) mediate this process by evaluating IL-1beta

80 re located upstream of CTSB, a gene encoding cathepsin B, a cysteine protease involved in keratinocyt

81 e VC(S) linker was designed to be cleaved by cathepsin B, a lysosomal cysteine protease.

82 inhibitor-binding site in cysteine protease cathepsin B, a potential drug target and prognostic mark

83 block proteolytic activities of host furin, cathepsin B, and caspases that mediate toxin's lethality

84 ysteine protease CPR-4, a homologue of human cathepsin B, as the first RIBE factor in nematodes, to o

85 tophagosome numbers, expression of lysosomal cathepsin B, cathepsin D, Beclin-1, and microtubule-asso

86 calcium binding protein A8 (S100A8), S100A9, cathepsin B, fibronectin, and galectin-3-binding protein

87 mice treated with a cathepsin inhibitor and cathepsin B-deficient mice suffer limited intestinal inj

88 f rats or mice (wild-type, trypsinogen 7, or cathepsin B-deleted) were stimulated with supramaximal c

89 trong association of acinar cell injury with cathepsin B-dependent intracellular activation of trypsi

90 Cathepsin B-mediated CD18 shedding regulates leukocyte r

91 ages and potentiate nerve invasion through a cathepsin B-mediated process.

92 studies in human specimens demonstrated that cathepsin B-producing macrophages were enriched in invad

93 Co-expression of cathepsin B and cathepsin B-resistant mutant LFABP in McA-RH7777 cells r

94 A cathepsin B-specific cleavable substrate (KGRR) conjugat

95 VPE activity was independent of cathepsin B.

96 Then, this caused degradation of CTSDmat by cathepsin B.

97 racellular sensing of the lysosomal protease cathepsin B.

98 -expression or pharmacological inhibition of cathepsin B.

99 plasma membrane, resulting in the release of Cathepsin B.

100 ing the derepression of the lysomal protease cathepsin B.

101 phagosomes and late endosomes to SiNP-filled cathepsin B/L-containing lysosomes rather than elevated

102 through impairing the proteolytic cascade of cathepsin B/urokinase-type plasminogen activator (uPA)/m

103 y increasing cathepsin D activity, levels of cathepsins B and D and two proteins known to interact wi

104 tides were released at the cleavage sites of cathepsins B and D, which thus play an important role.

105 Caco2 cells were also noted to produce cathepsins B and L, and inhibition of cathepsins suppres

106 ncreases the activity of cathepsin D but not cathepsins B or L.

107 on of cystatin B, an endogenous inhibitor of cathepsins B, H and L, on the development of NPC neuropa

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 nd non-ELR (CXCL9-12) chemokines by cysteine cathepsins B, K, L, and S at neutral pH by high resoluti

110 macrophages, singly or multiply deficient in cathepsins B, L, C, S and X.

111 and secreted proteins, including Tenascins, Cathepsin-B precursor, cystatin, and numerous Variant-sp

112 By contrast, cathepsin B3 protein and activity were upregulated by ER

113 s, we identified the lysosomal endopeptidase cathepsin Ba (ctsba) as the gene deficient in split top

114 The cysteine protease cathepsin C (CatC) activates granule-associated proinfla

115 60, which is currently in clinical trials as cathepsin C inhibitor for the treatment of cystic fibros

116 demonstrate that ABPs targeting the cysteine cathepsins can be used in murine models of atheroscleros

117 ivity-based probes (ABPs) targeting cysteine cathepsins can be used in murine models of atheroscleros

118 ayload release suggested that other cysteine cathepsins can cleave the VC(S) linker.

119 Thus, deletion of multiple cathepsins can lead to stage-dependent, compensatory mec

120 oprotein (GP) trimer, occludes access to the cathepsin-cleavage loop, and prevents the proteolytic cl

121 Lysosomal proteases such as cathepsins (Cts) regulate this process in other organs,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Cathepsin D plays a role in endothelial-pericyte interac

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

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

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

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

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

150 1 over other key aspartyl proteases, notably cathepsin D, and profoundly lowers CSF and brain Abeta l

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

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

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

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

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

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

157 decreased activity of the lysosomal enzyme, cathepsin D.

158 d decreased activity of the lysosomal enzyme cathepsin D.

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

160 olytic activation of the lysosomal hydrolase cathepsin D.

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

162 Cathepsin D: an Mvarphi-derived factor mediating increas

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

164 within the intestinal epithelial cells in a cathepsin-dependent manner.

165 t with lysosomal cell death (LCD), including cathepsin-driven caspase activation, and correlates with

166 mesothelin, gamma-glutamyltransferase 5, and cathepsin-E as the most interesting targets, because stu

167 rley plants silencing or over-expressing the cathepsin F-like HvPap-1 Cys protease show differential

168 , one of the proteinaceous inhibitors of the cathepsin F-like protease, also has important effects on

169 Here we establish the importance of the cathepsin G (CatG) in the context of arterial myeloid ce

170 Neutrophil serine proteases, such as cathepsin G (CG) and neutrophil elastase (NE), have been

171 mast cell chymase (HC) and human neutrophil cathepsin G (hCG) show relatively similar cleavage speci

172 ted than in uninfected B cells, induction of cathepsin G activity by EBV led to total degradation of

173 ypsin inhibitor-1 (SFTI-1) produced a potent cathepsin G inhibitor (Ki = 0.89 nM).

174 the most selective (>/=360-fold) engineered cathepsin G inhibitor reported to date.

175 a promising lead for further development of cathepsin G inhibitors targeting chronic inflammatory di

176 peptides MOG35-55 and MOG1-20 Inhibition of cathepsin G or citrullination of the arginine residue wi

177 The serine protease cathepsin G recapitulated the effects of MET-1 on DRG ne

178 Substituting preferred cathepsin G substrate sequences into sunflower trypsin i

179 ded substrate specificity (P4-P1) of the NSP cathepsin G using a peptide substrate library.

180 Cathepsin G's P2' preference was determined by screening

181 ntified by mass spectroscopy, five proteins, cathepsin G, glutaredoxin-1, thioredoxin, GP1b, and fibr

182 ial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured u

183 s to release the Ser proteases, elastase and cathepsin G, resulting in the proteolytic destruction of

184 adation by the endolysosomal serine protease cathepsin G.

185 oncogene homolog 1 (AKT1), and the protease cathepsin H (CTSH), for which we establish a role in fil

186 o HIV PIs acted in two complementary ways on cathepsin hydrolytic activities: directly on cathepsins

187 ta secretion, implicating roles for multiple cathepsins in both pro-IL-1beta synthesis and NLRP3 acti

188 Here we describe a novel role for cathepsins in CKD.

189 demonstrating non-invasive imaging of active cathepsins in fibrotic lesions of patients with IPF.

190 activity and selectively targets a subset of cathepsins in human cell proteomes.

191 cally from trypsin and chymotrypsin, and the cathepsins in the gut and saliva showed distinct propert

192 We show that cysteine cathepsins inactivate and in some cases degrade non-ELR

193 d retention of LDL, induction of endothelial cathepsins, increased endothelial permeability to LDL, a

194 osome maturation markers LAMP1 and lysosomal cathepsin, indicating delayed formation of a fully bioac

195 Finally, we found that mice treated with a cathepsin inhibitor and cathepsin B-deficient mice suffe

196 ioma cells was partly prevented by lysosomal cathepsin inhibitor E64 and antioxidant alpha-tocopherol

197 rotease inhibitor was more protective than a cathepsin inhibitor in SARS-CoV-infected mice.

198 (DAM), which encodes an endosomal/lysosomal cathepsin inhibitor named Cystatin F.

199 even when its cleavage was prevented with a cathepsin inhibitor, indicating that it is endocytic F t

200 Also, we evaluate endogenous cathepsin inhibitors cystatins C and B.

201 consideration of selective versus pan-family cathepsin inhibitors in cancer.

202 Finally, we find cathepsin inhibitors selectively block particle-induced

203 rate that both small molecule and endogenous cathepsin inhibitors suppress particle-induced IL-1beta

204 ar factor of activated T-cells, c1 (NFATc1), cathepsin K (Cstk), and tartrate-resistant acid phosphat

205 small molecule, odanacatib (ODN), which is a cathepsin K (Ctsk) inhibitor, was investigated to determ

206 Recent studies showed that cathepsin K (CTSK) might have functions in the immune sy

207 Our findings suggest that cathepsin K activity is dependent on LAM cell-fibroblast

208 In vitro, fibroblast extracellular cathepsin K activity was minimal at pH 7.5 but significa

209 oblast co-cultures, acidification paralleled cathepsin K activity, and both were reduced by sodium bi

210 gy, glutathione levels and protein levels of cathepsin K and those associated with Ca(2+) handling, c

211 provide a proof-of-concept for the use of a cathepsin K cleavable peptide-linked conjugate for targe

212 o that esterase activity will liberate 5 and cathepsin K cleavage of the Leu-Arg-PABA element will li

213 results in lower expression and activity of cathepsin K compared with resting unpolarized macrophage

214 ear factor of activated T cells type c-1 and cathepsin K expression is defective in these macrophages

215 Cathepsin K gene expression and protein and protease act

216 e expression profiling in whole lung tissue, cathepsin K gene expression was 40-fold overexpressed in

217 In lung nodules, cathepsin K immunoreactivity predominantly co-localized

218 In order to avoid previous problems of cathepsin K inhibitors associated with lysosomotropism o

219 Additionally, cathepsin K knockout mice attenuated cardiac oxidative s

220 Wild-type and cathepsin K knockout mice were rendered diabetic by stre

221 ocyte apoptosis, which were mitigated in the cathepsin K knockout mice.

222 Therefore, cathepsin K may represent a potential target in treating

223 disease and the lysosomal cysteine protease cathepsin K plays a critical role in cardiac pathophysio

224 , we tested the hypothesis that, knockout of cathepsin K protects against diabetes-associated cardiac

225 Immunohistochemistry confirmed cathepsin K protein was expressed in LAM but not control

226 fluorescence staining revealed a decrease in cathepsin K(+) and CD68(+) cells in anti-Netrin-1/anti-U

227 d increased both osteoclast activity (RankL, Cathepsin k) and osteoclast recruitment (Rank) in SCD mi

228 9c2 myoblasts, pharmacological inhibition of cathepsin K, or treatment with calcineurin inhibitor res

229 ia-derived IFN-gamma exhibited low levels of Cathepsin K, TRAP, RANK, and tumor necrosis factor recep

230 pounds exhibited reversible tight binding to cathepsin K, while the X-ray structural studies showed c

231 ydrase type II, but relatively low levels of cathepsin K.

232 uced the mRNAs encoding for RANKL, TRAP, and Cathepsin K.

233 Cathepsin L (Cat L) is a cysteine protease that can prot

234 The cysteine protease cathepsin L (CTSL) is often thought to act as a tumor pr

235 Cells and mice lacking cathepsin L accumulate full-length Ctr1 and hyper-accumu

236 ed in crowded and chilled salmon whereas the cathepsin L activity was found to be significantly affec

237 ty in vitro and partially inhibits lysosomal cathepsin L activity within live APCs.

238 p between the expression of cystatin E/M and cathepsin L and a direct relationship between the loss o

239 Mechanistically, both glomerular cathepsin L and heparanase expression were reduced.

240 vel substituents for the apolar S2 pocket of cathepsin L and was conducted entirely in a prospective

241 was a potent inhibitor of the major secreted cathepsin L cysteine proteases of F. hepatica, FhCL1 and

242 Deletion of CTSB reduced and deletion of cathepsin L increased intracellular trypsin activation.

243 The expressions of involucrin, loricrin, and cathepsin L is initially increased by day 19 but subsequ

244 of IL-10, whereas tumor necrosis factor and cathepsin L release was reduced, further confirming pola

245 rier function through influencing macrophage cathepsin L secretion, thus reducing activation of the g

246 In addition, cathepsin L was able to cleave the G protein in Vero cel

247 tion by three classes of proteases: plasmin, cathepsin L, and matrix metalloproteinases (MMP-2 and MM

248 pite close sequence homology to the protease cathepsin L, the silicateins seem to exhibit no signific

249 okinin (CCK) increased the activity of CTSB, cathepsin L, trypsin, chymotrypsin, and caspase 3 in viv

250 the major parasite-secreted proteases and/or cathepsin L-like proteases of its host.

251 evels, 53BP1 loss is caused by activation of cathepsin L-mediated degradation of 53BP1 protein.

252 lla spp. is a competitive inhibitor of human cathepsin L.

253 64), an inhibitor of thiol proteases such as cathepsin L.

254 Here, we identify the cathepsin L/B endolysosomal proteases functioning in a d

255 ate that the combination of cisplatin with a cathepsin L/B inhibitor enhances cisplatin uptake and ce

256 f F. hepatica, FhCL1 and FhCL2, and of human cathepsins L and K (Ki = 0.4-27 nm).

257 s selectivity toward FhCL1, FhCL2, and human cathepsins L and K.

258 Cathepsin-L, water soluble and total protein components

259 yolk platelet, leading to the activation of Cathepsin-like proteinases, but it is unknown how this p

260 Althoughthese substrates were cleaved by cathepsins, making them unsuitable for analysis of compl

261 containing protein with a CARD), caspase-1, cathepsin-mediated degradation, calcium mobilization, an

262 tered expression of endolysosomal proteases (cathepsins) mitigates the fast endolysosomal degradation

263 amine the hypothesis that multiple redundant cathepsins (not just cathepsin B) mediate this process b

264 selectivity versus related cysteine protease cathepsins, other proteases, and receptors.

265 mulation of Gallyas-positive aggregates, and cathepsin-positive vesicular clusters in axons in the sc

266 demonstrates the value of our complementary cathepsin probes and provides evidence for the existence

267 ur findings validate small molecule cysteine cathepsin probes for clinical PET imaging and suggest th

268 Lysosomal cathepsins regulate an exquisite range of biological fun

269 zed a pathogenic role in this dysfunction of cathepsin S (Cat-S), a cysteine protease that degrades e

270 egradation by different proteases, including cathepsin S (CatS) and the intramembrane protease signal

271 Cathepsin S (Ctss) is a cysteine protease that is active

272 1) repressed expression of the gene encoding cathepsin S (Ctss), a cysteine protease that cleaves inv

273 nt up-regulation of genes encoding proteases cathepsin S (CTSS), mast cell chymase (CMA1), tryptase (

274 trated that RO5444101 reduced immunoreactive cathepsin S (P < 0.05), elastin degradation (P = 0.01),

275 a specific fragment from the protease gene, cathepsin S (Rs-cps), was cloned into the binary vector

276 or the existence of specific localization of cathepsin S activity in dendritic cells.

277 e demonstrate that G-CSF injection increases Cathepsin S activity in spinal cord tissues.

278 Interestingly, cathepsin S activity was strongly up-regulated in sample

279 I and IL6, lesion matrix-degrading proteases cathepsin S and matrix metalloproteinase-9, and systemic

280 Systemic inhibition of cathepsin S attenuates the progression of atheroscleroti

281 The potent protease cathepsin S cleaves elastin and generates bioactive elas

282 We hypothesized that selective cathepsin S inhibition attenuates atherogenesis in hyper

283 Furthermore, cathepsin S inhibitor or siRNA significantly decreased e

284 6.6 or 60 mg/kg of the potent and selective cathepsin S inhibitor RO5444101 or a control diet.

285 Cathepsin S is one of the most important cysteine protei

286 Inhibition of cathepsin S molecules, blockade of costimulation through

287 olecule inhibitors and siRNA gene silencing, cathepsin S was identified as the major IL-36gamma-activ

288 ization of the probe with CD68, elastin, and cathepsin S, similar to that observed in the experimenta

289 teraction that responds to G-CSF by engaging Cathepsin S-CX3CR1-inducible NOS signaling.

290 mma-Ser18, identified as the main product of cathepsin S-dependent IL-36gamma cleavage, induced psori

291 activation of IL-36gamma and highlight that cathepsin S-mediated activation of IL-36gamma may be imp

292 f conventional protease-activated receptors, cathepsin S-mediated activation of MrgprC11 did not invo

293 -Le(X) neither required TAP-transporters nor Cathepsin-S and was still observed after prolonged intra

294 We have used synthetic membrane-permeable cathepsin substrates, which liberate fluorescent reporte

295 roduce cathepsins B and L, and inhibition of cathepsins suppressed the release of C3a.

296 Here we demonstrate that cysteine cathepsin-targeted imaging probes can be used to monitor

297 teases such as matrix metalloproteinases and cathepsins that contribute to disease formation and prog

298 tible mutant deficient in lysosomal cysteine cathepsins that manifests hallmarks of human lysosomal s

299 emonstrated the mislocalization of lysosomal cathepsins within the cytosol of Npc1-deficient Purkinje

300 d that the primary targets of the probe were cathepsins X, B, S, and L.