ライフサイエンスコーパス: cathepsin K

1 te, with cathepsin S predominantly degrading cathepsin K.

2 I (DPPI) (an in vitro activator of KLK4), or cathepsin K.

3 atrix is degraded by the lysosomal protease, cathepsin K.

4 r cathepsins B and L but no selectivity over cathepsin K.

5 xhibited only low levels or no expression of cathepsin K.

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

7 substrate-based inhibitor were developed for cathepsin K.

8 matrix metalloproteinase 3, cathepsin B, and cathepsin K.

9 o increased selectivity for cathepsin L over cathepsin K.

10 n increased selectivity for cathepsin L over cathepsin K.

11 nto the S1 subsite of the cysteine protease, cathepsin K.

12 suppress the IL-1alpha-induced expression of cathepsin K.

13 s were found to provide potent inhibitors of cathepsin K.

14 at different GAGs compete for the binding to cathepsin K.

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

16 NSC13345 binds to a novel allosteric site on cathepsin K.

17 s for the osteoclast markers Trap (Acp5) and cathepsin K.

18 one matrix resorption has been attributed to cathepsin K, a cysteine protease of the papain family th

19 Cathepsin K, a lysosomal cysteine protease of the papain

20 Cathepsin K, a lysosomal cysteine protease, has been imp

21 Cathepsin K, a lysosomal papain-like cysteine protease,

22 to the observed decrease in the induction of cathepsin K, a major bone matrix degrading protease.

23 tor of the collagenolytic cysteine peptidase cathepsin K, a major target for the treatment of osteopo

24 ed to study the catalytic mechanism of human cathepsin K, a member of the papain family of cysteine p

25 In contrast, levels of cathepsin K, a potent elastase, increased between 3 and

26 ability of mPEG-I and ST-PHPMA-I to inhibit cathepsin K activity in synovial fibroblasts was also ev

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

28 in sulfate present in bone and accessible to cathepsin K activity is sufficient for complex formation

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

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

31 tential to elucidate previously undetectable cathepsin K activity.

32 M NaF had no effect on KLK4, MMP20, DPPI, or cathepsin K activity.

33 Cathepsin-K activity levels of 42 GCF samples and 54 PIS

34 al implant group with regard to MBL measure, cathepsin-K activity, and GCF/PISF volume revealed no si

35 implant groups, despite higher MBL measures, cathepsin-K activity, and GCF/PISF volumes with the pres

36 the selective inhibition of cathepsin S over cathepsin K afforded by inhibitors with the P2-Phe side

37 Of note, cathepsin K also was expressed in repairing fibrocartila

38 with glycosaminoglycans (GAGs) is unique for cathepsin K among human papain-like cysteine proteases a

39 Assessment of odanacatib, an inhibitor of cathepsin K, an osteoclast enzyme required for resorptio

40 for the deacylation step is 16.7 kcal/mol in cathepsin K and 17.8 kcal/mol in aqueous solution.

41 ogue, 10, had a K(i,app) = 0.041 nM vs human cathepsin K and 89% oral bioavailability and an in vivo

42 xes at osteoclast target gene promoters like cathepsin K and acid 5 phosphatase without increasing ge

43 tes with C4-S are located in the R-domain of cathepsin K and are distant from its active site.

44 ding of proline residues in the S2 pocket of cathepsin K and are required for its unique collagenase

45 Biochemical analyses of cathepsin K and C4-S mixtures support the presence of a

46 M was determined for the interaction between cathepsin K and C4-S.

47 he coexpression of the alphavbeta3 integrin, cathepsin K and F-actin rings characteristic of active o

48 he complex is an oligomer consisting of five cathepsin K and five chondroitin sulfate molecules.

49 ism both for the catalyzed reaction in human cathepsin K and for the uncatalyzed reaction in water.

50 sion of osteoclast specific markers, such as cathepsin K and integrin beta3 at mRNA and protein level

51 ances osteoclastic activity by up-regulating cathepsin K and MMP9.

52 h a barrier height of 19.8 kcal/mol in human cathepsin K and of 29.3 kcal/mol in aqueous solution.

53 Cathepsin K and osteopontin mRNA expression increased in

54 tern blot analyses were performed to analyze cathepsin K and S expression in primary fibroblast-like

55 Cathepsin K and S protein expression was identified in t

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

57 entities and structural similarities between cathepsins K and L, only cathepsin K is capable of cleav

58 a, was determined and compared with those of cathepsins K and L.

59 Cathepsins K and S are papain-like cysteine proteases wi

60 cooperative or synergistic activity between cathepsins K and S is less described.

61 The specificities of cathepsins K and S partially match the cleavage site seq

62 matrix metalloproteinase-2, -9, and -12, and cathepsins K and S relative to their endogenous inhibito

63 Expression and localization of cathepsins K and S were determined by immunohistochemist

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

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

66 , FGF18 (fibroblast growth factor 18), CTSK (cathepsin K), and IL11 (interleukin 11), have therapeuti

67 express tartrate-resistant acid phosphatase, cathepsin K, and beta(3) integrin, suggesting that osteo

68 factor, tartrate-resistant acid phosphatase, cathepsin K, and beta3 integrin.

69 ssion of the osteoclast marker genes NFATc1, cathepsin K, and calcitonin receptor in a RANKL-dependen

70 loproteinase-9, matrix metalloproteinase-12, cathepsin K, and cathepsin G, and enhanced proliferation

71 c enzymes include matrix metalloproteinases, cathepsin K, and neutrophil elastase, and a variety of i

72 e cells express the osteoclast markers CD68, cathepsin K, and NFATc1, compared with their wild-type (

73 ted T-cells cytoplasmic 1, NF-kappaB ligand, cathepsin K, and serum tartrate-resistant acid phosphata

74 astogenic regulators including NFAT2, TRAF6, cathepsin K, and tartrate-resistant acid phosphatase.

75 RANK ligand (sRANKL), osteoprotegerin (OPG), cathepsin-K, and sclerostin.

76 alent binders is presented considering human cathepsin K as a test case.

77 Both cell cultures secreted mature cathepsin K as well as procathepsin K, and expressed act

78 We suggest cathepsin-K as a biochemical parameter for monitoring pe

79 copy, we demonstrate the specific binding of cathepsin K at the edge of the fibrillar gap region of c

80 fibroblasts expressed comparable amounts of cathepsin K at the transcript and protein levels.

81 The extension of a previously reported cathepsin K azepanone-based inhibitor template to the de

82 sc tissue demonstrated that ADAMTS-4 and -5; cathepsins K, B, and L; and MMP-3, -7, -12, and -13 were

83 ate structures and their activity to inhibit cathepsins K, B, L, and papain.

84 lagen-associated glycosaminoglycans prevents cathepsin K binding and subsequently fiber hydrolysis.

85 X-ray crystal structures of cathepsin K both unbound and complexed with inhibitors p

86 be the crystal structure of a 1:n complex of cathepsin K:C4-S inhibited by E64 at a resolution of 1.8

87 Expression of RANK, TRAP, cathepsin K, calcitonin receptor, matrix metalloproteina

88 sign has yielded highly potent inhibitors of cathepsin K (Cat K) with excellent physical properties,

89 is, in part, mediated by the collagenolytic cathepsin K (catK) and cathepsin L (catL), with a tempor

90 Here we reveal that cathepsin K (CatK) has a role in ischaemia-induced neova

91 Cathepsin K (catK) is a lysosomal cysteine protease with

92 Cathepsin K (CatK), a major lysosomal collagenase produc

93 Cathepsin K (CatK), a potent elastinolytic and collageno

94 cal changes, which correlate with changes in cathepsin K (CatK)-mediated degradation.

95 Excessive cathepsin K (catK)-mediated turnover of fibrillar type I

96 ectrophile into small molecule inhibitors of cathepsin K (CatK).

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

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

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

100 lagen degradation and suggest that targeting cathepsin K complex formation would be an effective and

101 The physiological relevance of cathepsin K complexes is supported by the findings that

102 Collectively, our data indicate that cathepsin K contributes to the development of obesity-as

103 t-mediated bone resorption via inhibition of cathepsin K could be an effective approach to prevent os

104 Inhibition of cathepsin K could potentially be an effective method to

105 The high potency for inhibition of cathepsin K coupled with the favorable rat and monkey ph

106 mated TLN1(fl/fl) mice with those expressing cathepsin K-Cre (CtsK-TLN1) to delete the gene in mature

107 mated VCL(fl/fl) mice with those expressing cathepsin K-Cre (CtsK-VCL) to delete the gene in mature

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

109 to increase expression of target genes like cathepsin K (Ctsk) and acid phosphatase 5 (Acp5) during

110 kappaB ligand) and the ECM-remodeling enzyme cathepsin K (CtsK) are expressed by ECC endothelial cell

111 r RANK, and the downstream remodeling enzyme cathepsin K (Ctsk) are expressed in the heart during val

112 of NFkappaB ligand (RANKL) signaling induces cathepsin K (CTSK) expression for extracellular matrix d

113 mediator of osteoclastogenesis and regulates cathepsin K (CTSK) expression, which is essential for no

114 esterol in late endosomes and show increased cathepsin K (Ctsk) expression.

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

116 Cathepsin K (CTSK) is an important protease responsible

117 Cathepsin K (CTSK) is secreted by osteoclasts to degrade

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

119 n osteoclasts for bone resorption, including cathepsin K (Ctsk), and lactation elevates their express

120 id phosphatase 5, tartrate resistant (Acp5), cathepsin K (Ctsk), and TNF superfamily member 11 (Tnfsf

121 al cis-regulatory element in the promoter of cathepsin K (Ctsk), which is expressed specifically in O

122 ver kinase b1 (Lkb1; also known as Stk11) in Cathepsin K (Ctsk)-Cre expressing cells.

123 osteoclasts (lysozyme M-Cre; LysMCre) or in cathepsin K (Ctsk)-expressing cells, previously thought

124 s and proteases, including cysteine protease cathepsin K (CTSK).

125 evels of cathepsin B, H, and S increased and cathepsin K decreased with advancing gestation.

126 dult-onset osteopetrotic phenotype caused by cathepsin K deficiency(23,24).

127 levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cell-specific transmembrane prote

128 riple-helical collagen-degrading activity of cathepsin K depends on the formation of complexes with b

129 Cathepsin K dimer and glycosaminoglycan binding sites re

130 ne-based inhibitors of the cysteine protease cathepsin K (EC 3.4.22.38) are described.

131 able and readily detected, the active mature cathepsin K eludes detection by in vitro methods due to

132 in situ activity was used to identify active cathepsin K enzyme in primary synovial fibroblast cultur

133 synovia due to an increase in the number of cathepsin K-expressing cells identifies this enzyme as a

134 The comparable increase in cathepsin K expression after stimulation of RA- and OA-d

135 itively correlated with TNF-alpha, IL-6, and cathepsin K expression and negatively correlated with Ru

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

137 Cathepsin K expression levels in normal synovium were lo

138 Cathepsin K expression was most prominent in young scars

139 vessels, inflammatory cell infiltration, and cathepsin K expression were assessed in soft tissue usin

140 in surgical scars showed strong cytoplasmic cathepsin K expression.

141 yrosine kinase-NF-kappaB pathway to regulate cathepsin K expression.

142 Our results show that cathepsin K function has different effects around the sk

143 The finding of this novel cathepsin K function provides insight into the pathomech

144 4/80- Ly-6C- CD31-) develop into TRAP+ CT-R+ cathepsin-k+ functional OC in a RANKL/RANK-dependent man

145 Cathepsin K gene expression and protein and protease act

146 erefore conclude that IL-1alpha up-regulates cathepsin K gene expression at the transcription level,

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

148 potent aggrecan-degrading activity and that cathepsin K-generated aggrecan cleavage products specifi

149 was further corroborated by the finding that cathepsin K has a potent aggrecan-degrading activity and

150 The cysteine protease cathepsin K has been implicated in pathogenesis of cardi

151 llagen-degrading activity, whereas monomeric cathepsin K has no collagenase activity.

152 of reversible ketoamides based inhibitors of cathepsin K have led to identification of potent and sel

153 Osteoclasts were identified by cathepsin K immunohistochemistry at various time points

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

155 in K was induced in Npc1-/- macrophages, and cathepsin K immunostaining and elastase activity were in

156 We now show increased cathepsin K immunostaining and increased cysteinyl prote

157 The selective and critical role of cathepsin K in articular cartilage and subchondral bone

158 well as procathepsin K, and expressed active cathepsin K in cytosolic vesicles.

159 ally defined manner that suggests a role for cathepsin K in degrading re-absorbed enamel matrix prote

160 ellular matrix, we studied the expression of cathepsin K in human skin and in cultured primary neonat

161 be linked to podosomes with the exception of cathepsin K in osteoclasts.

162 athepsin K(-/-) OCs and forced expression of cathepsin K in pre-OCs induced premature senescence and

163 TNF alpha on the expression and secretion of cathepsin K in primary cultures of synoviocytes was dete

164 However, the overexpression of cathepsin K in RA synovia due to an increase in the numb

165 s is the first study implicating bone marrow cathepsin K in regulation of biological activity of SPAR

166 Of note is the expression of cathepsin K in synovial fibroblasts and mononuclear macr

167 Here, we investigated the involvement of cathepsin K in the progression of prostate tumors in the

168 Expression levels of cathepsin K in the sublining and vascularized areas of i

169 To study the role of cathepsin K in the turnover of the cutaneous extracellul

170 ssociated with an increased protein level of cathepsin K in vitro after the GC treatments.

171 rtrate-resistant acid phosphatase (TRAP) and cathepsin K in vitro.

172 d significantly increased levels of RANK and cathepsin-K in mucositis.

173 In H9c2 myoblasts, silencing of cathepsin K inhibited palmitic acid-induced release of c

174 the P3 and P2 binding elements of the potent cathepsin K inhibitor 1 revealed that incorporation of e

175 rile compounds revealed 3 as a highly potent cathepsin K inhibitor but with cathepsin S activity and

176 d new lysosomotropic (water-soluble) polymer-cathepsin K inhibitor conjugates.

177 A representative cathepsin K inhibitor was shown to attenuate PTH-stimula

178 MIV-711 is a novel selective cathepsin K inhibitor with beneficial effects on bone an

179 A potent selective cathepsin K inhibitor, 1,5-bis(N-benzyloxycarbonylleucyl

180 Odanacatib, a cathepsin K inhibitor, reduces bone resorption while mai

181 6-, and 7-methyl-substituted azepanone-based cathepsin K inhibitors are described.

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

183 , and molecular docking studies, a series of cathepsin K inhibitors based on N-(functionalized benzoy

184 her deficient in cathepsin K or treated with cathepsin K inhibitors had significantly reduced secreti

185 pplied this method to determine occupancy of Cathepsin K inhibitors in bone tissues harvested from ra

186 pharmacokinetic properties of some of these cathepsin K inhibitors in rats make them suitable for ev

187 Inhibition of collagen breakdown by cathepsin K inhibitors suggests this mechanism of action

188 ations have resulted in potent and selective cathepsin K inhibitors that allow for improvements in th

189 versible, selective, and orally bioavailable cathepsin K inhibitors.

190 nones were identified that had widely varied cathepsin K inhibitory potency as well as pharmacokineti

191 y, we have engineered the S2 pocket of human cathepsin K into a cathepsin L-like subsite.

192 Cathepsin K is a major drug target for osteoporosis and

193 Cathepsin K is an attractive target because it is a coll

194 imilarities between cathepsins K and L, only cathepsin K is capable of cleaving interstitial collagen

195 esults demonstrated that bone marrow-derived cathepsin K is capable of processing and thereby modulat

196 we demonstrate that the lysosomal proteinase cathepsin K is expressed in the enamel organ in a develo

197 lpha further suggests that the expression of cathepsin K is independent of cellular alterations leadi

198 ains why the general proteolytic activity of cathepsin K is not affected by the binding of chondroiti

199 The primary substrate specificity of cathepsin K is not altered by complex formation, suggest

200 Cathepsin K is organized into elongated C-shaped proteas

201 Cathepsin K is the major collagenolytic enzyme produced

202 Cathepsin K is the major collagenolytic protease in bone

203 Cathepsin K is the major enzyme responsible for the degr

204 Cathepsin K is the predominant protease in osteoclasts t

205 Although the potent collagenase activity of cathepsin K is well known, its mechanism of action remai

206 Cathepsin-K is an enzyme involved in bone metabolism whi

207 apparent second-order rate constant against cathepsin K (k(obs)/[I] = 1.3 x 10(6) M(-1) s(-1)) simil

208 o the 4S-parent azepanone analogue, 1 (human cathepsin K, K(i,app) = 0.16 nM, rat oral bioavailabilit

209 specificity of the method was validated with cathepsin K knockdown using small interfering RNA (siRNA

210 Additionally, cathepsin K knockout alleviated whole-body glucose intol

211 Additionally, cathepsin K knockout mice attenuated cardiac oxidative s

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

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

214 All these changes were reconciled in cathepsin K knockout mice.

215 Cathepsin K knockout partly reversed the impaired cardio

216 d apoptotic markers, which were inhibited by cathepsin K knockout.

217 ot inhibit the cysteine proteinase papain or cathepsin K, L, or S.

218 mokines especially in the C-terminal region, cathepsins K, L, and S cleaved chemokines at the N termi

219 e now show that SQN-5, like SCCA1, inhibited cathepsins K, L, S, and V but not cathepsin B or H.

220 flammatory protein-1alpha, MMP-2, MMP-9, and cathepsins-K, -L, and -S and the ability of IL-13 to inh

221 MIP-1alpha) and proteases (MMP-2, MMP-9, and cathepsins-K, -L, and -S) and the inhibition of alpha1-a

222 fluid (GCF)/peri-implant sulcus fluid (PISF) cathepsin-K levels of natural teeth and dental implants,

223 bone metastases, we identified cathepsin G, cathepsin K, matrix metalloproteinase (MMP)-9, and MMP13

224 Our data suggest that cathepsin K may play an important role in the homeostasi

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

226 protein-protein interface completely inhibit cathepsin-K-mediated fiber degradation without affecting

227 d found that, only in the 129/Sv background, cathepsin K(-/-) mice exhibit many characteristics of th

228 We propose that one cathepsin K molecule binds to collagen-bound glycosamino

229 cosine curve-shaped strand of C4-S with each cathepsin K molecule interacting with three disaccharide

230 Multiple cathepsin K molecules bind specifically to a single cosi

231 We generated cathepsin K(-/-) mouse strains in the 129/Sv and C57BL/6

232 lls possessed significantly higher levels of Cathepsin K mRNA and Atg5 mRNA and protein.

233 Cathepsin K mRNA levels were assessed by PCR.

234 TRAP and cathepsin K mRNA paralleled the cell counts.

235 ient for complex formation and (ii) Y212C, a cathepsin K mutant that causes pycnodysostosis (a bone s

236 e and osteolysis in calvariae as a result of cathepsin K mutation.

237 oclast-promoting genes, including Dickkopf1, Cathepsin K, Nf-kbeta,; and Calcr, suggesting a role for

238 Cathepsin K, NFATc1, and osteopontin mRNA expression dec

239 The coincident up-regulation of SPARC and cathepsin K occurred both in vivo in experimental prosta

240 d tartrate-resistant acid phosphatase (TRAP)/cathepsin K(+) OCs expressing phosphorylated Janus kinas

241 and p21 were significantly reduced in 129/Sv cathepsin K(-/-) OCs and forced expression of cathepsin

242 stromal cells that were either deficient in cathepsin K or treated with cathepsin K inhibitors had s

243 9c2 myoblasts, pharmacological inhibition of cathepsin K, or treatment with calcineurin inhibitor res

244 Our data indicated that 129/Sv cathepsin K(-/-) osteoclasts (OCs) lacked normal apoptos

245 gen degradation and has good selectivity for cathepsin K over related enzymes.

246 7-8-fold) and protein expression (2-fold) of cathepsin K (P < 0.05) in primary synovial fibroblast cu

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

248 This is the first evidence that cathepsin K plays a key role in OC apoptosis and senesce

249 The collagenolytic activity of cathepsin K plays a pivotal role in bone resorption and

250 The presence of cathepsin K polypeptide in synovial fibroblasts and macr

251 Upon recruitment, the cathepsin K-positive DCs were observed in bone-resorbing

252 In addition, numerous mononucleated cathepsin K-positive osteoclast precursor cells emerged

253 In both AIA and CIA, multinucleated and cathepsin K-positive osteoclasts first were observed on

254 attached to bone) and osteoclast precursors (cathepsin K-positive, mononucleated or multinucleated, w

255 All osteoclasts (cathepsin K-positive, multinucleated, attached to bone)

256 sin S cannibalized the highly collagenolytic cathepsin K, preventing its activity.

257 Cathepsin K promoter activity was disrupted by dominant

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

259 We hypothesized that ablation of cathepsin K protects against obesity-associated cardiac

260 the structure of a collagenolytically active cathepsin K protein dimer.

261 Cathepsin K protein expression in the interstitial areas

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

263 Cathepsin K protein was localized in synovial fibroblast

264 hat IL-1alpha up-regulates the expression of cathepsin K protein, a key protease in bone resorption,

265 Furthermore, high-fat feeding resulted in cathepsin K release from lysosomes into the cytoplasm.

266 e mechanism of collagen fiber degradation by cathepsin K remained elusive.

267 f the double mutation into the S2 subsite of cathepsin K rendered the unique S2 binding preference of

268 It further implies that cathepsin K represents the only lysosomal collagenolytic

269 lex IV) subunit II (P < 0.05), and decreased cathepsin K RNA (P = 0.04) compared with levels in norma

270 ption volume and examined periodontal tissue cathepsin K, Runx2, TNF-alpha, and IL-6 expression.

271 Absence of synaptotagmin VII inhibits cathepsin K secretion and formation of the ruffled borde

272 Interestingly, AAV-sh-Ac45 impaired mature cathepsin K secretion more significantly than that by AA

273 ammation through impairing acidification and cathepsin K secretion.

274 Here, we report a cathepsin K-specific complex with chondroitin sulfate, w

275 d neonatal primary fibroblasts showed strong cathepsin K staining in the perinuclear endosomal compar

276 kin-6, -8) coincident with overexpression of cathepsin K suggest possible mechanisms by which this en

277 t genes encoding matrix metalloproteinase 9, cathepsin K, tartrate-resistant acid phosphatase, and ca

278 to show that murine osteoclasts secrete more cathepsin K than is stored intracellularly, and this was

279 Cathepsin K, the most potent mammalian collagenase, has

280 visualization, and quantification of mature cathepsin K to femtomole resolution using gelatin zymogr

281 ment with exogenous PDGF-BB or inhibition of cathepsin K to increase the number of preosteoclasts, an

282 does not impair the proteolytic activity of cathepsin K toward noncollagenous substrates.

283 ly potentiate the collagenolytic activity of cathepsin K toward type I and II collagens.

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

285 Comparison with the structures of cathepsins K, V, and L allows delineation of local inter

286 ries, the P1-P4 substrate specificity of the cathepsin K variant, Tyr67Leu/Leu205Ala, was determined

287 The expression of cathepsin K was also demonstrated in primary cell cultur

288 Cathepsin K was also found to be strongly expressed in k

289 In addition, cathepsin K was induced in Npc1-/- macrophages, and cath

290 Cathepsin K was localized to some perivascular cells by

291 candidate compounds with unknown activity on cathepsin K were finally selected for experimental evalu

292 clast markers (matrix metallopeptidase 9 and cathepsin K) were up-regulated at M14.

293 pounds 5, 6, and 9 were highly selective for cathepsin K when compared with cathepsins L and S, with

294 ely abolished the collagenolytic activity of cathepsin K whereas its overall gelatinolytic activity r

295 ates, enhance the collagenolytic activity of cathepsin K, whereas dermatan, heparan sulfate, and hepa

296 dation at 28 degrees C by all cathepsins but cathepsin K, whereas thermal destabilization at 37 degre

297 of magnitude less than those determined for cathepsin K, while for cathepsin B and papain, the value

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

299 emodeling (MMP12, MMP3, integrin alphaX, and cathepsins K, Z, B, and S).

300 Furthermore, cathepsin K zymography was used to show that murine oste