ライフサイエンスコーパス: cathepsin K

1 uced the mRNAs encoding for RANKL, TRAP, and 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 ydrase type II, but relatively low levels of 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 (i) = 0.0048 nM) and rat (K(i,app) = 4.8 nM) 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 te, with cathepsin S predominantly degrading cathepsin K.

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

20 4 of 20 when bound within the active site of cathepsin K, a feature subsequently confirmed by X-ray c

21 Cathepsin K, a lysosomal cysteine protease of the papain

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

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

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

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

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

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

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

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

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

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

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

33 tential to elucidate previously undetectable cathepsin K activity.

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

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

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

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

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

39 Cathepsin K also is expressed in a significant fraction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 15 nm, respectively) These data confirm that cathepsin K and not cathepsin L is the major protease re

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

56 Cathepsin K and osteopontin mRNA expression increased in

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

58 Cathepsin K and S protein expression was identified in t

59 This relationship between cathepsin K and the Mitf family helps explain the phenot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 This study identifies cathepsin K as a transcriptional target of Mitf and TFE3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 Cathepsin K (CTSK) is an important protease responsible

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

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

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

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

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

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

124 ive syndrome caused by cathepsin K mutation, cathepsin K-deficient mice, and mitf mutant rodent strai

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

126 Cathepsin K dimer and glycosaminoglycan binding sites re

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

128 Cathepsin K (EC 3.4.22.38), a cysteine protease of the p

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

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

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

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

133 petrosis and identifies likely regulators of cathepsin K expression in bone homeostasis and human mal

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

135 Cathepsin K expression levels in normal synovium were lo

136 Cathepsin K expression was most prominent in young scars

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

138 in surgical scars showed strong cytoplasmic cathepsin K expression.

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

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

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

142 4/80- Ly-6C- CD31-) develop into TRAP+ CT-R+ cathepsin-k+ functional OC in a RANKL/RANK-dependent man

143 Cathepsin K gene expression and protein and protease act

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

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

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

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

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

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

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

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

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

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

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

155 that IFN-gamma down-regulates mRNA levels of cathepsin K in a time- and dose-dependent manner.

156 d potent inhibitors of human cathepsin L and cathepsin K in an in vitro assay of human osteoclastic r

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

158 trates for the first time a critical role of cathepsin K in cartilage degradation by SFs in RA that i

159 ically up-regulated expression of endogenous cathepsin K in cultured human osteoclasts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 a major protease responsible for bone res

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

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

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

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

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

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

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

201 Cathepsin K is organized into elongated C-shaped proteas

202 Cathepsin K is the major collagenolytic enzyme produced

203 Cathepsin K is the major collagenolytic protease in bone

204 Cathepsin K is the major enzyme responsible for the degr

205 Cathepsin K is the predominant protease in osteoclasts t

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

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

208 f 20, a potent, selective inhibitor of human cathepsin K (K(i) = 0.16 nM) as well as 24, a potent inh

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

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

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

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

213 Additionally, cathepsin K knockout mice attenuated cardiac oxidative s

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

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

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

217 Cathepsin K knockout partly reversed the impaired cardio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 Multiple cathepsin K molecules bind specifically to a single cosi

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

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

235 Additionally, cathepsin K mRNA and protein were found to be deficient

236 Cathepsin K mRNA levels were assessed by PCR.

237 TRAP and cathepsin K mRNA paralleled the cell counts.

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

239 s, an autosomal recessive syndrome caused by cathepsin K mutation, cathepsin K-deficient mice, and mi

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

241 Cathepsin K, NFATc1, and osteopontin mRNA expression dec

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

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

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

245 9c2 myoblasts, pharmacological inhibition of cathepsin K, or treatment with calcineurin inhibitor res

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

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

248 7-8-fold) and protein expression (2-fold) of cathepsin K (P < 0.05) in primary synovial fibroblast cu

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

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

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

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

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

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

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

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

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

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

259 Cathepsin K promoter activity was disrupted by dominant

260 and TFE3 via three consensus elements in the cathepsin K promoter.

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

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

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

264 Cathepsin K protein expression in the interstitial areas

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

266 Cathepsin K protein was localized in synovial fibroblast

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

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

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

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

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

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

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

274 -amidotetrahydrofuran-4-one analogue 16 with cathepsin K showed the inhibitor to occupy the unprimed

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

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

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

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

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

280 Cathepsin K, the most potent mammalian collagenase, has

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

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

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

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

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

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

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

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

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

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

291 Cathepsin K was localized to some perivascular cells by

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

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

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

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

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

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

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

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

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

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