ライフサイエンスコーパス: stromelysin

1 er of structurally diverse inhibitors toward stromelysin.

2 ructure recently attained for70 complexed to stromelysin.

3 ynthase, inducible cyclooxygenase, IL-6, and stromelysin.

4 l thiadiazoles which were weak inhibitors of stromelysin.

5 lalanine can provide selective inhibitors of stromelysin.

6 on, at least in part, of gelatinase A and/or stromelysin.

7 matrix metalloproteinase gelatinase A and/or stromelysin.

8 ondylar cartilage, and induction of mRNA for stromelysin.

9 nding affinity of a competitive inhibitor of stromelysin.

10 ile collagenase (MMP 1), gelatinase (MMP 9), stromelysin 1 (MMP 3), and matrilysin (MMP 7) all proces

11 The high-affinity inhibition of stromelysin 1 (MMP-3) by tissue inhibitor of metalloprot

12 Stromelysin 1 (MMP-3) is a matrix metalloproteinase with

13 of the collagenases (MMPs 1, 8, and 13) and stromelysin 1 (MMP-3) was demonstrated in a proportion o

14 cting protease cascade involving plasmin and stromelysin 1 (MMP-3).

15 th serine proteinases and MMPs, particularly stromelysin 1 (MMP-3).

16 as tested by examining the arthritic paws of stromelysin 1 (SLN1)-deficient mice for loss of cartilag

17 s transition is the matrix metalloproteinase stromelysin 1 (Str-1).

18 vation of monomeric and dimeric pro-MMP-9 by stromelysin 1 revealed K(m) values in the nanomolar rang

19 ally, XL-Fb clots were solubilized by MMP-3 (stromelysin 1) by cleavage at gamma Gly 404-Ala 405, res

20 MMP-1 (interstitial collagenase) and MMP-3 (stromelysin 1) in astrocytes, and MMP-1, MMP-9 (gelatina

21 dontitis, matrix metalloproteinase-3 (MMP-3, stromelysin 1) is present at increased levels in active

22 -1 segments have been introduced into MMP-3 (stromelysin 1) starting from the C-terminal end.

23 the cartilage matrix-degrading enzyme MMP-3 (stromelysin 1).

24 (MMPs), membrane-type MMP-1, collagenase 1, stromelysin 1, and gelatinase B.

25 -, 17,000-, 90-, and 200-fold selective over stromelysin 1, collagenase 1, and gelatinases A and B, r

26 the Ki for a C-terminally truncated form of stromelysin 1, MMP-3(DeltaC), but do not disturb the con

27 near the site of the hydrolytic cleavage by stromelysin 1.

28 tude) of activation of the monomeric form by stromelysin 1.

29 Recombinant stromelysin 1/MMP3 alone was sufficient to drive branchi

30 ound between mRNA expression for matrilysin, stromelysins 1-3, TIMP-1, or TIMP-3 and secretion of the

31 ot of the pH dependence of kcat/KM for human stromelysin-1 (HS) exhibits a narrow range of maximal ac

32 Increased expression of stromelysin-1 (matrix metalloproteinase [MMP]-3) by the

33 ropeptide of a carboxyl-terminally truncated stromelysin-1 (mini-SL-1) were constructed and expressed

34 AAA wall expressed significantly more stromelysin-1 (MMP-3) (mean log(10) ratio [copy enzyme c

35 sition were found to be potent inhibitors of stromelysin-1 (MMP-3) and gelatinase A (MMP-2), in the r

36 Stromelysin-1 (MMP-3) and TIMP-3 were, however, over exp

37 previously reported structure of the TIMP-1/stromelysin-1 (MMP-3) complex shows that the mechanisms

38 Stromelysin-1 (MMP-3) degrades extracellular matrix and

39 We have studied mice with deficiencies of stromelysin-1 (MMP-3) or gelatinase B (MMP-9) in a dinit

40 asminogen activator inhibitor-1 (PAI-1), and stromelysin-1 (MMP-3) polymorphisms as risk factors for

41 The crystal structure of stromelysin-1 (MMP-3) was used to identify regions of th

42 ecorin (core protein), gelatinase-A (MMP-2), stromelysin-1 (MMP-3), and a tissue inhibitor of metallo

43 ned with antibodies to gelatinase A (MMP-2), stromelysin-1 (MMP-3), and gelatinase B (MMP-9).

44 e showed that the MMPs gelatinase B (MMP-9), stromelysin-1 (MMP-3), and the tissue inhibitor of MMPs

45 We describe here that stromelysin-1 (MMP-3), as well as the gelatinases A (MMP

46 yphimurium or Y. enterocolitica infection in stromelysin-1 (MMP-3)-deficient mice (mmp-3(-/-)) with m

47 that this is associated with an increase in stromelysin-1 (MMP3) transcripts in colonic tissues.

48 stable complex with the catalytic domain of stromelysin-1 (N-MMP-3).

49 l structure of the catalytic domain of human stromelysin-1 (SCD) complexed to a novel and potent, non

50 Human stromelysin-1 (SL-1) is a member of the stromelysin subf

51 cells expressing an inducible autoactivating stromelysin-1 (SL-1) transgene.

52 the results compared with the combination of stromelysin-1 (SL-1, a superactivator of FIB-CL) and FIB

53 th tetracycline-regulated expression of MMP3/stromelysin-1 (Str1) form epithelial glandular structure

54 The matrix metalloproteinase MMP-3/stromelysin-1 (Str1) is highly expressed during mammary

55 A/S68Y mutant is the strongest inhibitor for stromelysin-1 among all mutants characterized to date, w

56 itor was found to be similar with respect to stromelysin-1 and collagenase-1; however, subtle compara

57 These results indicate that stromelysin-1 and gelatinase B serve important functions

58 ity for six thiadiazole urea inhibitors with stromelysin-1 and gelatinase-A, two homologous MMPs that

59 Wild-type stromelysin-1 and the mutants were all expressed at dete

60 mRNA and protein for gelatinase A, stromelysin-1 and uPA were weakly induced, if at all, in

61 The increased selectivity for stromelysin-1 appears to be driven by (1) increased favo

62 Rabbit and human isoforms of stromelysin-1 are highly homologous, yet there are clear

63 reement with experimentally observed data on stromelysin-1 biological activity and binding-site topol

64 interstitial collagenase, gelatinase A, and stromelysin-1 by fibroblasts, and we have obtained cDNA

65 f this cysteine residue in the propeptide of stromelysin-1 by sulfhydryl reagents did not result in a

66 s by altering the cellular microenvironment, stromelysin-1 can act as a natural tumor promoter and en

67 Among these enzymes, stromelysin-1 can also activate the proenzymes of other

68 In contrast, stromelysin-1 could not rescue invasion inhibited by ant

69 Stromelysin-1 could provide a target for pharmacological

70 The striking acidic profile of stromelysin-1 defined by the combined ionization of Glu(

71 Thus misregulation of stromelysin-1 expression appears to be an important aspe

72 grins confer invasive behavior by regulating stromelysin-1 expression, whereas alpha6 integrins regul

73 both cell lines was critically dependent on stromelysin-1 expression.

74 ired in mice with a targeted deletion in the stromelysin-1 gene.

75 Stromelysin-1 has a third pK(a) near 6, resulting in a u

76 An intradermal injection of stromelysin-1 immediately before DNFB sensitization resc

77 ia led to increased expression of endogenous stromelysin-1 in stromal fibroblasts and up-regulation o

78 so inhibited the increase in collagenase and stromelysin-1 in the explant culture supernatants and th

79 he invasive cell line, FaDu, released active stromelysin-1 into the culture medium.

80 tes to the invasive phenotype, activation of stromelysin-1 is a key regulatory step for invasiveness

81 Stromelysin-1 is a member of the metalloproteinase famil

82 ng early wound contraction and indicate that stromelysin-1 is crucial for the organization of a multi

83 Stromelysin-1 is required for initiation of the response

84 ity in ODC-overexpressing cells and elevated stromelysin-1 mRNA expression in the stromal cells of in

85 that a given ligand will bind selectively to stromelysin-1 over gelatinase-A which is gratifying give

86 TEL bound sequences in the stromelysin-1 promoter and repressed the promoter in tra

87 near the TEL-binding sites in the endogenous stromelysin-1 promoter when TEL was expressed.

88 or, impaired TEL-dependent repression of the stromelysin-1 promoter.

89 These data implicate stromelysin-1 proteolysis during early wound contraction

90 Conversion of pIL-1 beta by stromelysin-1 required coincubation for at least 1 h, an

91 lished a transgenic mouse model in which rat stromelysin-1 targeted to the mammary gland augmented ex

92 ating mutant of the matrix metalloproteinase stromelysin-1 to mammary epithelia of transgenic mice re

93 mary gland stroma once the expression of the stromelysin-1 transgene commences.

94 that express an autoactivating form of MMP-3/stromelysin-1 under the control of the whey acidic prote

95 lial cells of mice expressing autoactivating stromelysin-1 underwent unscheduled apoptosis during lat

96 Stromelysin-1 was expressed in both malignant and nonmal

97 that the endogenous matrix metalloproteinase stromelysin-1 was repressed by TEL.

98 Expression of the stromal protease stromelysin-1 was unaffected by the absence of p53 sugge

99 Expression levels of 92 kDa gelatinase and stromelysin-1 were significantly increased early in the

100 PN is a novel substrate for two MMPs, MMP-3 (stromelysin-1) and MMP-7 (matrilysin).

101 er than the inhibition of the similar MMP-3 (stromelysin-1) catalytic domain (MMP-3cd) by TIMP-1.

102 s very efficient at generating active MMP-3 (stromelysin-1) from exogenously added pro-MMP-3.

103 expression of MMP-1 (collagenase) and MMP-3 (stromelysin-1) in a concentration- and time-dependent ma

104 to induce MMP-13 (collagenase-3) and MMP-3 (stromelysin-1) in the Ets2-deficient fibroblasts.

105 ression of matrix metalloproteinase-3 (MMP-3/stromelysin-1) is associated with a variety of tumor typ

106 gulation of MMP-1 (collagenase-1) and MMP-3 (stromelysin-1) mRNAs and proteins sustained for at least

107 effectors, matrix metalloproteinase-3 (MMP-3/stromelysin-1), and fibronectin.

108 Other metalloproteinases (collagenase-1, stromelysin-1, and 92-kD gelatinase) were not produced b

109 last production of interstitial collagenase, stromelysin-1, and gelatinase A (72-kDa type IV collagen

110 for their ability to inhibit collagenase-1, stromelysin-1, and gelatinase-B substrate hydrolysis.

111 hole-lung homogenates, whereas gelatinase B, stromelysin-1, and interstitial collagenase gene express

112 rolonged incubation of mature IL-1 beta with stromelysin-1, and to a lesser extent also with gelatina

113 these enzymes, the matrix metalloproteinase stromelysin-1, can actually cause cancer when expressed

114 ary gland augmented expression of endogenous stromelysin-1, disrupted functional differentiation, and

115 ective for human collagenase 3 over the MMPs stromelysin-1, gelatinase B, and collagenase 1, respecti

116 corneal epithelium and stroma, and of MMP-3/stromelysin-1, in DR corneal stroma.

117 MATRIX METALLOPROTEINASE-3 (MMP-3), or stromelysin-1, is an enzyme responsible for the degradat

118 that are associated with matrix deposition (stromelysin-1, MMP3), inflammation (IL-6), and lipid met

119 mRNAs for several other MMPs (stromelysin-1, stromelysin-3 and gelatinase A) and MMP i

120 Expression of stromelysin-1, stromelysin-3, and two different membrane

121 tachykinin-1, secretogranin-II, cathepsin-L, stromelysin-1, thymosin-beta4, alpha-tubulin, alphaB-cry

122 Gelatinase A, gelatinase B, stromelysin-1, urokinase, TIMP-1 and TIMP-2 mRNA and pro

123 might play in the APMA-induced activation of stromelysin-1, we have changed these residues by site-di

124 wounds 2 to 10 mm were made in the dermis of stromelysin-1-deficient and wild-type mice.

125 and epithelialization were unaffected in the stromelysin-1-deficient animals.

126 phocytes from lymph nodes of DNFB-sensitized stromelysin-1-deficient mice did not proliferate in resp

127 the age of the animal, excisional wounds in stromelysin-1-deficient mice failed to contract and heal

128 Stromelysin-1-deficient mice showed a markedly impaired

129 Unlike stromelysin-1-deficient mice, gelatinase B-deficient mic

130 rescued the impaired CHS response to DNFB in stromelysin-1-deficient mice.

131 r, in part, by transcriptional repression of stromelysin-1.

132 n expression of the matrix metalloproteinase stromelysin-1.

133 pha2 was reversed by addition of recombinant stromelysin-1.

134 the explant culture supernatants, especially stromelysin-1.

135 latinase B, collagenase-3, collagenase-2, or stromelysin-1.

136 e expression of the matrix metalloproteinase stromelysin-1.

137 ut retained the ETS domain failed to repress stromelysin-1.

138 We have previously investigated stromelysin-1/matrix metalloproteinase-3 (MMP-3), a stro

139 dative enzymes (MMP-2 [gelatinase-A], MMP-3 [stromelysin-1]), and a tissue inhibitor of metalloprotei

140 determined by NMR of the inhibitor bound to stromelysin (2, 3).

141 sin (matrix metalloproteinase 7 [MMP-7]) and stromelysin-2 (MMP-10), two MMPs induced by acute P. aer

142 Stromelysin-2 (MMP10) is expressed by macrophages in num

143 tumor components in most tumors, and neither stromelysin-2 nor neutrophil collagenase were detected i

144 Matrix metalloproteinase 10 (MMP-10, stromelysin-2) is a secreted metalloproteinase with func

145 evels of matrix metalloproteinase-10 (MMP-10/stromelysin-2) were significantly elevated in DR corneal

146 ntified 2,091 matrilysin-dependent and 1,628 stromelysin-2-dependent genes that were differentially e

147 ro array analysis found that TH up regulates stromelysin 3 (ST3, matrix metalloproteinase 11) in the

148 In normal mice, the MMPs MT1-MMP, stromelysin 3, and gelatinase B were expressed at low le

149 E4 substrates, such as the metalloproteinase stromelysin 3, is required for tumor cell invasion.

150 n of the matrix metalloproteinase (MMP) gene stromelysin-3 ( ST3 ) has been shown to be tightly assoc

151 The matrix metalloproteinase (MMP) stromelysin-3 (ST3) (MMP11) was first isolated as a brea

152 involvement of the matrix metalloproteinase stromelysin-3 (ST3) in tissue remodeling and pathogenesi

153 The MMP stromelysin-3 (ST3) is induced by T3, and its expression

154 We demonstrate here that three MMPs-stromelysin-3 (ST3), collagenases-3 (Col3), and collagen

155 Stromelysin-3 (STR-3) is a recently characterized matrix

156 However, the induction of stromelysin-3 after prolonged treatment with FGF-2 resul

157 atalytic domains are most closely related to stromelysin-3 and contain the consensus HEXXH zinc-bindi

158 mRNAs for several other MMPs (stromelysin-1, stromelysin-3 and gelatinase A) and MMP inhibitors (TIMP

159 Differences in the expression patterns of stromelysin-3 and the delayed response proteinases in th

160 ne MC3T3 was used to study the regulation of stromelysin-3 by FGF-2.

161 This study demonstrates dual regulation of stromelysin-3 by FGF-2: acute destabilization of stromel

162 gulation may be important in the function of stromelysin-3 in bone and in remodeling processes, such

163 sion of the unusual matrix metalloproteinase stromelysin-3 in human atherosclerotic lesions and impli

164 uman atherosclerotic plaques (n = 7) express stromelysin-3 in situ, whereas fatty streaks (n = 5) and

165 tumor necrosis factor alpha did not augment stromelysin-3 in vascular wall cells.

166 Stromelysin-3 is an unusual matrix metalloproteinase, be

167 Stromelysin-3 is up-regulated by TH with early kinetics,

168 In addition, stromelysin-3 mRNA and protein colocalized with CD40L an

169 Stromelysin-3 mRNA and protein colocalized with endothel

170 Acutely, FGF-2 decreased stromelysin-3 mRNA levels, whereas prolonged treatment c

171 ed that acute treatment with FGF-2 decreased stromelysin-3 mRNA stability but did not alter gene tran

172 melysin-3 by FGF-2: acute destabilization of stromelysin-3 mRNA, followed by induction of gene transc

173 s prolonged treatment caused an induction of stromelysin-3 mRNA.

174 Stromelysin-3 then cleaves and activates Notch.

175 Osteoblasts express stromelysin-3, a matrix metalloproteinase associated wit

176 Expression of stromelysin-1, stromelysin-3, and two different membrane type-MMPs was

177 ts reveal a stromal gene expression pattern (stromelysin-3, IGF-II and TIMP-1) identical to that obse

178 Furin processes stromelysin-3, membrane type 1 matrix metalloproteinase

179 The MMP-11 proteinase, also known as stromelysin-3, probably plays an important role in human

180 stromelysin-3, TIMP-2 and TIMP-3 mRNA while stromelysin-3, TIMP-2 and gelatinase A were seen in the

181 The skeletal muscle of the tongue expressed stromelysin-3, TIMP-2 and TIMP-3 mRNA while stromelysin-

182 erial specimens (n = 5) contain little or no stromelysin-3.

183 ed in atheroma, induced de novo synthesis of stromelysin-3.

184 andidate AP-1 target genes, collagenase-1 or stromelysin-3.

185 ar enzyme activation mechanism observed with stromelysin-3.

186 the IL-1 induction of stromelysin, the human stromelysin 5'-flanking region was screened by electroph

187 gned ribozymes that cleave the mRNA encoding stromelysin, a matrix metalloproteinase implicated in ca

188 ble to follow the course of reaction between stromelysin, a metalloprotease, and its substrate phage.

189 d on X-ray crystallography of the complex of stromelysin and 16.

190 d on X-ray crystallography of the complex of stromelysin and 4a.

191 e of an active uninhibited form of truncated stromelysin and a complex with a hydroxamate-based inhib

192 ut not IGF-II, modestly increased trabecular stromelysin and gelatinase B but not collagenase, gelati

193 Stromelysin and IL-1alpha steady-state messenger RNA (mR

194 was accompanied by a marked decrease in both stromelysin and IL-1alpha steady-state mRNA levels.

195 lso in other AP-1-dependent genes, including stromelysin and mitogen-activated protein kinase phospha

196 ly broad substrate profile, acting both as a stromelysin and noncanonical collagenase.

197 n synthesis and catabolism and production of stromelysin and tissue inhibitor of metalloproteinases 1

198 agenase, MMP9 is a gelatinase, MMP3/10a is a stromelysin, and MMP3/10b has an unusually broad substra

199 (TNF-alpha) and plasminogen on collagenase, stromelysin, and plasminogen activator inhibitor-1 (PAI-

200 uced expression of interstitial collagenase, stromelysin, and TF protein and activity.

201 he matrix metalloproteinases collagenase and stromelysin are also synthesized by resident corneal cel

202 ocated in the vicinity of the active site of stromelysin are conserved in gelatinase and collagenase,

203 Using stromelysin as an indicator, this study investigated whe

204 e was developed using thymidylate kinase and stromelysin as target proteins.

205 ibits IL-1 induction of both collagenase and stromelysin, as well as PGE2 production, in human synovi

206 added TGF-beta1 suppressed the induction of stromelysin by mediators that were elaborated by activat

207 becular meshwork expression of TIGR/MYOC and stromelysin by Northern blot analysis hybridization.

208 alyze the binding of three inhibitors to the stromelysin catalytic domain (SCD).

209 and 39% identical to human metalloelastase, stromelysin, collagenase-3, and matrilysin, respectively

210 y with other MMPs, particularly those of the stromelysin/collagenase subfamilies.

211 droxamate-phosphinamide-type inhibitor-bound stromelysin complex, formed by diffusion soaking, has be

212 suppression of IL-1-induced collagenase and stromelysin expression by IL-4 occurs at least in part a

213 for 30 minutes, induced typical increases in stromelysin expression in these organ cultures and in ce

214 onses to laser treatment, that is, to induce stromelysin expression or to trigger cell division, when

215 In contrast, stromelysin expression was induced at 6 hours and not at

216 In the normal glomeruli, stromelysin expression was markedly induced in resident

217 The ability of conditioned media to induce stromelysin expression was partially blocked by either t

218 ce-specific and dose-dependent inhibition of stromelysin expression were characterized.

219 nhibitor manoalide on cartilage degradation, stromelysin expression, and inflammatory cell accumulati

220 cytokines then mediate increased trabecular stromelysin expression.

221 Matrix metalloproteinases of the stromelysin family are expressed in the human endometriu

222 ide insight into the differential binding of stromelysin family members to TIMP-1.

223 specificity toward individual members of the stromelysin family, with potential therapeutic applicati

224 inetic inhibition analysis was conducted for stromelysin, gelatinase A, and gelatinase B with the var

225 Transcription of the stromelysin gene is induced by inflammatory cytokines su

226 repressor of IL-1-induced expression of the stromelysin gene.

227 n contrast, alteration of the S1' subsite of stromelysin (HFS:L214Y/V215A) to resemble matrilysin inc

228 ctants, which up-regulated collagenase I and stromelysin I as well.

229 AP-1 responsive collagenase I, stromelysin I, and NF-kappaB responsive IL-1 and IL-6 we

230 in-6 induced expression of collagenase I and stromelysin I, but not gelatinase A, were inhibited in t

231 95 (5'-G(T)TTTTTCCCCCCATCAAAG-3') termed the stromelysin IL-1 responsive element site.

232 ent by induction or augmentation of mRNA for stromelysin, IL-6, and IL-8, gene products important in

233 The juxtacanalicular stromelysin immunostaining increase was sustained for at

234 Stromelysin immunostaining was elevated dramatically in

235 ring TGF-betaR showed enhanced expression of stromelysin in response to IL-1beta, suggesting that end

236 ransfectants exhibited blunted expression of stromelysin in response to the Mphi-derived, inflammator

237 ases -- collagenase, a 92-kd gelatinase, and stromelysin -- in skin connective tissue and outer skin

238 ivo rat model and an in vivo rabbit model of stromelysin-induced cartilage degradation were used to f

239 alpha)- blocking antibodies to eliminate the stromelysin induction was evaluated.

240 Stromelysin inhibition was further improved using a pent

241 ulted in CGS 27023A, a potent, orally active stromelysin inhibitor that blocks the erosion of cartila

242 Examination of the tertiary structure of the stromelysin-inhibitor complex revealed few hydrogen-bond

243 An X-ray structure was obtained for a stromelysin-inhibitor complex which provided insights in

244 ethod is applied to the thiadiazole class of stromelysin inhibitors and it takes advantage of the fac

245 ies of ureas which were moderately effective stromelysin inhibitors, with Ki's between 0.3 and 1.0 mi

246 measurement of the dissociation constants of stromelysin inhibitors.

247 Stromelysin is a zinc-dependent proteinase and a member

248 The matrix metalloproteinase stromelysin is believed to be a key mediator in arthriti

249 The active site of stromelysin is located in a large, hydrophobic cleft.

250 It has long been proposed that stromelysin is one of the major degradative matrix metal

251 tide with the same efficiency as that of the stromelysin, k(cat)/K(m) approximately 1.07 x 10(6) M(-)

252 Stromelysin levels and activity were then evaluated at v

253 lelic polymorphism of the promoter region of stromelysin (matrix metalloproteinase 3) on susceptibili

254 levels, which suggests that collagenases and stromelysins may play a role in the pathogenesis of ster

255 Stromelysin message levels were significantly suppressed

256 In some experiments, levels of synovial stromelysin messenger RNA (mRNA) were assessed.

257 e inhibitors of the matrix metalloproteinase stromelysin (MMP-3) has been previously described.

258 Binding to stromelysin (MMP-3) was substantially weaker, with K(i)

259 undance of interstitial collagenase (MMP-1), stromelysin (MMP-3), 72 kD gelatinase (MMP-2), 92 kD gel

260 Interstitial collagenase (MMP-1), stromelysin (MMP-3), and 72-kD gelatinase (MMP-2) were i

261 creased interstitial collagenase (MMP-1) and stromelysin (MMP-3), and activated gelatinase A (MMP-2).

262 ntain at least 3 MMPs: gelatinase A (MMP-2), stromelysin (MMP-3), and gelatinase B (MMP-9).

263 e the biosynthesis of collagenase-1 (MMP-1), stromelysin (MMP-3), and macrophage elastase (MMP-12) wi

264 zymes, ie, interstitial collagenase (MMP-1), stromelysin (MMP-3), gelatinase B (MMP-9), and activated

265 M against fibroblast collagenase (MMP-1) and stromelysin (MMP-3), respectively.

266 r collagenase (MMP-1), gelatinase A (MMP-2), stromelysin (MMP-3), TIMP-1, and TIMP-2.

267 nase-1 (MMP-1) and only moderately inhibited stromelysin (MMP-3).

268 interstitial collagenase (MMP-1, 52 kDa) and stromelysin (MMP-3, 57 kDa).

269 rystal structures of the catalytic domain of stromelysin (MMP-3CD) complexed with inhibitors from clo

270 nd MMP-13), gelatinases (gelatinase A or B), stromelysins (MMP-3 and MMP-11), or matrilysin (MMP-7) a

271 ion of collagenases (MMP-1, -8, and -13) and stromelysins (MMP-3, -10, and -11) by human corneal epit

272 pha upregulate collagenases (MMP-1, -13) and stromelysins (MMP-3, -10, and -11) in human corneal epit

273 eries were incubated with MMP-3 (a member of stromelysins), MMP-9 (considered a gelatinase), and MMP-

274 Ribozymes inhibited IL-1-stimulated stromelysin mRNA expression in articular cartilage expla

275 Stromelysin mRNA increases also were localized primarily

276 significant decrease in both collagenase and stromelysin mRNA levels compared with IL-1 alone, with a

277 Stromelysin polymorphism may influence susceptibility an

278 There was minimal effect on stromelysin production (decrease from 107 +/- 16 ng/ml t

279 IL-1alpha-induced stromelysin production and proteoglycan loss from the ar

280 Interleukin-1alpha (IL-1alpha)-stimulated stromelysin production in rabbit synovial fibroblasts wa

281 inhibitor on IL-1alpha-induced MEK activity, stromelysin production, and cartilage degradation.

282 the transcriptional activation of the human stromelysin promoter, which contains palindromic Ets-bin

283 o cooperate with p300/CBP in stimulating the stromelysin promoter.

284 y small inhibitor could not deeply penetrate stromelysin's long narrow hydrophobic S1' pocket, the en

285 uman stromelysin-1 (SL-1) is a member of the stromelysin subfamily of matrix metalloproteinases (MMPs

286 a-Arg-NH(2) and, with higher efficiency, the stromelysin substrate Mca-Pro-Leu-Ala-Nva-Dpa-Ala-Arg-NH

287 The affinity of nonthiadiazole inhibitors of stromelysin-such as hydroxamic acids and others-can be d

288 amino acid appear to be more restrictive for stromelysin than for neutrophil collagenase, 72 kDa gela

289 otentially involved in the IL-1 induction of stromelysin, the human stromelysin 5'-flanking region wa

290 f 72 kDa gelatinase, fibroblast collagenase, stromelysin, tissue inhibitor of metalloproteinases (TIM

291 collagens from OA cartilage were denatured, stromelysin treated, and used for immunization and arthr

292 The production of p-ERK and stromelysin was also inhibited in IL-1alpha-stimulated r

293 or Mphi-conditioned medium, the induction of stromelysin was dramatically suppressed as compared with

294 This indicated that up-regulation of stromelysin was not essential for IL-1-induced cartilage

295 droxamic acid inhibitor of recombinant human stromelysin were systematically defined by taking advant

296 age degradation, such as IL-1beta, IL-6, and stromelysin, were also up-regulated in IL-17-treated cho

297 y to impart greater relative potency against stromelysin when larger hydrophobic groups are used.

298 oteinases collagenase, 92-kD gelatinase, and stromelysin, which degrade skin connective tissue and ma

299 bitor-1 (PAI-1) synthesis of collagenase and stromelysin, which remained predominantly in proenzyme f

300 e high levels of gelatinase A and B and some stromelysin, which suggests that this cell line may cont