ライフサイエンスコーパス: stromelysin 1

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

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

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

4 the explant culture supernatants, especially stromelysin-1.

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

6 e expression of the matrix metalloproteinase stromelysin-1.

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

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

9 n expression of the matrix metalloproteinase stromelysin-1.

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

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

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

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

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

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

16 The wild-type stromelysin-1 and the cysteine mutants (C75S and C75H) u

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

18 e matrix metalloproteinases gelatinase A and stromelysin-1 and the serine proteinase urokinase-type p

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

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

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

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

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

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

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

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

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

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

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

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

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

32 ated with matrix metalloproteinase 3 (MMP-3, stromelysin 1) but not with matrix metalloproteinase 2 (

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

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

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

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

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

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

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

40 -, 17,000-, 90-, and 200-fold selective over stromelysin 1, collagenase 1, and gelatinases A and B, r

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

42 Stromelysin-1 could provide a target for pharmacological

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

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

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

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

47 Stromelysin-1-deficient mice showed a markedly impaired

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

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

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

51 ansmembrane domain (DeltaMT-MMP1), a soluble stromelysin-1/DeltaMT-MMP1 chimera without the RRKR basi

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

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

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

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

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

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

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

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

60 the overexpression of both collagenase-1 and stromelysin-1 has been associated with the pathogenesis

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

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

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

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

65 Entactin (nidogen) was a specific target for stromelysin-1 in the extracellular matrix.

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

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

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

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

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

71 demonstrate that APMA-induced activation of stromelysin-1 involves protein interactions in addition

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

73 Stromelysin-1 is a member of the metalloproteinase famil

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

75 Stromelysin-1 is required for initiation of the response

76 cursor of matrix metalloproteinase 3 (MMP-3/ stromelysin 1) is activated in vitro by proteinases or m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 can stimulate keratinocyte collagenase-1 and stromelysin-1 production in a dose-dependent and matrix-

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

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

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

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

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

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

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

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

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

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

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

122 -1 segments have been introduced into MMP-3 (stromelysin 1) starting from the C-terminal end.

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

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

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

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

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

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

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

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

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

132 imals with mice expressing an autoactivating stromelysin-1 transgene targeted to mammary epithelial c

133 When stromelysin-1 transgenic mice were crossed with mice ove

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

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

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

137 Stromelysin-1 was expressed in both malignant and nonmal

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

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

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

141 ase A, MT-MMP, interstitial collagenase, and stromelysin-1 were localized to fibroblasts of tumor str

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