ライフサイエンスコーパス: collagenase-3

1 cleaved by MMP-1 (collagenase 1) or MMP-13 (collagenase 3).

2 22 x 10(6) m(-)(1) s(-)(1) for hydrolysis by collagenase 3.

3 ouse embryo fibroblasts bind and internalize collagenase-3.

4 entration of the proenzyme as well as active collagenase-3.

5 ssential for the triple helicase activity of collagenase-3.

6 tosolic extracts to AU-rich sequences in the collagenase 3 3'-untranslated region (UTR).

7 ent (FUSE)-binding protein 2 interacted with collagenase 3 3'-UTR sequences, and RNA interference dem

8 Matrix metalloproteinase-13 (collagenase-3), a member of the family of matrix metallo

9 activity levels for mixtures of MMPs such as collagenase 3 and gelatinase A.

10 nclusion, AU-rich sequences of the 3'-UTR of collagenase 3 and vinculin and FUSE-binding protein 2 re

11 Both collagenase-3 and Delta249-451 collagenase-3 hydrolyzed

12 The specific activities of both collagenase-3 and Delta249-451 collagenase-3 were found

13 a(v) integrins exert divergent regulation of collagenase-3 and osteocalcin expression during osteobla

14 Both collagenase-3 and osteocalcin mRNAs are expressed maxima

15 ctivation rate of the proenzyme initiated by collagenase-3 and our results indicate that progelatinas

16 However, FGF fails to induce MMP-13 (collagenase-3) and MMP-3 (stromelysin-1) in the Ets2-def

17 Interstitial collagenase, collagenase 3, and gelatinases are all likely to contrib

18 tical to human metalloelastase, stromelysin, collagenase-3, and matrilysin, respectively.

19 Gelatinase B, collagenase-3, and metalloelastase expression were more

20 by the recombinant catalytic domain of human collagenase 3 are identified.

21 ain interactions between progelatinase B and collagenase-3, as assessed using wild-type and C-termina

22 hodology described here required an improved collagenase-3-based mitochondrial isolation procedure an

23 evidence supporting a two-step mechanism of collagenase-3 binding and internalization involving both

24 In the present study, we show that collagenase-3 binding is calcium-dependent and occurs in

25 Ligand blot analysis shows that (125)I-collagenase-3 binds specifically to two proteins ( appro

26 of inhibition of wild-type and Delta249-451 collagenase-3 by wild-type and mutant tissue inhibitors

27 ngs support previous observations that human collagenase 3 can degrade aggrecan, type II and type IV

28 te here that three MMPs-stromelysin-3 (ST3), collagenases-3 (Col3), and collagenases-4 (Col4)-also ha

29 the gelatinase A/TIMP-2 axis, gelatinase B, collagenase-3, collagenase-2, or stromelysin-1.

30 of the catalytic domain of recombinant mouse collagenase-3, complexed to the hydroxamate inhibitor (R

31 Collagenase 3 degrades collagen fibrils and is necessary

32 effects of IL-6 and its soluble receptor on collagenase 3 expression in osteoblast-enriched cells fr

33 Consistent with this, collagenase-3 expression and cytokine production (interl

34 hese studies demonstrate that stimulation of collagenase-3 expression during osteoblast differentiati

35 o confer functional TGF-beta1-stimulation of collagenase-3 expression in MDA-MB231 cells.

36 lecule in metastatic bone cancer, stimulates collagenase-3 expression in the human breast cancer cell

37 Here, we show that TGF-beta 1 stimulates collagenase-3 expression in the rat osteoblastic cell li

38 are also required for TGF-beta 1-stimulated collagenase-3 expression in UMR 106-01 cells.

39 e JNK pathway, reduced TGF-beta 1-stimulated collagenase-3 expression, indicating that the p38 MAPK a

40 Human collagenase-3 expression, previously seen only in a brea

41 ncreases osteocalcin expression and inhibits collagenase-3 expression, suggesting that the RGD peptid

42 defect in IL-1--induced AP-1 activation and collagenase-3 expression.

43 hed fluorescent substrates, but Delta249-451 collagenase-3 failed to cleave native triple helical col

44 thways and their components in expression of collagenase-3 following TGF-beta 1 treatment in UMR 106-

45 -treated mice in situ hybridization revealed collagenase 3 gene induction in cells resembling macroph

46 hyroid hormone regulatory regions of the rat collagenase-3 gene and the proteins involved in this reg

47 oteins and transcriptional activation of the collagenase-3 gene by TGF-beta1.

48 ponsible for the developmental regulation of collagenase-3 gene expression in osteoblasts.

49 how that, in differentiating MC3T3-E1 cells, collagenase-3 gene expression increases in the presence

50 associated with decreased AP-1 activity and collagenase-3 gene expression.

51 response element, col3A, associated with the collagenase-3 gene in human U2OS osteosarcoma cells; col

52 g to the activator protein-1 site in the rat collagenase-3 gene in response to parathyroid hormone in

53 canine matrix metalloproteinase-13 (MMP-13), collagenase-3 gene promoter has been isolated and charac

54 Parathyroid hormone induces collagenase-3 gene transcription in rat osteoblastic cel

55 opmental expression is due to an increase in collagenase-3 gene transcription.

56 trating that these sites are responsible for collagenase-3 gene transcription.

57 ional analysis of the promoter region of the collagenase-3 gene was carried out, and we identified th

58 activator protein-1 (AP-1), as at the human collagenase-3 gene, and tested whether the identified in

59 of the rat interstitial collagenase (MMP-13; collagenase-3) gene from fibroblastic cells directly adj

60 nce elevated levels of both gelatinase B and collagenase-3 have been observed in arthritis and breast

61 Both collagenase-3 and Delta249-451 collagenase-3 hydrolyzed the large tenascin C isoform, f

62 The expression of collagenase 3 in medial tibial cartilage from 2-month-ol

63 Human progelatinase B was activated by collagenase-3 in a time-dependent fashion.

64 ecific chemokines, selectins, cytokines, and collagenase-3 in the synovium of IL-17R-/- mice.

65 tion of matrix-metalloproteinase 13 (MMP-13, collagenase 3) in the skin.

66 ation proceeds via bimolecular cleavage with collagenase-3 involving sequential cleavage of the prope

67 Collagenase-3 is normally expressed in hypertrophic chon

68 Matrix metalloproteinase (MMP) 13 (collagenase 3) is poised to play a crucial role in bone

69 , which is possibly the counterpart of human collagenase-3, is induced by interleukin-1beta plus tumo

70 cause we were most interested in determining collagenase 3 levels as a potential biological marker fo

71 metalloproteinases (MMPs), including MMP-13/collagenase-3, likely contribute to collagen catabolism

72 ive synthetic inhibitor of collagenase 2 and collagenase 3 (matrix metalloproteinase 8 [MMP-8] and MM

73 Collagenase-3 (matrix metalloproteinase 13, MMP-13) was

74 Collagenase-3 (matrix metalloproteinase-13) is expressed

75 ell type in the joint tissue, do not produce collagenase-3 message.

76 MMP-1]), neutrophil collagenase (MMP-8), and collagenase 3 (MMP-13) proteins and messenger RNA (mRNA)

77 The substrate specificity of human collagenase 3 (MMP-13), a member of the matrix metallopr

78 (-/-)/apoE(-/-)) or express wild-type MMP-13/collagenase-3 (Mmp-13(+/+)/apoE(-/-)).

79 ipoprotein E-deficient mice that lack MMP-13/collagenase-3 (Mmp-13(-/-)/apoE(-/-)) or express wild-ty

80 It has been suggested that increased collagenase-3 (MMP-13) activity plays a pivotal role in

81 The inhibitors were typically potent against collagenase-3 (MMP-13) and gelatinase A (MMP-2), while t

82 ery low levels in normal myocardium, such as collagenase-3 (MMP-13) and the membrane-type-1 MMPs, are

83 matrix metalloproteinase (MMP) interstitial collagenase-3 (MMP-13) and the previously studied MMP-1

84 l structure of the catalytic domain of human collagenase-3 (MMP-13) complexed to a potent, sulfonamid

85 structure of the catalytic fragment of human collagenase-3 (MMP-13) complexed with a sulfonamide deri

86 Collagenase-3 (MMP-13) is a member of this family and pr

87 at binds the alpha5beta1 integrin, stimulate collagenase-3 (MMP-13) production and cartilage destruct

88 unodetection have now provided evidence that collagenase-3 (MMP-13), an enzyme recently cloned from h

89 MMP and TIMP mRNAs [Str1, MT1-MMP, (MMP-14) collagenase-3 (MMP-13), gelatinase A (MMP-2), and TIMP-1

90 Collagenase-3 (MMP13), a member of the matrix metallopro

91 IL-6 and IL-6sR increased collagenase 3 mRNA in MC3T3 cells but only modestly in s

92 Cortisol increases collagenase 3 mRNA in osteoblasts by stabilizing collage

93 Here, we demonstrate that collagenase-3 mRNA expression in differentiating MC3T3-E

94 Collagenase-3 mRNA is initially detectable when osteobla

95 1300-, 11-, and 820-fold selective for human collagenase 3 over the MMPs stromelysin-1, gelatinase B,

96 hese data support the hypothesis that MMP-13/collagenase-3 plays a vital role in the regulation and o

97 Matrix metalloproteinase 13 (Mmp13, collagenase-3) plays an essential role in bone metabolis

98 The C-terminal domain of wild-type collagenase-3 promoted increased association rates with

99 site and the runt domain binding site in the collagenase-3 promoter act cooperatively in response to

100 he AP-1- and RD-binding sites also inhibited collagenase-3 promoter activation.

101 cooperative effect on TGF-beta 1-stimulated collagenase-3 promoter activity in these cells.

102 a1, and this transactivation is required for collagenase-3 promoter activity in UMR cells.

103 Transient transfection studies show that collagenase-3 promoter activity increases during cell di

104 fa1 in the signaling pathway for PTH-induced collagenase-3 promoter activity was analyzed.

105 PTH stimulation of collagenase-3 promoter activity was completely abrogated

106 anisms responsible for TGF-beta1 response on collagenase-3 promoter activity, a functional analysis o

107 -1 or the runt domain binding site decreased collagenase-3 promoter activity, demonstrating that thes

108 c-Jun or core-binding factor a1 to increase collagenase-3 promoter activity, suggesting that there i

109 aling is essential for TGF-beta 1-stimulated collagenase-3 promoter activity.

110 s as necessary for full TGF-beta1-stimulated collagenase-3 promoter activity.

111 eoblasts or core-binding factor a1 increased collagenase-3 promoter activity.

112 unD repressed core-binding factor a1-induced collagenase-3 promoter activity.

113 -binding factor a1 synergistically increased collagenase-3 promoter activity.

114 proteins, c-Fos.c-Jun and Cbfa, regulate the collagenase-3 promoter in parathyroid hormone-treated an

115 and Cbfa1/Runx2 at the distal RD site of the collagenase-3 promoter occurred in response to TGF-beta1

116 y bind the AP-1- and RD-binding sites in the collagenase-3 promoter.

117 Collagenase 3 protein was also abundant throughout the m

118 also found focal areas of collagenase 1 and collagenase 3 proteins localized to the extracellular ma

119 al contribution from two receptors, with the collagenase-3 receptor acting as a high affinity primary

120 nd internalization involving both a specific collagenase-3 receptor and the low density lipoprotein r

121 ggest that the 170-kDa protein is a specific collagenase-3 receptor.

122 We conclude that the internalization of collagenase-3 requires the participation of the low dens

123 synthetic peptide substrates made from human collagenase 3 selected phage clones reveals that some of

124 parison with the reported X-ray structure of collagenase-3 showed evidence of flexibility for the loo

125 tors also plays a role in induction of human collagenase-3, since it binds to the AP-1 site of this m

126 constructs, demonstrated that the 3'-UTR of collagenase 3 stabilizes c-fos mRNA in transcriptionally

127 , IL-6, in the presence of IL-6sR, increases collagenase 3 synthesis in osteoblasts by transcriptiona

128 bstrates tested have specific activities for collagenase 3 that are 37,000-, 17,000-, 90-, and 200-fo

129 reviously identified a specific receptor for collagenase-3 that mediates the binding, internalization

130 c day 13-15 mandibles, whereas gelatinase B, collagenase-3, TIMP-1 and TIMP-2 mRNA were found primari

131 as primarily localized to endothelial cells, collagenase-3 to isolated tumor cells, and metalloelasta

132 Binding of procollagenase-3 and active collagenase-3 to type I collagen is mediated by the C-te

133 agenase 3 mRNA in osteoblasts by stabilizing collagenase 3 transcripts.

134 enase 1), MMP-8 (collagenase 2), and MMP-13 (collagenase 3), truncated forms of MMP-8 and MMP-13 lack

135 ADAMTS-4 with MMP-1 (collagenase 1), MMP-13 (collagenase 3), trypsin, and thermolysin using triple-he

136 transient transfections of CMV-driven c-fos collagenase 3'-UTR chimeric constructs, demonstrated tha

137 Some procollagenase 3 and active collagenase 3 was also shown to be present.

138 collagenase was always detected, and active collagenase 3 was detectable in some experiments.

139 RetA, prointerstitial collagenase and active collagenase 3 were sometimes detected, but not in all ex

140 ities of both collagenase-3 and Delta249-451 collagenase-3 were found to be similar using two quenche

141 on of the pro-domain of MT1-MMP with that of collagenase 3) were functionally inactive in terms of bi

142 ryo fibroblasts bind but fail to internalize collagenase-3, whereas UMR 106-01 and wild-type mouse em

143 I collagen were susceptible to Delta249-451 collagenase-3, which indicates that the catalytic domain