ライフサイエンスコーパス: matrix metalloproteinase 3

1 -C motif) ligand 2, Nidogen1, urokinase, and matrix metalloproteinase 3.

2 ating factor, matrix metalloproteinase-9 and matrix metalloproteinase-3.

3 rable regulation of gene expression, notably matrix metalloproteinases 3, 10, and 13.

4 The protein abundance of matrix metalloproteinases 3, 8, 9, and 12 increased in T

5 Transcription levels of matrix metalloproteinases-3, -9, and -13, aggrecanase-1,

6 PTP-alpha promotes fibroblast expression of matrix metalloproteinase 3, a matrix-degrading proteinas

7 ion of the fibrogenic cytokine TGF-beta1 and matrix metalloproteinase-3, an important mediator in fib

8 ligands (Ccl2, Ccl7, Ccl9), lipocalin-2, and matrix metalloproteinase-3 and -12 of innate immunity we

9 otactic protein-1 mRNA levels while inducing matrix metalloproteinase-3 and CD36.

10 tivity corresponded to increased activity of matrix metalloproteinase-3 and degradation of fibrin(oge

11 Galectin-3 correlated significantly with matrix metalloproteinase-3 and monocyte chemoattractant

12 xploring the regulatory relationship between matrix metalloproteinase-3 and syndecan 4 in disc degene

13 ression of late responsive genes such as the matrix metalloproteinase-3 and the RE1 silencing transcr

14 Synovial interleukin-6 and matrix metalloproteinases 3 and 13 gene expression was a

15 ease of glycosaminoglycan, nitric oxide, and matrix metalloproteinases 3 and 13 were determined by di

16 w group also displayed reduced expression of matrix metalloproteinases-3 and -9 compared with the Bas

17 gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdow

18 iated with cGVHD, and only four (ST2, CXCL9, matrix metalloproteinase 3, and osteopontin) were necess

19 xpress high levels of C/EBPbeta, keratin-14, matrix metalloproteinase-3, and beta-catenin.

20 c-Myc, epidermal growth factor receptor and matrix metalloproteinase 3 as well as downregulation of

21 ble nitric oxide synthase, cyclooxygenase 2, matrix metalloproteinase 3, cathepsin B, and cathepsin K

22 Matrix metalloproteinase 3 cleaves insulin-like growth f

23 ein 1 (CHI3L1), CHI3L2, complement factor B, matrix metalloproteinase 3, ECM-1, haptoglobin, serum am

24 wer in MKK6(-/-), as were articular IL-6 and matrix metalloproteinase-3 expression.

25 This pathway transcriptionally activated the matrix metalloproteinase-3 gene and promoted oral SCC ce

26 Plasmin and matrix metalloproteinase-3 generate breakdown products o

27 bited IL-1beta-activated prostaglandin E(2), matrix metalloproteinase 3, IL-6, IL-8, and monocyte che

28 metalloproteinase-2, and tissue inhibitor of matrix metalloproteinase-3 inversely correlated with TGF

29 To date TIMP-3 (tissue inhibitor of matrix metalloproteinases-3) is the only endogenous inhi

30 Reductions in serum interleukin-6 and matrix metalloproteinase 3 levels also occurred as early

31 re seen for inducible nitric oxide synthase, matrix metalloproteinase 3, macrophage colony-stimulatin

32 d in psoriatic arthritis synovium, and serum matrix metalloproteinases-3 may be a reliable biomarker

33 Inactivation of RhoA/ROCK in MSCs induces matrix metalloproteinase-3-mediated CTGF cleavage, resul

34 of the 173 residue catalytic domain of human matrix metalloproteinase 3 (MMP-3(DeltaC)) affected by b

35 rosis factor alpha (TNFalpha) expression and matrix metalloproteinase 3 (MMP-3) and ADAMTS-4 messenge

36 to examine the protein expression levels of matrix metalloproteinase 3 (MMP-3) and MMP-13 in knee jo

37 wing injurious compression of the cartilage, matrix metalloproteinase 3 (MMP-3) and MMP-13 messenger

38 g was performed to examine the expression of matrix metalloproteinase 3 (MMP-3) and MMP-13, degraded

39 Matrix metalloproteinase 3 (MMP-3) and tissue inhibitor

40 Production of interferon-gamma, RANTES, and matrix metalloproteinase 3 (MMP-3) by NK cell and FLS co

41 f inducible nitric oxide synthase (iNOS) and matrix metalloproteinase 3 (MMP-3) were assessed in cult

42 The addition of procollagenase activators, matrix metalloproteinase 3 (MMP-3), and APMA to IL-1alph

43 ion, and expression of interleukin-6 (IL-6), matrix metalloproteinase 3 (MMP-3), and MMP-13 in joint

44 egradation of hyaluronan, release of HMGB-1, matrix metalloproteinase 3 (MMP-3), and MMP-13, and prot

45 of invasive properties and the induction of matrix metalloproteinase 3 (MMP-3), causing the cleavage

46 fibroblasts with PBEF promoted expression of matrix metalloproteinase 3 (MMP-3), CCL2, and CXCL8, an

47 The gene expressions of matrix metalloproteinase 3 (MMP-3), type II collagen, an

48 ecame thrombin-unclottable when treated with matrix metalloproteinase 3 (MMP-3, stromelysin 1) but no

49 The precursor of matrix metalloproteinase 3 (MMP-3/ stromelysin 1) is act

50 TNF and IL-1 increase matrix metalloproteinase-3 (MMP-3) expression in the tra

51 amined for matrix loss and the expression of matrix metalloproteinase-3 (MMP-3) following treatment w

52 el, both PYY and NPY increased expression of matrix metalloproteinase-3 (MMP-3) to a level sufficient

53 though CAFs promoted prostate cancer growth, matrix metalloproteinase-3 (MMP-3) was lower in CAFs but

54 We report here that matrix metalloproteinase-3 (MMP-3) was newly induced and

55 We report here that the active form of matrix metalloproteinase-3 (MMP-3) was released into the

56 e have previously investigated stromelysin-1/matrix metalloproteinase-3 (MMP-3), a stromal enzyme upr

57 IL-1beta, tumor necrosis factor-alpha, IL-8, matrix metalloproteinase-3 (MMP-3), MMP-9, and MMP-12.

58 MATRIX METALLOPROTEINASE-3 (MMP-3), or stromelysin-1, is

59 In periodontitis, matrix metalloproteinase-3 (MMP-3, stromelysin 1) is pre

60 Elevated expression of matrix metalloproteinase-3 (MMP-3/stromelysin-1) is asso

61 ry TGFalpha-induced morphogenetic effectors, matrix metalloproteinase-3 (MMP-3/stromelysin-1), and fi

62 Activated matrix metalloproteinase 3 (MMP3) and MMP12, which are i

63 TWIST1 induced matrix metalloproteinase 3 (MMP3) expression without dir

64 Because matrix metalloproteinase 3 (MMP3) is known to degrade ag

65 secreted frizzled-related protein 1 (SFRP1), matrix metalloproteinase 3 (MMP3), and dermatopontin (DP

66 Matrix metalloproteinase 3 (MMP3), is over expressed in

67 preferentially induced by BRAF, particularly matrix metalloproteinase 3 (MMP3), MMP9, and MMP13.

68 Here, we identify matrix metalloproteinase-3 (MMP3) as a regulator of Wnt

69 evious results showed that an endopeptidase, matrix metalloproteinase-3 (MMP3), was induced and activ

70 roteinase-2 (TIMP-2) and tissue inhibitor of matrix metalloproteinase-3 mRNA expression.

71 enesis inhibitor--either tissue inhibitor of matrix metalloproteinase-3 (n = 22) or a truncated solub

72 death/MI: intercellular adhesion molecule-1, matrix metalloproteinase-3, N-terminal pro-B-type natriu

73 omarkers (intercellular adhesion molecule-1, matrix metalloproteinase-3, N-terminal pro-B-type natriu

74 phism of the promoter region of stromelysin (matrix metalloproteinase 3) on susceptibility to primary

75 secretion (P = 0.03), increased secretion of matrix metalloproteinase-3 (P = 0.03), and increased sec

76 and synovial tissue turnover, levels of pro-matrix metalloproteinase 3 (pro-MMP-3), pro-MMP-1, and c

77 r IL-6, IL-8, matrix metalloproteinase-1 and matrix metalloproteinase-3 production.

78 enhanced not only fibronectin, but also pro-matrix metalloproteinase 3 (proMMP-3) expression.

79 urthermore, IL-1beta-induced IL-8, IL-6, and matrix metalloproteinase-3 protein production was signif

80 for miR-19a/b in the regulation of IL-6 and matrix metalloproteinase 3 release by controlling TLR2 e

81 +) matrix resulted in the strongest IL-6 and matrix metalloproteinase-3 release, and was even more pr

82 matory/prodestructive properties (e.g., IL-6/matrix metalloproteinase 3-release) in response to matri

83 In parallel, we found that both IL-6 and matrix metalloproteinase 3 secretion was significantly d

84 al ADAM17 inhibitor, the tissue inhibitor of matrix metalloproteinases-3 (TIMP3), or intravitreal inj

85 h polyangiitis (Churg-Strauss syndrome); and matrix metalloproteinase-3, tissue inhibitor of metallop

86 Gene expression of matrix metalloproteinase-3 was 4-fold greater in ETR sam