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 jury also increased the levels/activation of matrix metalloproteinase 3 and 9.

9 ype in cardiac fibroblasts, suppressing MMP (matrix metalloproteinase)-3 and MMP-8 synthesis and indu

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

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

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

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

14 tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-3 and pro-fibrotic gene express

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

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

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

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

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

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

21 s downstream metastasis-associated proteins, matrix metalloproteinase 3, and IL-8.

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

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

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

25 Taken together, we identified the KDM6A-matrix metalloproteinase 3 axis as a key mediator of KMT

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

27 Matrix metalloproteinase 3 cleaves insulin-like growth f

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

29 expression of Pax1 and of Mmp3, encoding the matrix metalloproteinase 3 enzyme implicated in matrix r

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

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

32 Plasmin and matrix metalloproteinase-3 generate breakdown products o

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

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

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

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

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

38 ate immune activation, in particular YKL-40, matrix metalloproteinase 3, macrophage inflammatory prot

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 ciated virus 9 (AAV9)-mediated expression of matrix metalloproteinase-3 (MMP-3) can increase outflow

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

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

60 Matrix metalloproteinase-3 (MMP-3) participates in norma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 hat produce protumorigenic factors including matrix metalloproteinase 3 (MMP3), which promotes BRCA1-

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

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

80 rowth factor-binding protein 6 (IGFBP6), and matrix metalloproteinase-3 (MMP3), which are implicated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 barrier repair (matrix metalloproteinase 7, matrix metalloproteinase 3, the integrins beta6 and beta

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

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

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