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1 MMP-3 and MMP-10) and 3D cultures (MMP-9 and MMP-10).
2 d with a cathepsin inhibitor, cystatin C, or MMP-10.
3  a very potent and selective non-hydroxamate MMP-10/-13 inhibitor.
4 from IL-1 plus OSM-stimulated cartilage, and MMP-10 activated proMMP-1, proMMP-8, and proMMP-13.
5  as matrix metalloproteinase (MMP)-1, MMP-3, MMP-10 and MMP-12, are key players in the development of
6 is of this new insight into the relevance of MMP-10 and MMP-13 within the MMP network and the ban of
7 induced expression of the HDAC7 target genes Mmp-10 and Nur77, and inhibits VEGF-induced vascular per
8                                              MMP-10 and PKCiota are coordinately overexpressed in pri
9 hted induction of the matrix metalloprotease MMP-10 and the extracellular matrix protein mindin (enco
10 ore, the detectable levels of synovial fluid MMP-10 and the histologic detection of this proteinase i
11                             Transcription of MMP-10 and tissue inhibitor of metalloprotease 1 was inc
12 MPs in both fibroblast monolayers (MMP-3 and MMP-10) and 3D cultures (MMP-9 and MMP-10).
13 lved a proteolytic axis composed of plasmin, MMP-10, and MMP-1.
14 es in a matrix metalloproteinase-1 (MMP-1)-, MMP-10-, and ADAM-15 (a disintegrin and metalloproteinas
15             The high potency (IC50 of 31 nM [MMP-10] and 5 nM [MMP-13]) and selectivity over MMP-1, -
16                       In contrast, MMP-1 and MMP-10 are strongly induced during EC tube formation to
17 ation, and decreased production of mmp-3 and mmp-10 by human conjunctival fibroblasts.
18              To understand the regulation of MMP-10 by tissue inhibitors of metalloproteinases (TIMPs
19 n alpha(3)beta(1), whereas in normal corneas MMP-10 decreased laminin-10 and integrin alpha(3)beta(1)
20  and cell-based models demonstrated that the MMP-10-dependent collagenolytic activity was a product o
21                           One family member, MMP-10, directly cleaves Htt and prevents cell death whe
22                                 Knockdown of MMP-10 expression blocks anchorage-independent growth an
23                Immunohistochemistry assessed MMP-10 expression in diseased joint tissues.
24 negative PKCiota inhibits tumorigenicity and MMP-10 expression in subcutaneous NSCLC tumors.
25 expression inhibits NSCLC transformation and MMP-10 expression in vitro.
26 expressed in primary NSCLC tumors, and tumor MMP-10 expression predicts poor survival in NSCLC patien
27 ion of ADAMTS-5 expression and regulation of MMP-10 expression suggest complex and context-dependent
28                                              MMP-10 expression was confirmed in both chondrocytes and
29 ulted in enhanced ADAMTS-5 expression, while MMP-10 expression was suppressed.
30 -deficient cells restores transformation and MMP-10 expression, whereas expression of Par6alpha mutan
31 invasion of NSCLC cells through induction of MMP-10 expression.
32 h activation of matrix metalloproteinase-10 (MMP-10) expression.
33 broblasts and articular chondrocytes express MMP-10 following treatment with procatabolic stimuli.
34 p-regulation of matrix metalloproteinase 10 (MMP-10) following treatment with the procatabolic stimul
35  to MMP-3, little is known about the role of MMP-10 in cartilage catabolism.
36 a demonstrate a critical role for macrophage MMP-10 in controlling the tissue remodeling activity of
37 in diseased joint tissues strongly implicate MMP-10 in the cartilage degradome during arthritis.
38 mmunohistochemistry revealed the presence of MMP-10 in the synovium and cartilage of an IL-1 plus OSM
39 sufficient to induce expression of MMP-9 and MMP-10, in a manner requiring its USP activity, but not
40                                     Although MMP-10 is closely related to MMP-3, little is known abou
41 rpose of this study was to determine whether MMP-10 is expressed in connective tissue cells and to as
42                 Matrix metalloproteinase-10 (MMP-10) is expressed by macrophages and epithelium in re
43               siRNA suppression of MMP-1 and MMP-10 markedly blocks tube regression without affecting
44                                              MMP-10 may be implicated in H. pylori-mediated extracell
45 th H. pylori led to an increase in levels of MMP-10 messenger RNA, protein secretion, and activity.
46 P-2 for the active catalytic domain of human MMP-10 (MMP-10cd) using multiple kinetic approaches.
47              Novel targets, including MMP-8, MMP-10, MMP-14, MMP-19, MMP-25 and MMP-28, are also bein
48                                              MMP-10 modulation occurs via EGFR activation in a proces
49 of PML decreases basal and TNF-alpha-induced MMP-10 mRNA accumulation.
50 ciation between HDAC7 and MEF2 and decreases MMP-10 mRNA accumulation.
51 teinase (MMP)-10, leading to accumulation of MMP-10 mRNA.
52                                              MMP-10 overexpressed in the diabetic corneal epithelium
53                                              MMP-10 secretion increased by 90% with binding to type I
54 sponded to CsA treatment with a reduction in MMP-10 secretion.
55                                    Exogenous MMP-10 significantly enhanced collagenolysis from IL-1 p
56                 Matrix metalloproteinase 10 (MMP-10, stromelysin-2) is a secreted metalloproteinase w
57  mRNA levels of matrix metalloproteinase-10 (MMP-10/stromelysin-2) were significantly elevated in DR
58 C cells and addition of catalytically active MMP-10 to PKCiota- or Par6alpha-deficient cells restores
59                               The ability of MMP-10 to superactivate procollagenases that are relevan
60 alloproteinase 7 [MMP-7]) and stromelysin-2 (MMP-10), two MMPs induced by acute P. aeruginosa pulmona
61                                              MMP-10 up-regulation was dependent on several MAPKs, but
62 ther IL-1 plus OSM or TNFalpha plus OSM, and MMP-10 was detected in synovial fluid samples from patie
63 s down-regulated 9-fold, while expression of MMP-10 was up-regulated 14-fold, and these responses wer
64                     Synovial fluid levels of MMP-10 were determined by specific immunoassay.
65 ocks tube regression by inhibiting MMP-1 and MMP-10 while having no influence on EC tube formation.

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