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1 MMP-3 and MMP-10) and 3D cultures (MMP-9 and MMP-10).
2 (MAPT, NEFL) and tissue remodelling (TMSB10, MMP-10).
3 h MMP-3 and disrupt unique interactions with MMP-10.
4 d with a cathepsin inhibitor, cystatin C, or MMP-10.
5 r the inhibition of MMP-3 in preference over MMP-10.
6 tro, suggesting ZO-1 as a novel substrate of MMP-10.
8 us to discover matrix metalloproteinase-10 (MMP-10), a secreted zinc-dependent endopeptidase, as one
10 gnificantly increased sHB-EGF, inhibition of MMP-10 activity using a broad spectrum MMP inhibitor had
11 This study investigated trophoblast mediated MMP-10 and HB-EGF expression and determined if there was
12 l analysis confirmed increased expression of MMP-10 and MET in bronchial epithelial cells and in sube
13 ing stringent false discovery rate analysis, MMP-10 and MET were significantly overexpressed in biops
14 as matrix metalloproteinase (MMP)-1, MMP-3, MMP-10 and MMP-12, are key players in the development of
15 is of this new insight into the relevance of MMP-10 and MMP-13 within the MMP network and the ban of
16 induced expression of the HDAC7 target genes Mmp-10 and Nur77, and inhibits VEGF-induced vascular per
18 l relatively novel proteins, such as TMSB10, MMP-10 and SMOC2, which have potential as novel biomarke
19 hted induction of the matrix metalloprotease MMP-10 and the extracellular matrix protein mindin (enco
20 ore, the detectable levels of synovial fluid MMP-10 and the histologic detection of this proteinase i
21 was a relationship between the secretion of MMP-10 and the release of soluble HB-EGF (sHB-EGF) from
24 usly shown that matrix metalloproteinase 10 (MMP-10) and Heparin binding-EGF like growth factor (HB-E
27 es in a matrix metalloproteinase-1 (MMP-1)-, MMP-10-, and ADAM-15 (a disintegrin and metalloproteinas
36 s, our findings illustrate that induction of MMP-10 could lead to podocyte injury by degrading ZO-1,
37 n alpha(3)beta(1), whereas in normal corneas MMP-10 decreased laminin-10 and integrin alpha(3)beta(1)
38 hanism where Piezo1 activity increased MMP-1/MMP-10, decreased collagen I and fibronectin, and increa
39 and cell-based models demonstrated that the MMP-10-dependent collagenolytic activity was a product o
46 expressed in primary NSCLC tumors, and tumor MMP-10 expression predicts poor survival in NSCLC patien
47 ion of ADAMTS-5 expression and regulation of MMP-10 expression suggest complex and context-dependent
51 -deficient cells restores transformation and MMP-10 expression, whereas expression of Par6alpha mutan
54 broblasts and articular chondrocytes express MMP-10 following treatment with procatabolic stimuli.
55 p-regulation of matrix metalloproteinase 10 (MMP-10) following treatment with the procatabolic stimul
56 1 variants bound to MMP-3 and counter-target MMP-10 how structural alterations within the N-terminal
58 a demonstrate a critical role for macrophage MMP-10 in controlling the tissue remodeling activity of
60 t SGHVMC-9, a human VSMC cell line, secreted MMP-10 in response to trophoblast conditioned medium (TC
62 mmunohistochemistry revealed the presence of MMP-10 in the synovium and cartilage of an IL-1 plus OSM
64 sufficient to induce expression of MMP-9 and MMP-10, in a manner requiring its USP activity, but not
67 rpose of this study was to determine whether MMP-10 is expressed in connective tissue cells and to as
73 th H. pylori led to an increase in levels of MMP-10 messenger RNA, protein secretion, and activity.
74 P-2 for the active catalytic domain of human MMP-10 (MMP-10cd) using multiple kinetic approaches.
81 ic mice with podocyte-specific expression of MMP-10, proteinuria was aggravated after injury induced
89 ed CSF level of matrix metalloproteinase 10 (MMP-10) showed a higher probability of progressing to de
93 mRNA levels of matrix metalloproteinase-10 (MMP-10/stromelysin-2) were significantly elevated in DR
94 six of these markers (DDC, CRH, MMP-3, ABL1, MMP-10, THOP1) was developed and validated in independen
95 C cells and addition of catalytically active MMP-10 to PKCiota- or Par6alpha-deficient cells restores
98 alloproteinase 7 [MMP-7]) and stromelysin-2 (MMP-10), two MMPs induced by acute P. aeruginosa pulmona
101 ther IL-1 plus OSM or TNFalpha plus OSM, and MMP-10 was detected in synovial fluid samples from patie
102 s down-regulated 9-fold, while expression of MMP-10 was up-regulated 14-fold, and these responses wer
103 ts with proteinuric chronic kidney diseases, MMP-10 was upregulated specifically in the podocytes of
107 ases also had elevated circulating levels of MMP-10, which correlated with the severity of kidney ins
108 nvolved in inflammatory processes, including MMP-10, which is suggested to have a role in high type-2
109 ocks tube regression by inhibiting MMP-1 and MMP-10 while having no influence on EC tube formation.