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Matrix metallopeptidase 13

Matrix Metalloproteinase 13, collagenase-3, MMP13
Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Most MMP's are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. The protein encoded by this gene cleaves type II collagen more efficiently than types I and III. It may be involved in articular cartilage turnover and cartilage pathophysiology associated with osteoarthritis. The gene is part of a cluster of MMP genes which localize to chromosome 11q22.3. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, V1a, HAD, POLYMERASE, Aggrecan
Papers on Matrix Metalloproteinase 13
Pulsed electromagnetic field (PEMF) treatment reduces expression of genes associated with disc degeneration in human intervertebral disc cells.
Lotz et al., San Francisco, United States. In Spine J, Feb 2016
Consistent with our previous results, after 4 days PEMF tended to reduce IL-1α-associated gene expression of IL-6 (25%, p = 0.07) in NP cells and MMP13 (26%, p = 0.10) in AF cells.
MicroRNA-320 regulates matrix metalloproteinase-13 expression in chondrogenesis and interleukin-1β-induced chondrocyte responses.
Liao et al., Guangzhou, China. In Osteoarthritis Cartilage, Feb 2016
The aim of this study was to determine whether microRNA-320 (miR-320) regulates the expression of MMP-13 in chondrogenesis and inflammation.
Reduced Response of Human Meniscal Cells to Osteogenic Protein 1 during Osteoarthritis and Pro-inflammatory Stimulation.
Ferguson et al., Winston-Salem, United States. In Osteoarthritis Cartilage, Feb 2016
RESULTS: OP1 treatment of normal meniscus cells resulted in significant, dose-dependent increases in ACAN (aggrecan) and COL2A1, and decreased MMP13 gene transcription, while only ACAN was upregulated (p<0.01) at the highest dose of OP1 in OA meniscus cells.
Chronic mild stress influences nerve growth factor through a matrix metalloproteinase-dependent mechanism.
Budziszewska et al., Kraków, Poland. In Psychoneuroendocrinology, Jan 2016
We have shown that NGF degradation in the hypothalamus of rats subjected to chronic mild stress is matrix metalloproteinase-dependent and related to an increase in the active forms of some metalloproteinases (MMP), including MMP2, MMP3, MMP9 and MMP13, while the NGF maturation process does not seem to be changed.
Effect of M3 muscarinic acetylcholine receptor deficiency on collagen antibody-induced arthritis.
Lips et al., Gießen, Germany. In Arthritis Res Ther, Dec 2015
Moreover, in M3R(-/-) mice, gene expression of markers for bone degradation (matrix metalloproteinase 13, cathepsin K and receptor activator of nuclear factor-κB ligand) was already increased in mice with low arthritis score.
Blood-brain barrier damage in vascular dementia.
Nakagawa et al., Japan. In Neuropathology, Dec 2015
In addition, mRNA expression of osteopontin, matrix metalloproteinase-13 (MMP-13), and CD36 was increased in vessels showing BBB damage in hypertensive SHRSP.
MicroRNAs: exploring new horizons in osteoarthritis.
Nugent, Dublin, Ireland. In Osteoarthritis Cartilage, Dec 2015
Many of the dysregulated miRNAs have been shown to regulate expression of inflammatory pathways such as interleukin-mediated or matrix metalloproteinase-13 (MMP-13)-mediated degradation of the articular cartilage extracellular matrix (ECM).
Secreted and O-GlcNAcylated MIF binds to the human EGF receptor and inhibits its activation.
Lu et al., Houston, United States. In Nat Cell Biol, Oct 2015
Activation of EGFR through mutation or its ligand binding enhances the secretion of MMP13, which degrades extracellular MIF, and results in abrogation of the negative regulation of MIF on EGFR.
Selective regulation of Mmp13 by 1,25(OH)2D3, PTH, and Osterix through distal enhancers.
Pike et al., Madison, United States. In J Steroid Biochem Mol Biol, Oct 2015
UNASSIGNED: Matrix metalloproteinase 13 (MMP13, collagenase-3) is a vital component for chondrocyte and osteoblast maturation, and is aberrantly expressed in numerous disease states.
Regulation of the catabolic cascade in osteoarthritis by the zinc-ZIP8-MTF1 axis.
Chun et al., Kwangju, South Korea. In Cell, 2014
ZIP8-mediated Zn2+ influx upregulated the expression of matrix-degrading enzymes (MMP3, MMP9, MMP12, MMP13, and ADAMTS5) in chondrocytes.
Osteoarthritis year 2013 in review: genetics and genomics.
Gonzalez, Santiago de Compostela, Spain. In Osteoarthritis Cartilage, 2013
The role of DNA methylation in regulation of NOS2, SOX9, MMP13 and IL1B has been further clarified.
Markers of breast cancer stromal fibroblasts in the primary tumour site associated with lymph node metastasis: a systematic review including our case series.
Brentani et al., São Paulo, Brazil. In Biosci Rep, 2012
Biomarkers evaluated in these studies may be divided in two groups, according to their ontology: extracellular matrix components [MMP13 (matrix metalloproteinase 13), TIMP2 (tissue inhibitor of metalloproteinases-2), THBS1 (thrombospondin 1), LGALS1 (lectin, galactoside-binding, soluble, 1)] and response to wounding [PDPN (podoplanin), PLAU (plasminogen activator, urokinase), PLAUR (plasminogen activator, urokinase receptor), CAV1 (caveolin 1), THBS1, LGALS1].
MicroRNA-125b down-regulates matrix metallopeptidase 13 and inhibits cutaneous squamous cell carcinoma cell proliferation, migration, and invasion.
Pivarcsi et al., Stockholm, Sweden. In J Biol Chem, 2012
a novel molecular mechanism by which MMP13 is up-regulated in cSCCs and indicate that miR-125b plays a tumor suppressive role in cSCC.
Defining requirements for collagenase cleavage in collagen type III using a bacterial collagen system.
Brodsky et al., United States. In J Biol Chem, 2012
The minimum collagen type III sequence necessary for cleavage by MMP1 and MMP13 was 5 GXY triplets, including 4 residues before and 11 residues after the cleavage site (P4-P11').
β-adrenergic receptor stimulation transactivates protease-activated receptor 1 via matrix metalloproteinase 13 in cardiac cells.
Blaxall et al., Rochester, United States. In Circulation, 2012
demonstrate that beta-adrenergic receptor stimulation leads to MMP-13 transactivation of protease-activated receptor 1 in both cardiac fibroblasts and cardiomyocytes
Matrix metalloproteinase 13 genotype in rs640198 polymorphism is associated with severe coronary artery disease.
Vítovec et al., Brno, Czech Republic. In Dis Markers, 2011
T allele of MMP-13 intron polymorphism rs640198 is associated with the severity of coronary artery disease.
Identification of a central role for complement in osteoarthritis.
Robinson et al., Palo Alto, United States. In Nat Med, 2011
Further, MAC colocalized with matrix metalloprotease 13 (MMP13) and with activated extracellular signal-regulated kinase (ERK) around chondrocytes in human osteoarthritic cartilage.
AT1 receptors activation enhances the expression of MMP-2, MMP-13 and VEGF but not MMP-9 in B16F10 melanoma cells.
Falahtpishe et al., Tehrān, Iran. In Pak J Biol Sci, 2011
Data show that angiotensin II through activation of AT1 receptors can stimulate the expression of MMP-2, MMP-13 and VEGF, but not MMP-13, in B16F10 melanoma cells.
Hypoxia-inducible factor-2alpha is a catabolic regulator of osteoarthritic cartilage destruction.
Chun et al., Kwangju, South Korea. In Nat Med, 2010
HIF-2alpha directly induces the expression in chondrocytes of genes encoding catabolic factors, including matrix metalloproteinases (MMP1, MMP3, MMP9, MMP12 and MMP13), aggrecanase-1 (ADAMTS4), nitric oxide synthase-2 (NOS2) and prostaglandin-endoperoxide synthase-2 (PTGS2).
Transcriptional regulation of endochondral ossification by HIF-2alpha during skeletal growth and osteoarthritis development.
Kawaguchi et al., Tokyo, Japan. In Nat Med, 2010
Chondrocyte hypertrophy followed by cartilage matrix degradation and vascular invasion, characterized by expression of type X collagen (COL10A1), matrix metalloproteinase-13 (MMP-13) and vascular endothelial growth factor (VEGF), respectively, are central steps of endochondral ossification during normal skeletal growth and osteoarthritis development.
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