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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 26 Jul 2015.

Matrix metallopeptidase 3

MMP-3, Matrix Metalloproteinase 3, stromelysin-1, MEF2
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. This gene encodes an enzyme which degrades fibronectin, laminin, collagens III, IV, IX, and X, and cartilage proteoglycans. The enzyme is thought to be involved in wound repair, progression of atherosclerosis, and tumor initiation. 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: matrix metalloproteinase, MMP-9, CAN, HAD, Interleukin-6
Papers using MMP-3 antibodies
Isolation and characterization of the cyanogen bromide peptides from the l(II) chain of chick cartilage collagen.
Supplier
Buehler Markus J., In PLoS ONE, 1970
... mercuric acetate (APMA) for 1 hr at 37°C or by the recombinant active catalytic domain of MMP-3 (Merck-Calbiochem) at 1∶100 molar ratio ...
Papers on MMP-3
The pro-inflammatory cytokine s14-3-3ε is a ligand of CD13/Aminopeptidase N in cartilage.
New
Jacques et al., Paris, France. In J Cell Sci, 24 Aug 2015
14-3-3ε-induced (MMP-3) and MMP-13 was significantly reduced with CD13/APN knockdown, which suggests its critical role in 14-3-3ε signal transduction.
The effect of gender and genetic polymorphisms on MMPs and TIMPs plasma levels in different infectious and non-infectious conditions.
New
Valle-Garay et al., Oviedo, Spain. In Clin Exp Immunol, 22 Aug 2015
MMP-1(-1607 1G/2G), MMP-3(-1612 5A/6A), MMP-8(-799C/T), MMP-9(-1562 C/T), and MMP-13(-77A/G) SNPs were genotyped.
IRF2BP2 Reduces Macrophage Inflammation and Susceptibility to Atherosclerosis.
New
Stewart et al., Ottawa, Canada. In Circ Res, 20 Aug 2015
Promoter studies revealed that IRF2BP2 is required for MEF2-dependent activation of KLF2.
Adiponectin is required for cardiac MEF2 activation during pressure overload induced hypertrophy.
New
Sweeney et al., Toronto, Canada. In J Mol Cell Cardiol, 18 Aug 2015
UNASSIGNED: Cardiomyocyte (CM) hypertrophy and increased heart mass in response to pressure overload is associated with hyper-activation of the myocyte enhancer factor-2 (MEF2) family of transcriptional regulators, and concomitant initiation of the fetal gene program.
The Class IIa histone deacetylase HDAC4 and neuronal function: nuclear nuisance and cytoplasmic stalwart?
Review
New
Fitzsimons, Palmerston North, New Zealand. In Neurobiol Learn Mem, 11 Jul 2015
In the nucleus, HDAC4 is a repressor of transcriptional programmes, although vertebrate HDAC4 is itself catalytically inactive and repression is facilitated through direct inhibition of transcription factors such as MEF2.
Marek's disease: Genetic regulation of gallid herpesvirus 2 infection and latency.
Review
New
Muylkens et al., Namur, Belgium. In Vet J, 07 Jun 2015
kb mRNA, and also modulates expression of cellular genes, such as Bcl-2 and matrix metalloproteinase 3. GaHV-2 expresses viral telomerase RNA subunit (vTR), which forms a complex with the cellular telomerase reverse transcriptase (TERT), thus contributing to tumorigenesis, while vTR independent of telomerase activity is implicated in metastasis.
Pathophysiological aspects of thyroid hormone disorders/thyroid peroxidase autoantibodies and reproduction.
Review
New
Bisschop et al., Amsterdam, Netherlands. In Hum Reprod Update, May 2015
T3 increases the expression of matrix metalloproteinases (MMP), MMP-2, MMP-3, fetal fibronectin and integrin α5β1T3 in early placental extravillous trophoblasts.
Matrix metalloproteinases as therapeutic targets for stroke.
Review
New
Rosenberg et al., Albuquerque, United States. In Brain Res, May 2015
Normally the constitutive enzymes, MMP-2 and membrane type MMP (MMP-14), are activated in a spatially specific manner and act close to the site of activation, while the inducible enzymes, MMP-3 and MMP-9, become active through the action of free radicals and other enzymes during neuroinflammation.
Aberrant protein S-nitrosylation contributes to the pathophysiology of neurodegenerative diseases.
Review
New
Lipton et al., San Diego, United States. In Neurobiol Dis, Apr 2015
Specifically, we discuss the pathological consequences of S-nitrosylated parkin, myocyte enhancer factor 2 (MEF2), dynamin-related protein 1 (Drp1), protein disulfide isomerase (PDI), X-linked inhibitor of apoptosis protein (XIAP), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) under neurodegenerative conditions.
Genome-Wide Gene Expression Analysis Shows AKAP13-Mediated PKD1 Signaling Regulates the Transcriptional Response to Cardiac Hypertrophy.
New
Carnegie et al., San Francisco, United States. In Plos One, Dec 2014
Under cardiac hypertrophic conditions AKAP13 anchored PKD1 activates the transcription factor MEF2 leading to subsequent fetal gene activation and hypertrophic response.
The Hippo transducer YAP1 transforms activated satellite cells and is a potent effector of embryonal rhabdomyosarcoma formation.
New
Impact
Camargo et al., Boston, United States. In Cancer Cell, Sep 2014
YAP1-TEAD1 upregulate pro-proliferative and oncogenic genes and maintain the ERMS differentiation block by interfering with MYOD1 and MEF2 pro-differentiation activities.
Isogenic human iPSC Parkinson's model shows nitrosative stress-induced dysfunction in MEF2-PGC1α transcription.
Impact
Lipton et al., Los Angeles, United States. In Cell, 2014
We report a pathway whereby basal and toxin-induced nitrosative/oxidative stress results in S-nitrosylation of transcription factor MEF2C in A53T hNs compared to corrected controls.
MEF2 is an in vivo immune-metabolic switch.
Impact
Dionne et al., London, United Kingdom. In Cell, 2013
We show that Mef2 is required in the fat body for anabolic function and the immune response.
A role for matrix metalloproteinases in regulating mammary stem cell function via the Wnt signaling pathway.
Impact
Werb et al., San Francisco, United States. In Cell Stem Cell, 2013
Here, we identify matrix metalloproteinase-3 (MMP3) as a regulator of Wnt signaling and mammary stem cell (MaSC) activity.
Exercise, GLUT4, and skeletal muscle glucose uptake.
Review
Impact
Hargreaves et al., Copenhagen, Denmark. In Physiol Rev, 2013
AMPK and CaMKII are key signaling kinases that appear to regulate GLUT4 expression via the HDAC4/5-MEF2 axis and MEF2-GEF interactions resulting in nuclear export of HDAC4/5 in turn leading to histone hyperacetylation on the GLUT4 promoter and increased GLUT4 transcription.
Limited cleavage of tau with matrix-metalloproteinase MMP-9, but not MMP-3, enhances tau oligomer formation.
GeneRIF
Giese et al., München, Germany. In Exp Neurol, 2012
In this study, we identify MMP-3 and MMP-9 as potential tau proteinases
miR-92b regulates Mef2 levels through a negative-feedback circuit during Drosophila muscle development.
GeneRIF
Han et al., Ann Arbor, United States. In Development, 2012
The negative feedback circuit between miR-92b and Mef2 efficiently maintains the stable expression of both components that is required for homeostasis during Drosophila muscle development.
Zebrafish Mef2ca and Mef2cb are essential for both first and second heart field cardiomyocyte differentiation.
GeneRIF
Hughes et al., London, United Kingdom. In Dev Biol, 2012
Mef2ca single mutants have delayed heart development, but form an apparently normal heart. Mef2cb single mutants have a functional heart and are viable adults.
Neurotoxin-induced selective ubiquitination and regulation of MEF2A isoform in neuronal stress response.
GeneRIF
Mao et al., Atlanta, United States. In J Neurochem, 2012
MEF2A, but not MEF2C or MEF2D, is modified by ubiquitination in dopaminergic neuronal cell line SN4741 cells.
[Association of the MMP3, MMP9, ADAM33 and TIMP3 genes polymorphic markers with development and progression of chronic obstructive pulmonary disease].
GeneRIF
Victorova et al., In Mol Biol (mosk), 2012
The MMP3 gene polymorphism may be an important risk factor for the development and progression of chronic obstructive pulmonary disease.
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