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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Matrix metallopeptidase 20

Matrix Metalloproteinase 20, MMP-20, MT6-MMP
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 degrades amelogenin, the major protein component of dental enamel matrix, and thus thought to play a role in tooth enamel formation. A mutation in this gene, which alters the normal splice pattern and results in premature termination of the encoded protein, has been associated with amelogenesis imperfecta. This gene is part of a cluster of MMP genes located on chromosome 11q22.3. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: Amelogenin, KLK4, CAN, Kallikrein, HAD
Papers on Matrix Metalloproteinase 20
Matrix metalloproteinase-20 mediates dental enamel biomineralization by preventing protein occlusion inside apatite crystals.
New
Moradian-Oldak et al., Los Angeles, United States. In Biomaterials, Jan 2016
A mutation in the Matrix Metalloproteinase-20 (MMP-20) gene results in hypomineralized enamel that is thin, disorganized and breaks from the underlying dentin.
High-Level Expression and Prognostic Significance of Matrix Metalloprotease-19 and Matrix Metalloprotease-20 in Human Pancreatic Ductal Adenocarcinoma.
New
Tang et al., Hefei, China. In Pancreas, Jan 2016
OBJECTIVE: Matrix metalloproteinase (MMP)-19 and MMP-20 are important members of the MMP family, and their roles in tumor survivorship and progression are continually reported.
Truncated amelogenin and LRAP transgenes improve Amelx null mouse enamel.
New
Pugach et al., Cambridge, United States. In Matrix Biol, Dec 2015
Soon after secretion by ameloblasts, M180 is cleaved by MMP20 resulting in C-terminal truncated (CTRNC) amelogenin.
Inactivation of C4orf26 in toothless placental mammals.
New
Gatesy et al., Riverside, United States. In Mol Phylogenet Evol, Dec 2015
UNASSIGNED: Previous studies have reported inactivated copies of six enamel-related genes (AMBN, AMEL, AMTN, ENAM, KLK4, MMP20) and one dentin-related gene (DSPP) in one or more toothless vertebrates and/or vertebrates with enamelless teeth, thereby providing evidence that these genes are enamel or tooth-specific with respect to their critical functions that are maintained by natural selection.
MMP20 and ARMS2/HTRA1 Are Associated with Neovascular Lesion Size in Age-Related Macular Degeneration.
New
Nagahama Cohort Research Group et al., Kyoto, Japan. In Ophthalmology, Nov 2015
RESULTS: In the discovery stage, rs10895322 in MMP20 showed a genome-wide significant P value of 6.95×10(-8), and rs2284665 in ARMS2/HTRA1 showed a P value of 1.55×10(-7).
Store-operated Ca2+ Entry Modulates the Expression of Enamel Genes.
New
Lacruz et al., New York City, United States. In J Dent Res, Oct 2015
Our results demonstrate that stimulating LS8 cells or murine primary enamel organ cells with thapsigargin to activate SOCE leads to increased expression of Amelx, Ambn, Enam, Mmp20.
Immunohistochemical expression of WNT5A and MMPs in odontogenic epithelial tumors and cysts.
New
Nunes et al., São Paulo, Brazil. In Acta Histochem, Oct 2015
MMP20 expression was higher in ameloblastoma when compared to adenomatoid odontogenic tumor (AOT), DC and GOC.
Analysis of the association between polymorphisms in MMP2, MMP3, MMP9, MMP20, TIMP1, and TIMP2 genes with white spot lesions and early childhood caries.
New
Paixão et al., Nova Friburgo, Brazil. In Int J Paediatr Dent, Oct 2015
AIM: This study aimed to evaluate the association between polymorphisms in MMP2, MMP3, MMP9, MMP20, TIMP1, and TIMP2 with white spot lesions (WSL) and early childhood caries (ECC).
Hypoxia increases the expression of enamel genes and cytokines in an ameloblast-derived cell line.
New
Reseland et al., Oslo, Norway. In Eur J Oral Sci, Aug 2015
Hypoxia increased expression of the structural enamel matrix genes amelogenin (Amelx), ameloblastin (Ambn), and enamelin (Enam), and the enamel protease matrix metalloproteinase-20 (Mmp20).
Cell cycle control, DNA damage repair, and apoptosis-related pathways control pre-ameloblasts differentiation during tooth development.
Zheng et al., Chengdu, China. In Bmc Genomics, 2014
Moreover, coexpression network analysis uncovered two highly conserved sub-networks contributing to differentiation, containing transcription regulators (RUNX2, ETV1 and ETV5), solute carrier family members (SLC15A1 and SLC7A11), enamel matrix protein (MMP20), and a polymodal excitatory ion channel (TRPA1).
Modulation of cell-cell junctional complexes by matrix metalloproteinases.
Review
Smith et al., Cambridge, United States. In J Dent Res, 2013
Matrix metalloproteinases (MMPs) facilitate cell movement in various tissues during development, and in this review we suggest that the tooth-specific MMP, enamelysin (MMP20), facilitates ameloblast movements during enamel development.
Dental enamel development: proteinases and their enamel matrix substrates.
Review
Bartlett, Cambridge, United States. In Isrn Dent, 2012
This review focuses on recent discoveries and delves in detail about what is known about each of the proteins (amelogenin, ameloblastin, and enamelin) and proteinases (matrix metalloproteinase-20 and kallikrein-related peptidase-4) that are secreted into the enamel matrix.
Genetic variation in MMP20 contributes to higher caries experience.
GeneRIF
Vieira et al., Rio de Janeiro, Brazil. In J Dent, 2012
Variation in MMP20 may be associated with caries experience mainly in Caucasian subjects with poor oral health habits.
Biochemical characterization and N-terminomics analysis of leukolysin, the membrane-type 6 matrix metalloprotease (MMP25): chemokine and vimentin cleavages enhance cell migration and macrophage phagocytic activities.
GeneRIF
Overall et al., Vancouver, Canada. In J Biol Chem, 2012
MT6-MMP regulates neutrophil and monocyte chemotaxis and by generating "eat-me" signals upon vimentin cleavage potentially increases phagocytic removal of neutrophils to resolve inflammation.
Amelogenesis imperfecta: an introduction.
Review
Malik et al., In Br Dent J, 2012
Amelogenesis imperfecta (AI) is an inherited disorder that is associated with mutations in five genes (AMEL; ENAM; MMP20; KLK4 and FAM83H) with a wide range of clinical presentations (phenotypes).
A multidisciplinary approach for the diagnosis of hypocalcified amelogenesis imperfecta in two Chilean families.
GeneRIF
Cifuentes et al., Santiago, Chile. In Acta Odontol Scand, 2012
hypocalcified amelogenesis imperfecta, Witkop type III, was unrelated to previously described mutations in the ENAM or MMP-20 genes
Matrix metalloproteinase 20 promotes a smooth enamel surface, a strong dentino-enamel junction, and a decussating enamel rod pattern.
GeneRIF
Smith et al., Cambridge, United States. In Eur J Oral Sci, 2011
required for ameloblast cell movement necessary to form the decussating enamel rod patterns, for the prevention of ectopic mineral formation, and to maintain a functional dentin-enamel junction
Defining a new candidate gene for amelogenesis imperfecta: from molecular genetics to biochemistry.
Review
Cifuentes et al., Santiago, Chile. In Biochem Genet, 2011
These disorders are considered clinically and genetically heterogeneous in etiology, involving a variety of genes, such as AMELX, ENAM, DLX3, FAM83H, MMP-20, KLK4, and WDR72.
Genetics and genomics of human ageing.
Review
Kim et al., Stanford, United States. In Philos Trans R Soc Lond B Biol Sci, 2011
The genomic convergence approach has been used to implicate the gene MMP20 in human kidney ageing.
MMP20 cleaves E-cadherin and influences ameloblast development.
GeneRIF
Smith et al., Cambridge, United States. In Cells Tissues Organs, 2010
MMP20 may influence ameloblast developmental progression through hydrolysis of cadherin extracellular domains with associated release of transcription factor(s).
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