Matrix Metalloproteinase 14
"Matrix Metalloproteinase 14" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A transmembrane domain-containing matrix metalloproteinase. It is synthesized as an inactive zymogen that is activated by the action of PROPROTEIN CONVERTASES such as FURIN. Matrix metalloproteinase 14 plays a direct role in the cleavage of proteins in the pericellular environment. In addition, it can function indirectly by enzymatically activating the proprotein form of MATRIX METALLOPROTEINASE 15.
Descriptor ID |
D053511
|
MeSH Number(s) |
D08.811.277.656.300.480.525.300.500 D08.811.277.656.675.374.525.300.500
|
Concept/Terms |
Matrix Metalloproteinase 14- Matrix Metalloproteinase 14
- Metalloproteinase 14, Matrix
- Membrane-Type Matrix Metalloproteinase 1
- Membrane Type Matrix Metalloproteinase 1
- MMP-14 Metalloproteinase
- MMP 14 Metalloproteinase
- Metalloproteinase, MMP-14
- MT1-MMP
- MMP14 Metalloproteinase
- Metalloproteinase, MMP14
- MT-MMP-1
- MT1-Matrix Metalloproteinase
- MT1 Matrix Metalloproteinase
- Metalloproteinase, MT1-Matrix
- Membrane-Type 1 Matrix Metalloproteinase
- Membrane Type 1 Matrix Metalloproteinase
- MMP-X1 Protein
- MMP X1 Protein
|
Below are MeSH descriptors whose meaning is more general than "Matrix Metalloproteinase 14".
Below are MeSH descriptors whose meaning is more specific than "Matrix Metalloproteinase 14".
This graph shows the total number of publications written about "Matrix Metalloproteinase 14" by people in this website by year, and whether "Matrix Metalloproteinase 14" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
Year | Major Topic | Minor Topic | Total |
---|
2004 | 0 | 1 | 1 |
2006 | 0 | 2 | 2 |
2007 | 3 | 0 | 3 |
2008 | 0 | 1 | 1 |
2009 | 2 | 1 | 3 |
2010 | 3 | 0 | 3 |
2011 | 1 | 0 | 1 |
2012 | 1 | 1 | 2 |
2013 | 1 | 0 | 1 |
2014 | 1 | 0 | 1 |
2016 | 1 | 1 | 2 |
To return to the timeline,
click here.
Below are the most recent publications written about "Matrix Metalloproteinase 14" by people in Profiles.
-
Differential hypertensive protease expression in the thoracic versus abdominal aorta. J Vasc Surg. 2017 11; 66(5):1543-1552.
-
Regulation of membrane type-1 matrix metalloproteinase activity and intracellular localization in clinical thoracic aortic aneurysms. J Thorac Cardiovasc Surg. 2017 03; 153(3):537-546.
-
Mechanistic relationship between membrane type-1 matrix metalloproteinase and the myocardial response to pressure overload. Circ Heart Fail. 2014 Mar 01; 7(2):340-50.
-
Gender differences in non-ischemic myocardial remodeling: are they due to estrogen modulation of cardiac mast cells and/or membrane type 1 matrix metalloproteinase. Pflugers Arch. 2013 May; 465(5):687-97.
-
Differential membrane type 1 matrix metalloproteinase substrate processing with ischemia-reperfusion: relationship to interstitial microRNA dynamics and myocardial function. J Thorac Cardiovasc Surg. 2013 Jan; 145(1):267-275, 277.e1-4; discussion 275-7.
-
Regulation of invadopodia formation and activity by CD147. J Cell Sci. 2012 Feb 01; 125(Pt 3):777-88.
-
Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodeling. Am J Physiol Heart Circ Physiol. 2011 Oct; 301(4):H1656-66.
-
Heterogeneity in MT1-MMP activity with ischemia-reperfusion and previous myocardial infarction: relation to regional myocardial function. Am J Physiol Heart Circ Physiol. 2010 Dec; 299(6):H1947-58.
-
Cardiac restricted overexpression of membrane type-1 matrix metalloproteinase causes adverse myocardial remodeling following myocardial infarction. J Biol Chem. 2010 Sep 24; 285(39):30316-27.
-
Alterations in membrane type-1 matrix metalloproteinase abundance after the induction of thoracic aortic aneurysm in a murine model. Am J Physiol Heart Circ Physiol. 2010 Jul; 299(1):H114-24.