2srt
From Proteopedia
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{{STRUCTURE_2srt| PDB=2srt | SCENE= }} | {{STRUCTURE_2srt| PDB=2srt | SCENE= }} | ||
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===CATALYTIC DOMAIN OF HUMAN STROMELYSIN-1 AT PH 5.5 AND 40OC COMPLEXED WITH INHIBITOR=== | ===CATALYTIC DOMAIN OF HUMAN STROMELYSIN-1 AT PH 5.5 AND 40OC COMPLEXED WITH INHIBITOR=== | ||
+ | {{ABSTRACT_PUBMED_7656014}} | ||
- | + | ==Disease== | |
+ | [[http://www.uniprot.org/uniprot/MMP3_HUMAN MMP3_HUMAN]] Defects in MMP3 are the cause of susceptibility to coronary heart disease type 6 (CHDS6) [MIM:[http://omim.org/entry/614466 614466]]. A multifactorial disease characterized by an imbalance between myocardial functional requirements and the capacity of the coronary vessels to supply sufficient blood flow. Decreased capacity of the coronary vessels is often associated with thickening and loss of elasticity of the coronary arteries. Note=A polymorphism in the MMP3 promoter region is associated with the risk of coronary heart disease and myocardial infarction, due to lower MMP3 proteolytic activity and higher extracellular matrix deposition in atherosclerotic lesions.<ref>PMID:8662692</ref><ref>PMID:12477941</ref> | ||
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+ | ==Function== | ||
+ | [[http://www.uniprot.org/uniprot/MMP3_HUMAN MMP3_HUMAN]] Can degrade fibronectin, laminin, gelatins of type I, III, IV, and V; collagens III, IV, X, and IX, and cartilage proteoglycans. Activates procollagenase. | ||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
- | <ref group="xtra">PMID:007656014</ref><references group="xtra"/> | + | <ref group="xtra">PMID:007656014</ref><references group="xtra"/><references/> |
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Stromelysin 1]] | [[Category: Stromelysin 1]] |
Revision as of 02:32, 25 March 2013
Contents |
CATALYTIC DOMAIN OF HUMAN STROMELYSIN-1 AT PH 5.5 AND 40OC COMPLEXED WITH INHIBITOR
Template:ABSTRACT PUBMED 7656014
Disease
[MMP3_HUMAN] Defects in MMP3 are the cause of susceptibility to coronary heart disease type 6 (CHDS6) [MIM:614466]. A multifactorial disease characterized by an imbalance between myocardial functional requirements and the capacity of the coronary vessels to supply sufficient blood flow. Decreased capacity of the coronary vessels is often associated with thickening and loss of elasticity of the coronary arteries. Note=A polymorphism in the MMP3 promoter region is associated with the risk of coronary heart disease and myocardial infarction, due to lower MMP3 proteolytic activity and higher extracellular matrix deposition in atherosclerotic lesions.[1][2]
Function
[MMP3_HUMAN] Can degrade fibronectin, laminin, gelatins of type I, III, IV, and V; collagens III, IV, X, and IX, and cartilage proteoglycans. Activates procollagenase.
About this Structure
2srt is a 1 chain structure with sequence from Homo sapiens. This structure supersedes the now removed PDB entry 1srt. Full experimental information is available from OCA.
See Also
Reference
- Gooley PR, O'Connell JF, Marcy AI, Cuca GC, Salowe SP, Bush BL, Hermes JD, Esser CK, Hagmann WK, Springer JP, et al.. The NMR structure of the inhibited catalytic domain of human stromelysin-1. Nat Struct Biol. 1994 Feb;1(2):111-8. PMID:7656014
- ↑ Ye S, Eriksson P, Hamsten A, Kurkinen M, Humphries SE, Henney AM. Progression of coronary atherosclerosis is associated with a common genetic variant of the human stromelysin-1 promoter which results in reduced gene expression. J Biol Chem. 1996 May 31;271(22):13055-60. PMID:8662692
- ↑ Yamada Y, Izawa H, Ichihara S, Takatsu F, Ishihara H, Hirayama H, Sone T, Tanaka M, Yokota M. Prediction of the risk of myocardial infarction from polymorphisms in candidate genes. N Engl J Med. 2002 Dec 12;347(24):1916-23. PMID:12477941 doi:10.1056/NEJMoa021445