Sandbox 985
From Proteopedia
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=== Hypertension === | === Hypertension === | ||
MMP-9 activity is induced very early with the development of hypertension, contributing to collagen breakdown and arterial distensibility. An increase in fibrillar collagen in the compensated stage of hypertension is associated with increased MMP-9 activity. An increased arterial pressure and altered remodeling in the blood vessels lead to a pressure overload of the heart. Under these conditions, both vascular and cardiac tissues undergo additional compensatory remodeling. MMP-9 activity is increased in arteries with high pressure compared with vessels under normal pressure. | MMP-9 activity is induced very early with the development of hypertension, contributing to collagen breakdown and arterial distensibility. An increase in fibrillar collagen in the compensated stage of hypertension is associated with increased MMP-9 activity. An increased arterial pressure and altered remodeling in the blood vessels lead to a pressure overload of the heart. Under these conditions, both vascular and cardiac tissues undergo additional compensatory remodeling. MMP-9 activity is increased in arteries with high pressure compared with vessels under normal pressure. | ||
| - | == | + | == Regulation == |
| + | Activators: | ||
| + | Ca2+ and Zn2+ | ||
| - | + | Gelatinase B activity is under strict control at various levels: transcription of the gene by cytokines and cellular interactions; activation of the pro-enzyme by a cascade of enzymes comprising serine proteases and other MMPs; and regulation by specific tissue inhibitors of MMPs (TIMPs) or by unspecific inhibitors, such as alpha2-macroglobulin.<ref> </Opdenakker, G., PE Van Der Steen, B. Dubois, I. Nelissen, E. Van Coillie, S. Masure, P. Proost, and J. Van Damme. "Gelatinase B Functions as Regulator and Effector in Leukocyte Biology." Gelatinase B Functions as Regulator and Effector in Leukocyte Biology 69.6 (2001): 851-59. Gelatinase B Functions as Regulator and Effector in Leukocyte Biology. Journal of Leukocyte Biology, June 2001. Web. 04 May 2015.> | |
| - | This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes. | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
| - | <ref/> | + | <ref><Opdenakker, G., PE Van Der Steen, B. Dubois, I. Nelissen, E. Van Coillie, S. Masure, P. Proost, and J. Van Damme. "Gelatinase B Functions as Regulator and Effector in Leukocyte Biology." Gelatinase B Functions as Regulator and Effector in Leukocyte Biology 69.6 (2001): 851-59. Gelatinase B Functions as Regulator and Effector in Leukocyte Biology. Journal of Leukocyte Biology, June 2001. Web. 04 May 2015./> |
Revision as of 16:53, 4 May 2015
MMP family members share similar fundamental structural characteristics and are classified according to their substrate specificity. By this classification, MMP-9 belongs to the gelatinase subgroup and is known as gelatinase B due to its ability to degrade gelatin. MMP9 is composed of the following domains: a gelatin-binding domain consisting of three fibronectin type II units, a catalytic domain containing the zinc-binding site, a proline-rich type V collagen-homologous domain and a hemopexin-like domain. The zinc binding motif HEXXHXXGXXH in the catalytic domain, and the “cysteine switch” motif PRCGXPD in the propeptide are common structural signatures, where three histidines in the zinc binding motif coordinate and the cysteine in the propetide coordinate with the catalytic zinc ion. MMP9 is produced by the several cell types, normal alveolar macrophages and granulocytes.
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