Anti-Human MMP2 Antibody Pair

Product Description: MMP2 is an enzyme that plays a crucial role in extracellular matrix remodeling and tissue repair. It functions by cleaving type IV collagen, a major component of basement membranes, and is involved in various physiological processes such as menstruation, angiogenesis, and bone remodeling. MMP2 has been implicated in several pathological conditions, including chronic kidney disease (CKD) and multicentric osteolysis, nodulosis, and arthropathy (MONA).In CKD, MMP2 exhibits a dual role. During early stages, it promotes extracellular matrix production and accelerates kidney fibrosis. However, in advanced stages, MMP2 activity decreases, leading to reduced extracellular matrix degradation and exacerbating fibrosis. Mutations in the MMP2 gene can cause MONA, a rare inherited bone disease characterized by progressive bone loss and joint problems. These mutations eliminate MMP2 function, disrupting the balance between bone creation and breakdown during remodeling. Protein Function: Ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, and atherosclerotic plaque rupture. As well as degrading extracellular matrix proteins, can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. Also cleaves KISS at a Gly-, -Leu bond. Appears to have a role in myocardial cell death pathways. Contributes to myocardial oxidative stress by regulating the activity of GSK3beta. Cleaves GSK3beta in vitro. Involved in the formation of the fibrovascular tissues in association with MMP14 , PEX, the C-terminal non-catalytic fragment of MMP2, possesses anti-angiogenic and anti-tumor properties and inhibits cell migration and cell adhesion to FGF2 and vitronectin. Ligand for integrinv/beta3 on the surface of blood vessels , Mediates the proteolysis of CHUK/IKKA and initiates a primary innate immune response by inducing mitochondrial-nuclear stress signaling with activation of the pro-inflammatory NF-kappaB, NFAT and IRF transcriptional pathways [The Uniprot Consortium]