SCUBA

MMP2 — Matrix metallopeptidase 2

MMP2 belongs to a gene co-expression module in 2 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

MMP2's module in each cell type

Cell typeModuleShares the module with
FibroblastsBasement Membrane ECM
ECM production
BSG, COL6A1, COL6A2, COMT, ECE1, ECM1, FNDC3B, LAMB1 +2 moreView in SCUBA
PericytesBMP-Stromal Signaling
Developmental
BMP4, CXCL14, F3, NBL1, PDGFRA, POSTN, TMEM176A, TMEM176BView in SCUBA

About the gene

SynonymsCLG4, CLG4A, TBE-1
Chromosome16: 55389700-55506691
Predicted locationIntracellular, Secreted
Essential geneNo
Protein classCancer-related genes, Candidate cardiovascular disease genes, Disease related genes, Enzymes, Human disease related genes, Plasma proteins, Potential drug targets, Predicted intracellular proteins, Predicted secreted proteins
Molecular functionHydrolase, Metalloprotease, Protease
Biological processAngiogenesis, Collagen degradation

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

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.