TIMP3 — TIMP metallopeptidase inhibitor 3
TIMP3 belongs to a gene co-expression module in 4 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.
TIMP3's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Endothelial | Endothelial Quiescence Endothelial cell development | AMD1, AQP7, ARMH4, CDC14B, FBXO34, GATA2, GLUL, KLF3 +7 more | View in SCUBA |
| Glial cells | Peripheral Glial Myelination Myelination | FAM210B, FRMD6, GNAS, KDSR, MAF, MYL9, OLFML2A, OLFML3 +7 more | View in SCUBA |
| Lymphatic endothelial | Anticoagulant Barrier endothelial development | AP2A2, ERICH1, JUP, KBTBD11, MMRN1, MYCT1, PARD6G, TFPI | View in SCUBA |
| Smooth muscle cells | Vascular Tone Signaling Contractility | ADCY3, CPEB4, CYSTM1, DBI, EPAS1, EPS8, IER5L, NR2F2 +5 more | View in SCUBA |
About the gene
| Synonyms | SFD |
|---|---|
| Chromosome | 22: 32801705-32863041 |
| Predicted location | Secreted |
| Essential gene | No |
| Protein class | Cancer-related genes, Disease related genes, Human disease related genes, Predicted secreted proteins |
| Molecular function | Metalloenzyme inhibitor, Metalloprotease inhibitor, Protease inhibitor |
| Biological process | Sensory transduction, Vision |
Function
Mediates a variety of processes including matrix regulation and turnover, inflammation, and angiogenesis, through reversible inhibition of zinc protease superfamily enzymes, primarily matrix metalloproteinases (MMPs). Regulates extracellular matrix (ECM) remodeling through inhibition of matrix metalloproteinases (MMP) including MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-13, MMP-14 and MMP-15. Additionally, modulates the processing of amyloid precursor protein (APP) and apolipoprotein E receptor ApoER2 by inhibiting two alpha- secretases ADAM10 and ADAM17. Functions as a tumor suppressor and a potent inhibitor of angiogenesis. Exerts its anti- angiogenic effect by directly interacting with vascular endothelial growth factor (VEGF) receptor-2/KDR, preventing its binding to the VEGFA ligand. Selectively induces apoptosis in angiogenic endothelial cells through a caspase-independent cell death pathway. Mechanistically, inhibits matrix-induced focal adhesion kinase PTK2 tyrosine phosphorylation and association with paxillin/PXN and disrupts the incorporation of ITGB3, PTK2 and PXN into focal adhesion contacts on the matrix.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.