TIMP-3 (Tissue Inhibitor of Metalloproteinase-3) Antibody - With BSA and Azide
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| IHC-P, IF, FC |
---|---|
Primary Accession | P35625 |
Other Accession | 7078, 644633, 714168 |
Reactivity | Human, Mouse, Rat, Bovine, Horse, Dog |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit / IgG |
Clone Names | |
Calculated MW | 30kDa |
Gene ID | 7078 |
---|---|
Other Names | Metalloproteinase inhibitor 3, Protein MIG-5, Tissue inhibitor of metalloproteinases 3, TIMP-3, TIMP3 |
Application Note | IHC-P~~N/A IF~~1:50~200 FC~~1:10~50 |
Format | 200ug/ml of Ab purified from rabbit anti-serum by Protein A. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA at 1.0mg/ml. |
Storage | Store at 2 to 8°C.Antibody is stable for 24 months. |
Precautions | TIMP-3 (Tissue Inhibitor of Metalloproteinase-3) Antibody - With BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | TIMP3 |
---|---|
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 (PubMed:17913923). 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 (PubMed:12652295). Selectively induces apoptosis in angiogenic endothelial cells through a caspase-independent cell death pathway (PubMed:25558000). 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 (PubMed:25558000). |
Cellular Location | Secreted, extracellular space, extracellular matrix |

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Provided below are standard protocols that you may find useful for product applications.
Background
TIMP3 (tissue inhibitor of metalloproteinases 3), along with family members TIMP1, TIMP2, and TIMP4, are inhibitors of the matrix metalloproteinases (MMPs), a group of peptidases involved in degradation of the extracellular matrix (ECM). An imbalance between MMPs and the associated TIMPs may play a significant role in the invasive phenotype of malignant tumors. TIMP s inhibit the proteolytic invasiveness of tumor cells and normal placental trophoblast cells. TIMP-3 may be involved in regulating trophoblastic invasion of the uterus as well as in regulating remodeling of the extracellular matrix during the folding of epithelia, and in the formation, branching and expansion of epithelial tubes.
References
Nagase, H. et al. (2006) Cardiovasc Res 69, 562-73. | Visse, R. and Nagase, H. (2003) Circ Res 92, 827-39. |

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