|Application ||WB, IHC, IF, FC, IP|
|Other Accession||P39876, P48032|
|Reactivity||Human, Mouse, Rat|
|Other Names||Metalloproteinase inhibitor 3, Protein MIG-5, Tissue inhibitor of metalloproteinases 3, TIMP-3, TIMP3|
|Target/Specificity||The amino acid sequence (aa175-211), used as the immunogen for TIMP3 Ab, is 100% homologous in human, cow, dog and horse, and 94% homologous in mouse and rat.|
|Application Note||Flow Cytometry : 0.5-1ug/million cells|
Immunofluorescence : 1-2ug/ml
Western Blotting : 0.5-1.0 µg/ml
Immunoprecipitation : 1-2ug/500ug protein lysate
Immunohistology (formalin-fixed) : 1-2ug/ml for 30 minutes at RT
(Staining of formalin-fixed tissues requires boiling tissue sections in 10mM citrate buffer, pH 6.0, for 10-20 min followed by cooling at RT for 20 minutes).
|Format||0.5 ml at 200ug/ml with BSA and azide|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||TIMP-3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Complexes with metalloproteinases (such as collagenases) and irreversibly inactivates them by binding to their catalytic zinc cofactor. May form part of a tissue-specific acute response to remodeling stimuli. Known to act on MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-13, MMP-14 and MMP-15.|
|Cellular Location||Secreted, extracellular space, extracellular matrix|
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Provided below are standard protocols that you may find useful for product applications.
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.
1. Nagase, H. et al. (2006) Cardiovasc Res 69, 562-73.
2. Visse, R. and Nagase, H. (2003) Circ Res 92, 827-39.
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