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> Antibody > Rabbit PAb Antibody > MMP-2 / CLG4A Antibody (Antigen Affinity Purified) MMP-2 / CLG4A Antibody (Antigen Affinity Purified)
| Catalog | Size (Price) | Quantity | In Stock | Operation | Other Information |
| 10082-RP02 |
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YES |
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MMP-2 / CLG4A Antibody ( Antigen Affinity Purified )
| Order or Inquire for MMP-2 Antibody product | ![]() |
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| Detection limit is 4 ng/lane in WB | |||
| Detection limit is 0.00975 ng/well in ELISA |
MMP-2 / CLG4A Antibody Product Information
| Immunogen : |
Recombinant human MMP-2 protein ( Catalog#10082-HNAH ) |
| Antibody Type : | Rabbit Polyclonal Antibody ( Antibody Purification Platform ) |
| Ig Type : |
Rabbit IgG |
| Formulation : | 0.2 μm filtered solution in PBS with 5% trehalose |
| Preparation : |
Produced in rabbits immunized with purified, human cell-derived, recombinant human MMP2 ( rh MMP-2 ; Catalog#10082-HNAH ; NP_004521.1 ; Met 1 - Cys 660 ). MMP-2 specific IgG was purified by human MMP-2 affinity chromatography |
MMP-2 / CLG4A Antibody Usage Guide
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Specificity : |
Human MMP-2 / CLG4A |
| Western blot : | This antibody can be used at 0.1 - 0.2 μg/mL with the appropriate secondary reagents to detect human MMP2 in WB. Using a DAB detection system, the detection limit for human MMP2 is approximately 4 ng/lane under non-reducing conditions and 8 ng/lane under reducing conditions |
| Direct ELISA : | This antibody can be used at 0.1 - 0.2 μg/mL with the appropriate secondary reagents to detect human MMP-2. The detection limit for human MMP-2 is approximately 0.00975 ng/well |
| Storage : | This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free. Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles. |
MMP-2 / CLG4A Antibody Related Products & Topics
Related Areas:
Enzyme>>Protease & Regulator>>Metalloprotease & Regulator>>Matrix Metalloproteinase>>MMP-2/MMP2
Cancer>>Angiogenesis>>Matrix Metalloproteinase>>MMP-2/MMP2
Cancer>>Cancer Biomarkers>>MMP-2/MMP2
Proteins:
| MMP-2/MMP2 | Human | MMP-2/MMP2 Protein, Recombinant | 10082-HNAH |
Antibodies:
| Human MMP-2/MMP2 |
WB, ELISA | MMP-2/MMP2 Antibody, Rabbit PAb | 10082-RP01 |
MMP-2 / CLG4A Antibody Background
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade components of the extracellular matrix (ECM) and play essential roles in various physiological processes such as morphogenesis, differentiation, angiogenesis and tissue remodeling, as well as pathological processes including inflammation, arthritis, cardiovascular diseases, pulmonary diseases and tumor invasion. 72 kDa type IV collagenase, also known as Matrix metalloproteinase-2, Gelatinase A, MMP-2, and CLG4A, is a secreted protein which belongs to thepeptidase M10A family. MMP-2/MMP2 contains threefibronectin type-II domains and four hemopexin-like domains. MMP-2/MMP2 is ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, atherosclerotic plaque rupture, as well as degrading extracellular matrix proteins. MMP-2/MMP2 can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. MMP-2/MMP2 cleaves KISS at a Gly-|-Leu bond and appears to have a role in myocardial cell death pathways. MMP-2/MMP2 contributes to myocardial oxidative stress by regulating the activity of GSK3beta. Defects in MMP-2/MMP2 are the cause of Torg-Winchester syndrome (TWS), also known as multicentric osteolysis nodulosis and arthropathy (MONA). TWS is an autosomal recessive osteolysis syndrome. It is severe with generalized osteolysis and osteopenia.
References
- Brooks P.C. et al., 1998, Cell 92:391-400.
- Fernandez-Patron C. et al., 1999, Circ. Res. 85:906-11.
- Fernandez-Patron C. et al., 2000, Circ. Res. 87:670-6.
- Bello L., et al., 2001, Cancer Res. 61:8730-6.
- Kandasamy A.D. et al., 2009, Cardiovasc. Res. 83:698-706.
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