| Field | Specification |
|---|---|
| Mfr No | |
| Alternative Names | Macrophage metalloelastase;MME;3.4.24.65;Matrix metalloproteinase-12;MMP-12;Mmp12;Mme, Mmel; |
| Assay Time | |
| Assay Type | |
| Detection Range | |
| Expression System | |
| Gene ID | |
| Immunogen | Expression system for standard: NS0; Immunogen sequence: A18-C462 |
| Product Type | |
| Reactivity | |
| Sample Type(s) | cell culture supernatants, serum and plasma (heparin). |
| Sensitivity | |
| Storage | |
| Target | |
| UniProt # |
Background
Also known as: Macrophage metalloelastase, MME, 3.4.24.65, Matrix metalloproteinase-12, MMP-12, Mmp12, Mmel.
Mouse MMP-12 (MMP12) is widely studied as a molecular readout in experimental models where changes in protein abundance reflect underlying biology. This target is frequently investigated in Molecular & Cellular Biology research contexts. Proteases and extracellular matrix (ECM) components are central to tissue architecture and remodeling. In many experimental contexts, changes in ECM-related proteins reflect shifts in cell adhesion, migration, barrier integrity, or matrix turnover.
Biological function and remodeling context
Matrix remodeling is influenced by the balance between synthesis and degradation, often regulated by inflammatory cues, mechanical stress, and growth-factor signaling. Protease activity can unmask or release bioactive fragments, while altered ECM composition can feed back on cell behavior through mechanotransduction and receptor engagement.
Why it matters in research
- Remodeling readout: Quantification can support studies of fibrosis, wound repair, and invasion models.
- Microenvironment state: Levels may reflect stromal activation, barrier disruption, or matrix turnover.
- Mechanistic linkage: Pairing with inflammatory and growth-factor markers can clarify drivers of remodeling.
Disease and translational relevance
ECM remodeling and protease regulation are frequently discussed in the literature across oncology, cardiovascular, pulmonary, and inflammatory disease models. Interpretation of abundance should consider whether the measured analyte represents pro-forms, active forms, or fragments, and whether binding partners in the matrix influence detectability.
Sample data
| Concentration (pg/ml) | 0 | 62.5 | 125 | 250 | 500 | 1000 | 2000 | 4000 |
| O.D. | 0.054 | 0.19 | 0.299 | 0.505 | 0.81 | 1.285 | 1.801 | 2.101 |
Intra/inter assay consistency
| Intra-Assay Precision | Inter-Assay Precision | |||||
|---|---|---|---|---|---|---|
| Sample | 1 | 2 | 3 | 1 | 2 | 3 |
| n | 16 | 16 | 16 | 24 | 24 | 24 |
| Mean (pg/ml) | 127 | 628 | 1430 | 134 | 684 | 1370 |
| Standard deviation | 9.27 | 46.47 | 100.1 | 11.12 | 57.45 | 97.27 |
| CV (%) | 7.3% | 7.4% | 7% | 8.3% | 8.4% | 7.1% |
Kit components
Description|Quantity Pre-coated 96-well strip microplate|1 Standard|2 vials Biotinylated antibody (100x)|100ul Avidin-Biotin-Peroxidase Complex (100x)|100ul Sample Diluent|30ml Antibody Diluent|12ml Avidin-Biotin-Peroxidase Diluent|12ml Color Developing Reagent (TMB)|10ml Stop Solution|10ml Wash Buffer (25x)|20ml Adhesive plate sealers|4Materials required but not provided
- Microplate Reader capable of reading absorbance at 450nm.
- Incubator.
- Automated plate washer (optional).
- Pipettes and pipette tips capable of precisely dispensing 0.5 µl through 1 ml volumes of aqueous solutions.
- Multichannel pipettes are recommended for large amount of samples.
- Deionized or distilled water.
- 500ml graduated cylinders.
- Test tubes for dilution.
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- Michiko et al. (2023). Apoptosis inhibitor of macrophage (AIM)/CD5L is involved in the pathogenesis of COPD. RESPIRATORY RESEARCH.
- Suzuki et al. (2020). ADAM17 protects against elastase-induced emphysema by suppressing CD62L+ leukocyte infiltration in mice. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY.
- Zang et al. (2016). Pulmonary C Fibers Modulate MMP-12 Production via PAR2 and Are Involved in the Long-Term Airway Inflammation and Airway …. JOURNAL OF VIROLOGY.
- Huang et al. (2024). DACH1 Attenuates Airway Inflammation in COPD by Activating NRF2 Signaling. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY.