Application
| WB, IHC, ICC, IP |
---|---|
Primary Accession | B7ZLR4 |
Other Accession | NP_000044.2 |
Host | Mouse |
Isotype | IgG1 |
Reactivity | Human, Mouse, Rat |
Clonality | Monoclonal |
Description | Mouse Anti-Human Copper Transporting ATPase 2 Monoclonal IgG1 |
Target/Specificity | Detects ~160kDa in rat brain membrane preparations. |
Other Names | ATP7B Antibody, ATPase Cu++ transporting beta polypeptide Antibody, ATPase Cu(2+) transporting beta polypeptide Antibody, Copper pump 2 Antibody, Copper transporting ATPase 2 Antibody, PWD Antibody, Toxic milk Antibody, tx Antibody, WC1 Antibody, WD Antibody, Wilson disease associated protein Antibody, WND Antibody, WND/140 kDa Antibody |
Clone Names | S62-29 |
Immunogen | Synthetic peptide amino acids 3-21 (cytoplasmic N-terminus) of human Copper-transporting ATPase2 |
Purification | Protein G Purified |
Storage | -20ºC |
Storage Buffer | PBS pH7.4, 50% glycerol, 0.09% sodium azide |
Shipping Temperature | Blue Ice or 4ºC |
Certificate of Analysis | 1 µg/ml of SMC-399 was sufficient for detection of Copper-transporting ATPase2 in 20 µg of rat brain lysate by colorimetric immunoblot analysis using Goat IgG:HRP as the secondary antibody. |
Cellular Localization | Cytoplasm | Mitochondrion | Golgi Apparatus | Trans-Golgi Network Membrane |
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Provided below are standard protocols that you may find useful for product applications.
Background
The copper efflux transporters ATP7A and ATP7B sequester intracellular copper into the vesicular secretory pathway for export from the cell. ATP7b is an important protein for copper transport and elimination of excess copper from the body. ATP7b transports metals in and out of cells using ATP. There are 3 known isoforms of the ATP7b gene; A is found in the liver, kidney, and brain, the shorter form B is found in brain tissue, and the third isoform, known as WND/140 KDA is found in mitochondria. Mutations in the ATP7b gene can cause Wilson's disease, an inherited disorder causing copper poisoning in the brain and liver, characterized by neurological symptoms and hepatic damage.
References
1. Tanzi R.E., et al. (1993) Nature Genetics. 5: 344-350.
2. Ghr/nlm.gov/gene/ATP7B