||Recombinant Human ATPase, Cu++ transporting, alpha polypeptide expressed inE.coliwas cloned from human cDNA with a C-terminal purification tag. The second soluble domain of the human Menkes protein (residues 169-240 swissprot accession Q04656). The C-terminal tag is cleaved during the purification. MW=8.4kDa.
||ATP7A (ATPase, Cu++ transporting, alpha polypeptide (Menkes syndrome)) is a human gene that provides instructions to make a protein that is important for regulating copper levels in the body. This protein is found in most tissues, but it is absent from the liver. In the small intestine, the ATP7A protein helps control the absorption of copper from food. In other organs and tissues, the ATP7A protein has a dual role and shuttles between two locations within the cell. The protein normally resides in a cell structure called the Golgi apparatus, which modifies and transports newly produced enzymes and other proteins. Here, the ATP7A protein supplies copper to certain enzymes that are critical for the structure and function of bone, skin, hair, blood vessels, and the nervous system. If copper levels in the cell environment are elevated, however, the ATP7A protein moves to the cell membrane and eliminates excess copper from the cell.
||>95% by SDS-PAGE. The protein was observed as a single band migrating at amolecular weight of (<14kDa).
||1.0mg at 1.0mg/ml in 50mM Tris/Mes pH8.0, 2mM DTT (Dithiothreitol). The concentration is calculated from the absorbance at 280nm (e280=1400M-1cm-1).
||Under the above described conditions, to avoid precipitation or protein dimerization, the product can be concentrated to a maximum of 2mM.
||-20ºC. The protein is stable at 4ºC for at least 2 weeks and at 25ºC for at least several hours. After initial defrost, aliquot product into individual tubes and refreeze at -20ºC. Avoid repeated freeze/defrost cycles.