Cloned (Comment) | Organism |
---|---|
DNA sequence and genetic structure analysis of ATP7B from renal and hepatic tissue and comparison, recombinant ATP7B expressed in renal cells is similar to hepatic protein in size and trafficking, ATP7B lacking the exon 1 sequence shows cell-specific trafficking in polarized renal and hepatic cells, overview | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
membrane | - |
Homo sapiens | 16020 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + H2O + Cu2+/in | Homo sapiens | kidney-specific regulation of ATP7B, unlike ATP7A, or hepatic ATP7B, which traffics from the TGN to export copper, renal ATP7B does not traffic and therefore is unlikely to mediate copper export. Role for renal ATP7B in intracellular copper storage | ADP + phosphate + Cu2+/out | - |
? | |
additional information | Homo sapiens | inactivation of Cu-ATPases ATP7A and ATP7B causes Menkes disease and Wilson disease, respectively. In Menkes disease, copper accumulates in kidneys and causes tubular damage, indicating that the renal ATP7B does not compensate for the loss of ATP7A function, copper efflux by ATP7A does not contribute to the lack of trafficking response by ATP7B | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Posttranslational Modification | Comment | Organism |
---|---|---|
additional information | ATP7B in Hep-G2 and HEK-293 cells differ in size, but not in post-translational modifications | Homo sapiens |
phosphoprotein | ATP7B is phosphorylated in HEK-293 and Hep-G2 cells, overview | Homo sapiens |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HEK-293 cell | ATP7A and ATP7B | Homo sapiens | - |
Hep-G2 cell | - |
Homo sapiens | - |
hepatocyte | primary and cultured | Homo sapiens | - |
kidney | - |
Homo sapiens | - |
kidney | ATP7A and ATP7B | Homo sapiens | - |
liver | ATP7A and ATP7B | Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + H2O + Cu2+/in | - |
Homo sapiens | ADP + phosphate + Cu2+/out | - |
? | |
ATP + H2O + Cu2+/in | kidney-specific regulation of ATP7B, unlike ATP7A, or hepatic ATP7B, which traffics from the TGN to export copper, renal ATP7B does not traffic and therefore is unlikely to mediate copper export. Role for renal ATP7B in intracellular copper storage | Homo sapiens | ADP + phosphate + Cu2+/out | - |
? | |
additional information | inactivation of Cu-ATPases ATP7A and ATP7B causes Menkes disease and Wilson disease, respectively. In Menkes disease, copper accumulates in kidneys and causes tubular damage, indicating that the renal ATP7B does not compensate for the loss of ATP7A function, copper efflux by ATP7A does not contribute to the lack of trafficking response by ATP7B | Homo sapiens | ? | - |
? |
Subunits | Comment | Organism |
---|---|---|
More | ATP7B from HEK-293 and Hep-G2 cells have different electrophoretic properties, ATP7B in Hep-G2 and HEK-293 cells differ in size, but not in post-translational modifications | Homo sapiens |
Synonyms | Comment | Organism |
---|---|---|
ATP7A | - |
Homo sapiens |
ATP7B | - |
Homo sapiens |
Cu-ATPase | - |
Homo sapiens |
Temperature Optimum [°C] | Temperature Optimum Maximum [°C] | Comment | Organism |
---|---|---|---|
37 | - |
copper transport assay at | Homo sapiens |
pH Optimum Minimum | pH Optimum Maximum | Comment | Organism |
---|---|---|---|
7.4 | - |
copper transport assay at | Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
ATP | - |
Homo sapiens |