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Literature summary for 7.2.2.9 extracted from
- Roles and mechanisms of copper transporting ATPases in cancer pathogenesis (2009), Med. Sci. Monit., 15, RA1-RA5.
Activating Compound
| Activating Compound | Comment | Organism | Structure |
|---|---|---|---|
| glutaredoxin-1 | is essential in interaction with ATP7A and ATP7B via their N-termini for stabilizing their activities | Homo sapiens |
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| overexpression of ATP7A and ATP7B in Me32a cells mediating resistance to bioavailable platinum analogue agents DDP and JM118, expression of ATP7A and ATP7B in the two-hydrid expression system for interaction analysis | Homo sapiens |
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| membrane | - |
Homo sapiens | 16020 | - |
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + H2O + Cu2+/in | Homo sapiens | the enzyme is involved in copper transport, copper homeostasis, and in human cancer progression, overview. When the copper concentration in the hepatocyte increases, ATP7B relocates to the canalicular compartment and excretes excess copper to the bile, intestinal ATPA7 exports the absorbed copper from the enterocytes into the blood stream to supply the copper for the systemic need in a process that involves trafficking of he transporter towards the basolateral membrane. Copper is delivered by specific cytosolic chaperones. ATP7A is essential for the function of a copper-dependent enzyme tyrosinase in the secretory pathway in melanosomes | ADP + phosphate + Cu2+/out | - |
? |  |
| additional information | Homo sapiens | inactivation of the enzyme leads to severe neurodegenerative disorders. ATP7A and ATP7B need a an extensive network of tightly regulated and coordinated protein interactions to facilitate and modulate their activities, the functional deficit of ATP7B causes the Wilson disease | ? | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
isozymes ATP7A and ATP7B | - |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| carcinoma cell | - |
Homo sapiens | - |
| enterocyte | ATP7A | Homo sapiens | - |
| hepatocyte | - |
Homo sapiens | - |
| intestine | high levels of ATP7A | Homo sapiens | - |
| kidney | high levels of ATP7B | Homo sapiens | - |
| liver | high levels of ATP7B | Homo sapiens | - |
| additional information | when the copper concentration in the hepatocyte increases, ATP7B relocates to the canalicular compartment and excretes excess copper to the bile, intestinal ATPA7 exports the absorbed copper from the enterocytes into the blood stream to supply the copper for the systemic need in a process that involves trafficking of he transporter towards the basolateral membrane | Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + H2O + Cu2+/in | the enzyme is involved in copper transport, copper homeostasis, and in human cancer progression, overview. When the copper concentration in the hepatocyte increases, ATP7B relocates to the canalicular compartment and excretes excess copper to the bile, intestinal ATPA7 exports the absorbed copper from the enterocytes into the blood stream to supply the copper for the systemic need in a process that involves trafficking of he transporter towards the basolateral membrane. Copper is delivered by specific cytosolic chaperones. ATP7A is essential for the function of a copper-dependent enzyme tyrosinase in the secretory pathway in melanosomes | Homo sapiens | ADP + phosphate + Cu2+/out | - |
? | |
| ATP + H2O + Cu2+/in | copper is transferred to ATP7A and ATP7B by ATOX1, i.e. HAH1, a cytosolic metallochaperone protein interacting via the N-terminal domain of Cu-ATPases | Homo sapiens | ADP + phosphate + Cu2+/out | - |
? | |
| additional information | inactivation of the enzyme leads to severe neurodegenerative disorders. ATP7A and ATP7B need a an extensive network of tightly regulated and coordinated protein interactions to facilitate and modulate their activities, the functional deficit of ATP7B causes the Wilson disease | Homo sapiens | ? | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| ATP7A | - |
Homo sapiens |
| ATP7B | - |
Homo sapiens |
| copper transporting ATPase | - |
Homo sapiens |
| copper-transporting ATPase | - |
Homo sapiens |
| Cu-ATPase | - |
Homo sapiens |
Cofactor
| Cofactor | Comment | Organism | Structure |
|---|---|---|---|
| ATP | - |
Homo sapiens | |
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