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Literature summary for 7.2.2.9 extracted from

  • Petrukhin, K.; Lutsenko, S.; Chernov, I.; Ross, B.M.; Kaplan, J.H.; Giliam, T.C.
    Characterization of the Wilson disease gene encoding a P-type copper transporting ATPase: genomic organization, alternative splicing, and structural function predictions (1994), Hum. Mol. Genet., 3, 1647-1656.
    View publication on PubMed
Search for more literature for 7.2.2.9

Cloned(Commentary)

Cloned (Comment) Organism
cloning of the 5'-end of the Wilson disease gene ATP7B Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + H2O + Cu2+/in Homo sapiens autosomal recessive Wilson disease is characterized by copper toxicity believed to result from the loss of ability to export copper from liver to bile and incorporate copper into ceruloplasmin in the liver. Mechanism of alternative splicing serves to regulate the amount of functional Wilson disease protein produced in brain, kidney and placenta ADP + phosphate + Cu2+/out
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Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
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Source Tissue

Source Tissue Comment Organism Textmining
brain
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 Homo sapiens
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kidney
-
 Homo sapiens
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placenta
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 Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + H2O + Cu2+/in
-
 Homo sapiens ADP + phosphate + Cu2+/out
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 ?
ATP + H2O + Cu2+/in autosomal recessive Wilson disease is characterized by copper toxicity believed to result from the loss of ability to export copper from liver to bile and incorporate copper into ceruloplasmin in the liver. Mechanism of alternative splicing serves to regulate the amount of functional Wilson disease protein produced in brain, kidney and placenta Homo sapiens ADP + phosphate + Cu2+/out
-
 ?