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Literature summary extracted from

  • Sudhahar, V.; Okur, M.N.; Bagi, Z.; OBryan, J.P.; Hay, N.; Makino, A.; Patel, V.S.; Phillips, S.A.; Stepp, D.; Ushio-Fukai, M.; Fukai, T.
    Akt2 (protein kinase B beta) stabilizes ATP7A, a copper transporter for extracellular superoxide dismutase, in vascular smooth muscle novel mechanism to limit endothelial dysfunction in type 2 diabetes mellitus (2018), Arterioscler. Thromb. Vasc. Biol., 38, 529-541 .
    View publication on PubMedView publication on EuropePMC

Application

EC Number Application Comment Organism
7.2.2.8 medicine ATP7A protein is markedly downregulated in vessels isolated from high-fat diet-induced or db/db type 2 diabetes mellitus mice. Downregulation of ATP7A in type 2 diabetes mellitus mice vessels is restored by constitutive active Akt or in protein-tyrosine phosphatase 1B-deficient type 2 diabetes mellitus mice. Insulin stimulates Akt2 binding to ATP7A to induce phosphorylation at residues Ser1424/1463/1466. Superoxide dismutase SOD3 activity is reduced in Akt2-/- vessels or vascular smooth muscle cells, which is rescued by ATP7A overexpression Mus musculus
7.2.2.8 medicine ATP7A protein is markedly downregulated in vessels isolated from type 2 diabetes mellitus patients. Akt2 (protein kinase B beta) activated by insulin promotes ATP7A stabilization via preventing ubiquitination/degradation as well as translocation to plasma membrane in vascular smooth muscle cells Homo sapiens

Organism

EC Number Organism UniProt Comment Textmining
7.2.2.8 Homo sapiens Q04656
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7.2.2.8 Mus musculus Q64430
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Source Tissue

EC Number Source Tissue Comment Organism Textmining
7.2.2.8 vascular smooth muscle cell
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 Homo sapiens
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7.2.2.8 vascular smooth muscle cell
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 Mus musculus
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General Information

EC Number General Information Comment Organism
7.2.2.8 physiological function ATP7A protein is markedly downregulated in vessels isolated from high-fat diet-induced or db/db type 2 diabetes mellitus mice. Downregulation of ATP7A in type 2 diabetes mellitus mice vessels is restored by constitutive active Akt or in protein-tyrosine phosphatase 1B-deficient type 2 diabetes mellitus mice. Insulin stimulates Akt2 binding to ATP7A to induce phosphorylation at residues Ser1424/1463/1466. Superoxide dismutase SOD3 activity is reduced in Akt2-/- vessels or vascular smooth muscle cells, which is rescued by ATP7A overexpression Mus musculus