EC Number   |
Application |
Reference |
|---|
   7.2.2.8 | analysis |
method to probe Cu flow through human Atox1 and copper chaperone ATP7B proteins when expressed in yeast. |
751473 |
| 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 |
749770 |
| 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 |
749770 |
| 7.2.2.8 | medicine |
cisplatin-resistant cell sublines show cross-resistance to carboplatin and oxaliplatin. ATP7A expression in cisplatin-resistant cell sublines is much higher than in cisplatin-sensitive cell lines at both mRNA and protein levels. ATP7A-targeted siRNA in cisplatin-resistant cancer cells partially reverses cisplatin-resistance. It also increases cell apoptosis at different cisplatin concentrations |
751166 |
| 7.2.2.8 | medicine |
deletion of isoform ATP7A in H-RAS transformed tumorigenic mouse embryonic markedly suppresses tumorigenesis relative to wild type parental cells, associated with hyperaccumulation of copper and sensitivity to reactive oxygen species and hypoxia. Tumor grafts lacking ATP7A are markedly more sensitive to cisplatin chemotherapy compared to ATP7A-expressing control tumors |
751167 |
| 7.2.2.8 | medicine |
mutation T994I is located in the sixth transmembrane domain of ATP7A, and is associated with the an adult-onset isolated distal motor neuropathy, and with an abnormal interaction with p97/valosin-containing protein. T994I substitution results in conformational exposure of the UBX domain in the third lumenal loop of ATP7A, which then binds the N-terminal domain of p97/VCP. This abnormal interaction occurs at or near the cell plasma membrane |
751122 |
