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Literature summary for 7.2.2.8 extracted from

  • Nyasae, L.K.; Schell, M.J.; Hubbard, A.L.
    Copper directs ATP7B to the apical domain of hepatic cells via basolateral endosomes (2014), Traffic, 15, 1344-1365.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 7.2.2.8

Localization

Localization Comment Organism GeneOntology No. Textmining
apical plasma membrane luminal acidification is required for the cell to redirect ATP7B to the apical domain and maintain it there under conditions of high Cu. Deacidification prevents Cu-directed delivery to apical domain Homo sapiens 16324
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endosome Cu2+ directs ATP7B to the apical domain of hepatic cells via basolateral endosomes Homo sapiens 5768
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plasma membrane enzyme localization at high copper concentration Homo sapiens 5886
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plasma membrane enzyme localization at high copper concentration. Deacidification prevents Cu-directed delivery to apical domain Homo sapiens 5886
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trans-Golgi network enzyme localization at low copper concentration Homo sapiens 5802
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vesicle
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 Homo sapiens 31982
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vesicle Cu induces an increase in the number of ATP7B vesicles, which traverse large basolateral endosomes en route to the apical domain Homo sapiens 31982
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Metals/Ions

Metals/Ions Comment Organism Structure
Cu2+ copper directs ATP7B to the apical domain of hepatic cells via basolateral endosomes Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P35670 ATP7B
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Homo sapiens Q04656 ATP7A
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Source Tissue

Source Tissue Comment Organism Textmining
hepatocyte Cu-regulated localization in hepatocytes Homo sapiens
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liver Cu2+ directs ATP7B to the apical domain of hepatic cells via basolateral endosomes Homo sapiens
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additional information Cu-directed trafficking of both endogenous and exogenous ATP7B Homo sapiens
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WIF-B cell Cu levels regulate the reversible trafficking of endogenous ATP7B in polarized WIF-B cells Homo sapiens
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Synonyms

Synonyms Comment Organism
ATP7A
-
 Homo sapiens
ATP7B
-
 Homo sapiens
Cu ATPase
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction Menkes disease results from loss-of-function mutations in ATP7A Homo sapiens
malfunction Wilson's disease results from loss-of-function mutations in ATP7B. Loss of ATP7B function leads to excess Cu accumulation in the brain, kidney and particularly in the liver, owing to defective biliary Cu excretion across the apical surface of hepatocytes. Wilson's disease mutation affects the intracellular trafficking of ATP7B, while having little effect on ATPase activity itself, indicating that a mislocalization of ATP7B is sufficient to cause the disease Homo sapiens
additional information Cu-directed trans-Golgi network-to-apical trafficking occurs via a basolateral compartment in hepatocytes in vivo Homo sapiens
physiological function cellular Cu homeostasis is highly regulated and is achieved in part by two intracellular Cu-transporting P-type ATPases, ATP7A and ATP7B. When Cu is low, the enzymes pump cytosolic Cu into the luminal spaces in the secretory pathway to supply Cu to newly synthesized cuproenzymes. When Cu is high, Cu ATPases exit the trans-Golgi network in vesicles and move near the plasma membrane, where they extrude Cu from the cell Homo sapiens
physiological function cellular Cu homeostasis is highly regulated and is achieved in part by two intracellular Cu-transporting P-type ATPases, ATP7A and ATP7B. When Cu is low, the enzymes pump cytosolic Cu into the luminal spaces in the secretory pathway to supply Cu to newly synthesized cuproenzymes. When Cu is high, Cu ATPases exit the trans-Golgi network in vesicles and move near the plasma membrane, where they extrude Cu from the cell. Cu induces an increase in the number of ATP7B vesicles, which traverse large basolateral endosomes en route to the apical domain Homo sapiens