Deletion of hepatic Ctrl reveals its function in copper acquisition and compensatory mechanisms for copper homeostasis

American Journal of Physiology - Gastrointestinal and Liver Physiology

Volumn 296, Issue 2, 2009, Pages

  Kim, Heejeong ^a   Son, Hwa Young ^b   Bailey, Sarah M ^a   Lee, Jaekwon ^a  

^a UNIVERSITY OF NEBRASKA LINCOLN   (United States)

^b Chungnam National University   (South Korea)

Author keywords

Bile; Copper excretion; Cuproenzymes; Liver specific copper transporter 1 deletion; Urine

Indexed keywords

COPPER; COPPER ZINC SUPEROXIDE DISMUTASE; CYTOCHROME C OXIDASE; IRON; MENKES PROTEIN; MENKES PROTEIN 1; UNCLASSIFIED DRUG; ZINC; CATION TRANSPORT PROTEIN; CERULOPLASMIN; CTR1 PROTEIN, MOUSE; SUPEROXIDE DISMUTASE;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; BILIARY EXCRETION; CONTROLLED STUDY; COPPER DEFICIENCY; COPPER METABOLISM; ENZYME ACTIVITY; GENE DELETION; GROWTH RETARDATION; HOMEOSTASIS; IMMUNOBLOTTING; KIDNEY CONCENTRATING CAPACITY; LIVER LEVEL; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; TISSUE LEVEL; URINARY EXCRETION; URINE LEVEL; AGE; AGING; ANIMAL; BILE; BLOOD; ENZYMOLOGY; FEMALE; GENETICS; GROWTH DISORDER; LIVER; MALE; METABOLISM; MOUSE MUTANT; URINE;

AGE FACTORS; AGING; ANIMALS; BILE; CATION TRANSPORT PROTEINS; CERULOPLASMIN; COPPER; ELECTRON TRANSPORT COMPLEX IV; FEMALE; GROWTH DISORDERS; HOMEOSTASIS; IRON; LIVER; MALE; MICE; MICE, KNOCKOUT; SUPEROXIDE DISMUTASE; ZINC;

EID: 59449094867     PISSN: 01931857     EISSN: 15221547     Source Type: Journal    
DOI: 10.1152/ajpgi.90632.2008     Document Type: Article

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