Loss of OATP1B3 function causes Rotor syndrome

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Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver.

Bilirubin, a breakdown product of heme, is normally glucuronidated and excreted by the liver into bile. Failure of this system can lead to a buildup of conjugated bilirubin in the blood, resulting in jaundice. The mechanistic basis of bilirubin excretion and hyperbilirubinemia syndromes is largely understood, but that of Rotor syndrome, an autosomal recessive disorder characterized by conjugate...

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ژورنال

عنوان ژورنال: Cancer Biology & Therapy

سال: 2012

ISSN: 1538-4047,1555-8576

DOI: 10.4161/cbt.22010