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Defective SLCO1B3 causes hyperbilirubinemia, Rotor type (HBLRR)

Summary

Organism

Homo sapiens (human)

Reactome

R-HSA-5619058

PubChem

R-HSA-5619058

Description

In the body, solute carrier organic anion transporter family member 1B3 (SLCO1B3) is expressed on the basolateral surfaces of hepatocytes and may play a role in the uptake of bilirubin (BIL), a breakdown product of heme that requires conjugation and excretion from the body. Defects in SLCO1B3 can cause hyperbilirubinemia, Rotor type (HBLRR; MIM:237450), an autosomal recessive form of primary conjugated hyperbilirubinemia. Mild jaundice, not associated with hemolysis, develops shortly after birth or in childhood (van de Steeg et al. 2012, Sticova & Jirsa 2013, Keppler 2014).

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SPV: a JavaScript Signaling Pathway Visualizer, Bioinformatics, 2018

Displaying 1 entry
UniProt ID	Protein Name	Gene Symbol	Pathway Viewer
Q9NPD5	Solute carrier organic anion transporter family member 1B3	LST2 OATP1B3 OATP8 SLC21A8 SLCO1B3	view

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