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Details on Person In the body, solute carrier organic anion transporter family...
| Class:Id | Summation:5661179 |
|---|---|
| _displayName | In the body, solute carrier organic anion transporter family... |
| _timestamp | 2019-09-18 14:23:15 |
| created | [InstanceEdit:5661189] Jassal, Bijay, 2015-01-09 |
| modified | [InstanceEdit:9661797] Jassal, Bijay, 2019-09-18 |
| text | 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. SLCO1B3 mutations that can cause HBLRR are a 7.2-kb deletion, removing exon 12 and causing premature termination of the C-terminal 3 transmembrane domains (not shown here) and I562* (van de Steeg et al. 2012). |
| (summation) | [FailedReaction:5661198] Defective SLCO1B3 does not transport BIL from extracellular region (blood) to cytosol (hepatocyte) [Homo sapiens] |
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No pathways have been reviewed or authored by In the body, solute carrier organic anion transporter family... (5661179)
