Search results for SLCO1B1

Showing 11 results out of 11

×

Species

Types

Compartments

Reaction types

Search properties

Species

Types

Compartments

Reaction types

Search properties

Protein (3 results from a total of 3)

Identifier: R-HSA-194133
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLCO1B1: Q9Y6L6
Identifier: R-HSA-5661200
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLCO1B1: Q9Y6L6
Identifier: R-HSA-5661185
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: Q9Y6L6

Set (1 results from a total of 1)

Identifier: R-HSA-5661192
Species: Homo sapiens
Compartment: plasma membrane

Reaction (5 results from a total of 5)

Identifier: R-HSA-9631987
Species: Homo sapiens
Compartment: plasma membrane
Three organic anion transporting polypeptides (OATPs; now called solute carrier organic anion transporters, SLCOs) are able to mediate the transport of thyroid hormones, predominantly thyroxine (T4) and triiodothyronine (T3) (Fujiwara et al. 2001). SLCO1B1 (formerly OATP-C), which can also transport bile salts, is mainly expressed in the liver (Abe et al. 1999, Hsiang et al. 1999).
Identifier: R-HSA-194083
Species: Homo sapiens
Compartment: plasma membrane
A molecule of extracellular glycocholate (GCCA) or taurocholate (TCCA) is transported into the cytosol, mediated by OATP-C (SLCO1B1) in the plasma membrane. GCCA and TCCA exist in the blood as complexes with serum albumin (ALB), and its uptake by OATP-C must involve disruption of this complex, but the molecular mechanism coupling disruption and uptake is unknown. In the body, OATP-C is expressed on the basolateral surfaces of hepatocytes and may play a role in the uptake of GCCA and TCCA by the liver under physiological conditions (Kullak-Ublick et al. 2004, Trauner & Boyer 2002).
Identifier: R-HSA-5661184
Species: Homo sapiens
Compartment: plasma membrane, extracellular region
The solute carrier organic anion transporter family member 1B1 (SLCO1B1) is expressed on the basolateral surfaces of hepatocytes and mediates the uptake of bilirubin (BIL), a breakdown product of heme degradation, to the liver where it is conjugated and excreted from the body. Defects in SLCO1B1 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. Mutations in SLCO1B1 that can cause HBLRR include R580* and R253* (van de Steeg et al. 2012).
Identifier: R-HSA-9661397
Species: Homo sapiens
Compartment: cytosol, extracellular region, plasma membrane
Bilirubin (BIL), the end product of heme catabolism, is taken up from the blood circulation into the liver. The organic anion transporting polypeptide SLCO1B1 (OATP, OATP2, OATPC, SLC21A6), localised on the basolateral (sinusoidal side) hepatocyte membrane, can mediate the uptake of BIL and various other lipophilic anions into the human liver (Konig et al. 2000, Cui et al. 2001).
Identifier: R-HSA-879575
Species: Homo sapiens
Compartment: plasma membrane
Three organic anion transporting polypeptides (OATPs; now called solute carrier organic anion transporters, SLCOs) are able to mediate the transport of thyroid hormones, predominantly thyroxine (T4) and triiodothyronine (T3) (Fujiwara et al. 2001). SLCO1B1 (formerly OATP-C), which can also transport bile salts, is mainly expressed in the liver (Abe et al. 1999; Hsiang et al. 1999). SLCO4A1 (formerly OATP-E) is mainly expressed in peripheral tissue and has a broad substrate specificty (Tamai et al. 2000). SLCO1C1 (formerly OATP-F) is highly expressed in brain and is also a high affinity thyroid hormone transporter (Pizzagalli et al. 2002).

The monocarboxylate transporter 8 (MCT8, SLC16A2 is also a very active and specific thyroid hormone transporter in its dimeric form (Visser et al. 2009). Defects in SLC16A2 can cause severe X-linked psychomotor retardation. SLC16A2 mutations that inhibited SLC16A2 dimerisation resulted in defective transport function of SLC16A2 (Fischer et al. 2015).

Pathway (2 results from a total of 2)

Identifier: R-HSA-5619110
Species: Homo sapiens
The solute carrier organic anion transporter family member 1B1 (SLCO1B1) is expressed on the basolateral surfaces of hepatocytes and mediates the uptake of bilirubin (BIL), a breakdown product of heme degradation, to the liver where it is conjugated and excreted from the body. Defects in SLCO1B1 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).
Identifier: R-HSA-159418
Species: Homo sapiens
Of the 20-40 grams of bile salts released daily by the liver, all but approximately 0.5 grams are reabsorbed from the intestine, returned to the liver, and re-used. This recycling involves a series of transport processes: uptake by enterocytes mediated by ASBT (SLC10A2), traversal of the enterocyte cytosol mediated by ileal bile acid binding protein (I-BABP - FABP6), efflux from enterocytes mediated by MRP3 (ABCC3), travel through the portal blood as a complex with albumin, and uptake by hepatocytes mediated by Na+-taurocholate transporting protein (NTPC - SLC10A1) and, to a lesser extent by organic anion transporting proteins A, C, and 8 (OATPA - SLCO1A2, OATPC - SLCO1B1, and OATP-8 - SLCO1B3). Once returned to the hepatocyte cytosol, bile acids (generated in the intestine by the action of bacteria on secreted bile salts) are activated by conjugation with coenzyme A, then coupled to glycine or taurine, regenerating bile salts for re-export into the bile, mediated by the bile salt export pump, ABCB11 (Kullak-Ublick et al. 2004; Mihalik et al. 2002; Trauner and Boyer 2003). Unmodified bile salts returned to the hepatocyte cytosol can be re-exported by ABCB11 without further modification.
Cite Us!