Catalyzes the transport of the major hydrophobic bile salts, such as taurine and glycine-conjugated cholic acid across the canalicular membrane of hepatocytes in an ATP-dependent manner, therefore participates in hepatic bile acid homeostasis and consequently to lipid homeostasis through regulation of biliary lipid secretion in a bile salts dependent manner. Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts. Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion. ATP + cholate(in) + H2O = ADP + cholate(out) + H(+) + phosphate ATP + H2O + taurocholate(in) = ADP + H(+) + phosphate + taurocholate(out) ATP + glycocholate(in) + H2O = ADP + glycocholate(out) + H(+) + phosphate ATP + glycochenodeoxycholate(in) + H2O = ADP + glycochenodeoxycholate(out) + H(+) + phosphate ATP + H2O + taurochenodeoxycholate(in) = ADP + H(+) + phosphate + taurochenodeoxycholate(out) ATP + glycoursodeoxycholate(in) + H2O = ADP + glycoursodeoxycholate(out) + H(+) + phosphate ATP + H2O + tauroursodeoxycholate(in) = ADP + H(+) + phosphate + tauroursodeoxycholate(out) ATP + H2O + taurodeoxycholate(in) = ADP + H(+) + phosphate + taurodeoxycholate(out) ATP + H2O + taurolithocholate 3-sulfate(in) = ADP + H(+) + phosphate + taurolithocholate 3-sulfate(out) ATP + H2O + pravastatin(in) = ADP + H(+) + phosphate + pravastatin(out) The uptake of taurocholate is inhibited by taurolithocholate sulfate with an IC(50) of 9 uM. Pravastatin competitively inhibits the transport of taurocholic acid. Cyclosporin A, glibenclamide, rifampicin and troglitazonestrongly competitively inhibit the transport activity of taurocholate. The canalicular transport activity of taurocholate is strongly dependent on canalicular membrane cholesterol content. The uptake of taurocholate is increased by short- and medium-chain fatty acids. Cholesterol increases transport capacity of taurocholate without affecting the affinity for the substrate. Interacts with HAX1 (By similarity). Interacts with the adapter protein complex 2 (AP-2) throught AP2A2 or AP2A1; this interaction regulates cell membrane expression of ABCB11 through its internalization in a clathrin-dependent manner and its subsequent degradation (By similarity). Internalized at the canalicular membrane through interaction with the adapter protein complex 2 (AP-2). At steady state, localizes in the canalicular membrane but is also present in recycling endosomes. ABCB11 constantly and rapidly exchanges between the two sites through tubulo-vesicles carriers that move along microtubules. Microtubule-dependent trafficking of ABCB11 is enhanced by taurocholate and cAMP and regulated by STK11 through a PKA-mediated pathway. Trafficking of newly synthesized ABCB11 through endosomal compartment to the bile canalicular membrane is accelerated by cAMP but not by taurocholate (By similarity). Cell membrane expression is up-regulated by short- and medium-chain fatty acids (By similarity). Expressed predominantly, if not exclusively in the liver, where it was further localized to the canalicular microvilli and to subcanalicular vesicles of the hepatocytes by in situ. Multifunctional polypeptide with two homologous halves, each containing a hydrophobic membrane-anchoring domain and an ATP binding cassette (ABC) domain. N-glycosylated. Ubiquitinated; short-chain ubiquitination regulates cell-Surface expression of ABCB11. Belongs to the ABC transporter superfamily. ABCB family. Multidrug resistance exporter (TC 3.A.1.201) subfamily.