241 human active and 13 inactive phosphatases in total;
194 phosphatases have substrate data;
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336 protein substrates;
83 non-protein substrates;
1215 dephosphorylation interactions;
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299 KEGG pathways;
876 Reactome pathways;
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last scientific update: 11 Mar, 2019
last maintenance update: 01 Sep, 2023
The hepatic sodium/bile acid uptake system exhibitsbroad substrate specificity and transports various non-bile acidorganic compounds as well It is strictly dependent on theextracellular presence of sodium (Microbial infection) Acts as a receptor for hepatitis Bvirus
Bile is a vital secretion, essential for digestion and absorption of fats and fat-soluble vitamins in the small intestine. Moreover, bile is an important route of elimination for excess cholesterol and many waste product, bilirubin, drugs and toxic compounds. Bile secretion depends on the function of membrane transport systems in hepatocytes and cholangiocytes and on the structural and functional integrity of the biliary tree. The hepatocytes generate the so-called primary bile in their canaliculi. Cholangiocytes modify the canalicular bile by secretory and reabsorptive processes as bile passes through the bile ducts. The main solutes in bile are bile acids, which stimulate bile secretion osmotically, as well as facilitate the intestinal absorption of dietary lipids by their detergent properties. Bile acids are also important signalling molecules. Through the activation of nuclear receptors, they regulate their own synthesis and transport rates.
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