Molecular Regulation of Canalicular ABC Transporters

The ATP-binding cassette (ABC) transporters expressed at the canalicular membrane of hepatocytes mediate the secretion of several compounds into the bile canaliculi and therefore play a key role in bile secretion. Among these transporters, ABCB11 secretes bile acids, ABCB4 translocates phosphatidylc...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-02, Vol.22 (4), p.2113
Main Authors: Ben Saad, Amel, Bruneau, Alix, Mareux, Elodie, Lapalus, Martine, Delaunay, Jean-Louis, Gonzales, Emmanuel, Jacquemin, Emmanuel, Aït-Slimane, Tounsia, Falguières, Thomas
Format: Article
Language:English
Subjects:
ABC transporters
ABCB1
ABCB11
ABCB4
ABCC2
ABCG5/G8
Animals
ATP-Binding Cassette Transporters - genetics
ATP-Binding Cassette Transporters - metabolism
Bile
Bile acids
Bile Canaliculi - metabolism
Bile ducts
bile secretion
Biosynthesis
Cholesterol
Endocytosis
Endoplasmic reticulum
Gallbladder diseases
Glycosylation
Hepatocytes
Hepatocytes - metabolism
Humans
Kinases
Lecithin
Life Sciences
Liver
Lymphocyte receptors
Membrane trafficking
Membranes
Phosphatidylcholine
Plasma
Protein folding
Quality control
Review
Secretion
Ubiquitination
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Summary:The ATP-binding cassette (ABC) transporters expressed at the canalicular membrane of hepatocytes mediate the secretion of several compounds into the bile canaliculi and therefore play a key role in bile secretion. Among these transporters, ABCB11 secretes bile acids, ABCB4 translocates phosphatidylcholine and ABCG5/G8 is responsible for cholesterol secretion, while ABCB1 and ABCC2 transport a variety of drugs and other compounds. The dysfunction of these transporters leads to severe, rare, evolutionary biliary diseases. The development of new therapies for patients with these diseases requires a deep understanding of the biology of these transporters. In this review, we report the current knowledge regarding the regulation of canalicular ABC transporters' folding, trafficking, membrane stability and function, and we highlight the role of molecular partners in these regulating mechanisms.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22042113