Molecular Regulation of Canalicular ABC Transporters

被引：24

作者：

Ben Saad, Amel ^{[1
,2
]}

Bruneau, Alix ^{[2
,3
]}

Mareux, Elodie ^{[1
]}

Lapalus, Martine ^{[1
]}

Delaunay, Jean-Louis ^{[2
]}

Gonzales, Emmanuel ^{[1
,4
]}

Jacquemin, Emmanuel ^{[1
,4
]}

Ait-Slimane, Tounsia ^{[2
]}

Falguieres, Thomas ^{[1
]}

机构：

[1] Univ Paris Saclay, Physiopathogenese & Traitement Malad Foie, INSERM, UMR S 1193, F-91400 Orsay, France

[2] Sorbonne Univ, INSERM, UMR S 938, Ctr Rech St Antoine CRSA,Inst Cardiometab & Nutr, F-75012 Paris, France

[3] Charite Univ Med Berlin, Dept Hepatol & Gastroenterol, D-13353 Berlin, Germany

[4] CHU Bicetre, Paediat Hepatol & Paediat Liver Transplant Dept, Reference Ctr Rare Paediat Liver Dis, FILFOIE,ERN RARE LIVER,AP HP,Fac Med Saclay, F-94270 Le Kremlin Bicetre, France

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2021年 / 22卷 / 04期

关键词：

bile secretion; ABCB1; ABCB4; ABCB11; ABCC2; ABCG5; G8; molecular partners;

D O I：

10.3390/ijms22042113

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：1 / 17

页数：17

共 140 条

[1] Protein Quality Control in the Endoplasmic Reticulum [J].