ATP‐binding cassette transporters and cholesterol translocation

IUBMB Life - Tập 65 Số 6 - Trang 505-512 - 2013
Ge Li1, Hongmei Gu1, Dawei Zhang2,1
1Department of Pediatrics and Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB, Canada
2Department of Biochemistry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada

Tóm tắt

AbstractCholesterol, a major component of mammalian cell membranes, plays important structural and functional roles. However, accumulation of excessive cholesterol is toxic to cells. Aberrant cholesterol trafficking and accumulation is the molecular basis for many diseases, such as atherosclerotic cardiovascular disease and Tangier's disease. Accumulation of excessive cholesterol is also believed to contribute to the early onset of Alzheimer's disease. Thus, cellular cholesterol homeostasis is tightly regulated by uptake, de novo synthesis, and efflux. Any surplus of cholesterol must either be stored in the cytosol in the form of esters or released from the cell. Recently, several ATP‐binding cassette (ABC) transporters, such as ABCA1, ABCG1, ABCG5, and ABCG8 have been shown to play important roles in the regulation of cellular cholesterol homeostasis by mediating cholesterol efflux. Mutations in ABC transporters are associated with several human diseases. In this review, we discuss the physiological roles of ABC transporters and the underlying mechanisms by which they mediate cholesterol translocation. © 2013 IUBMB Life, 65(6):505–512, 2013

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Tài liệu tham khảo

10.1038/11905

10.1038/72869

10.1126/science.290.5497.1771

10.1038/ng.803

10.1161/CIRCULATIONAHA.111.066589

10.1172/JCI32057

10.1073/pnas.97.8.4245

10.1172/JCI0215748

10.1161/CIRCULATIONAHA.106.621433

10.1073/pnas.0403506101

10.1074/jbc.M505368200

10.1194/jlr.M500546-JLR200

10.1194/jlr.M600218-JLR200

10.1515/bc.2011.006

10.1073/pnas.252582399

10.1172/JCI0216001

10.1194/jlr.M300078-JLR200

10.1074/jbc.M704590200

10.1073/pnas.96.20.11358

10.1074/jbc.M107938200

10.1074/jbc.M513783200

10.1074/jbc.M102348200

10.1074/jbc.M309888200

10.1074/jbc.M412602200

10.1371/journal.pone.0045959

10.1371/journal.pone.0030984

10.1016/j.bbalip.2011.07.010

10.1074/jbc.M507515200

Vulevic B., 2001, Cloning and characterization of human adenosine 5′‐triphosphate‐binding cassette, sub‐family A, transporter 2 (ABCA2), Cancer Res., 61, 3339

10.1056/NEJMoa032178

10.1016/S0006-291X(03)01097-0

10.1016/j.bbalip.2011.07.012

10.1016/j.cmet.2005.01.002

10.1161/01.ATV.0000237629.29842.4c

10.1161/01.ATV.0000240051.22944.dc

10.1161/01.ATV.0000242275.92915.43

10.1016/j.bbamem.2008.06.010

10.1016/j.atherosclerosis.2011.11.024

10.1161/ATVBAHA.110.213215

10.1172/JCI41280

10.1161/01.ATV.0000200082.58536.e1

Yvan‐Charvet L., 2007, Combined deficiency of ABCA1 and ABCG1 promotes foam cell accumulation and accelerates atherosclerosis in mice, J. Clin. Invest., 117, 3900

10.1126/science.1189731

10.1073/pnas.1113021108

10.1161/01.ATV.0000218998.75963.02

10.1016/j.bbalip.2013.01.019

10.1194/jlr.M033209

10.1096/fj.07-9944com

10.1016/j.bbalip.2012.09.007

10.1194/M900250-JLR200

von Kampen O., 2012, Genetic and functional identification of the likely causative variant for cholesterol gallstone disease at the ABCG5/8 lithogenic locus, Hepatology

10.1016/j.bbalip.2011.07.019

10.1016/j.febslet.2007.08.052

10.1021/bi902064g

10.1021/bi800292v