Function and regulation of ABCA1 – membrane meso‐domain organization and reorganization

Nagao, Kazunori; Tomioka, Maiko; Ueda, Kazumitsu

doi:10.1111/j.1742-4658.2011.08170.x

Cited by 57 publications

(49 citation statements)

References 149 publications

(191 reference statements)

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“…The resulting protrusions promote transient binding of apoA-1 to the membrane and a solubilization of the exovesiculated lipid domain leading to the loading of apoA-1 with phospholipids and cholesterol for the generation of nascent HDL particles (52)(53)(54). Other models stress the importance of the interconversion of ABCA1 monomers to dimers and membrane meso-domain organization in apoA-1 binding and HDL formation (55,56).…”

Section: Discussionmentioning

confidence: 99%

Differential Phospholipid Substrates and Directional Transport by ATP-binding Cassette Proteins ABCA1, ABCA7, and ABCA4 and Disease-causing Mutants

Quazi

Molday

2013

Journal of Biological Chemistry

186

159

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Background: Lipid transport by the A-subfamily of ATP-binding cassette (ABC) transporters implicated in human disorders is poorly understood. Results: ABCA1 and ABCA7 export phosphatidylcholine and phosphatidylserine across membranes, whereas ABCA4 imports phosphatidylethanolamine. Conclusion: ABCA transporters actively flip phospholipids across membranes, a function severely reduced for disease-causing mutants. Significance: ABCA-dependent phospholipid transport plays a crucial role in cellular lipid homeostasis.

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Section: Discussionmentioning

confidence: 99%

Differential Phospholipid Substrates and Directional Transport by ATP-binding Cassette Proteins ABCA1, ABCA7, and ABCA4 and Disease-causing Mutants

Quazi

Molday

2013

Journal of Biological Chemistry

186

159

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“…ABCA1 is a key player in the biogenesis of HDL, which is responsible for reverse cholesterol transport, a physiological process for eliminating excess cholesterol from peripheral tissues by returning it to the liver 67) . The loss of ABCA1 function causes Tangier disease, which is characterized by the accumulation of cholesterol (esters) throughout the body due to HDL deficiency, resulting in an increased risk of atherosclerosis and cardiovascular events in patients with Tangier disease 3–5) .…”

Section: Atp-binding Cassette Transporter A1mentioning

confidence: 99%

Transporters for the Intestinal Absorption of Cholesterol, Vitamin E, and Vitamin K

Yamanashi

Takada

Kurauchi

et al. 2017

J Atheroscler Thromb

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Humans cannot synthesize fat-soluble vitamins such as vitamin E and vitamin K. For this reason, they must be obtained from the diet via intestinal absorption. As the deficiency or excess of these vitamins has been reported to cause several types of diseases and disorders in humans, the intestinal absorption of these nutrients must be properly regulated to ensure good health. However, the mechanism of their intestinal absorption remains poorly understood. Recent studies on cholesterol using genome-edited mice, genome-wide association approaches, gene mutation analyses, and the development of cholesterol absorption inhibitors have revealed that several membrane proteins play crucial roles in the intestinal absorption of cholesterol. Surprisingly, detailed analyses of these cholesterol transporters have revealed that they can also transport vitamin E and vitamin K, providing clues to uncover the molecular mechanisms underlying the intestinal absorption of these fat-soluble vitamins. In this review, we focus on the membrane proteins (Niemann-Pick C1 like 1, scavenger receptor class B type I, cluster of differentiation 36, and ATP-binding cassette transporter A1) that are (potentially) involved in the intestinal absorption of cholesterol, vitamin E, and vitamin K and discuss their physiological and pharmacological importance. We also discuss the related uncertainties that need to be explored in future studies.

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“…111,185) ApoA-I mediates the formation of nascent HDL particles from cellular FC and PL through the interaction with the cell surface transporter ABCA1. 186,187) The majority of apoA-I is secreted from the liver. ApoA-I molecules are also accommodated in CM.…”

Section: )mentioning

confidence: 99%

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Morita

2016

Biological & Pharmaceutical Bulletin

133

108

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Increased levels of apolipoprotein B (apoB)-containing lipoproteins, such as low density lipoproteins (LDL) and chylomicron remnants, are associated with the development of atherosclerosis. Chylomicrons containing apoB-48 are secreted from the intestine during the postprandial state, whereas very low density lipoproteins (VLDL) containing apoB-100 are constitutively formed in the liver. Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces. The hepatic uptake of these remnants is facilitated by apolipoprotein E (apoE), but is inhibited by apolipoproteins C-I, C-II and C-III. In the plasma, VLDL remnants are further converted into LDL by the hydrolysis of triglycerides. ApoB-100 is responsible for the hepatic uptake of LDL. LDL receptor, LDL receptor-related protein and heparan sulfate proteoglycans are involved in the hepatic clearance of lipoproteins containing apoB-100 and/or apoE. The subendothelial retention and modification of apoB-containing lipoproteins are crucial events in the initiation of atherosclerosis. In the subendothelium, the uptake of modified lipoproteins by macrophages leads to the formation of foam cells storing excess amounts of cholesteryl esters and subsequently to apoptosis. This review describes the current knowledge about the metabolism and modification of apoB-containing lipoproteins involved in dyslipidemia and atherogenesis. In particular, I focus on the effects of apolipoproteins, lipid composition and particle size on lipoprotein metabolism and on the roles of cholesterol, sphingomyelinase and apoB denaturation in macrophage foam cell formation and apoptosis. A detailed understanding of these mechanisms will help to develop new therapeutic strategies.

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Function and regulation of ABCA1 – membrane meso‐domain organization and reorganization

Cited by 57 publications

References 149 publications

Differential Phospholipid Substrates and Directional Transport by ATP-binding Cassette Proteins ABCA1, ABCA7, and ABCA4 and Disease-causing Mutants

Differential Phospholipid Substrates and Directional Transport by ATP-binding Cassette Proteins ABCA1, ABCA7, and ABCA4 and Disease-causing Mutants

Transporters for the Intestinal Absorption of Cholesterol, Vitamin E, and Vitamin K

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

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