Naturally occurring mutations in the largest extracellular loops of ABCA1 can disrupt its direct interaction with apolipoprotein A-I (Q24300380)

cholesterol transfer activity

GOA release 2020-03-11

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GOA release 2020-03-11

Mason W Freeman

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author name string

Michael L Fitzgerald

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Andrea L Morris

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Jeongmi S Rhee

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Lorna P Andersson

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Armando J Mendez

Journal of Biological Chemistry

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language of work or name

English

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publication date

6 September 2002

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published in

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volume

277

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issue

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page(s)

33178-87

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A point mutation in ABC1 gene in a patient with severe premature coronary heart disease and mild clinical phenotype of Tangier disease

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Decreased cellular cholesterol efflux is a common cause of familial hypoalphalipoproteinemia: role of the ABCA1 gene mutations

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Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency

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The gene encoding ATP-binding cassette transporter 1 is mutated in Tangier disease

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Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1

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ABC1 promotes engulfment of apoptotic cells and transbilayer redistribution of phosphatidylserine

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Transport of lipids from golgi to plasma membrane is defective in tangier disease patients and Abc1-deficient mice

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Cholesterol efflux to apolipoprotein AI involves endocytosis and resecretion in a calcium-dependent pathway

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High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1

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Cell toxicity induced by inhibition of acyl coenzyme A:cholesterol acyltransferase and accumulation of unesterified cholesterol

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Functional changes in scavenger receptor binding conformation are induced by charge mutants spanning the entire collagen domain

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Specific binding of ApoA-I, enhanced cholesterol efflux, and altered plasma membrane morphology in cells expressing ABC1.

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ABCA1 is the cAMP-inducible apolipoprotein receptor that mediates cholesterol secretion from macrophages

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ATP-binding cassette transporter A1 contains an NH2-terminal signal anchor sequence that translocates the protein's first hydrophilic domain to the exoplasmic space.

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Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease

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