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Silvia Santamarina-Fojo

Researcher at National Institutes of Health

Publications -  87
Citations -  7816

Silvia Santamarina-Fojo is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Cholesterol & Hepatic lipase. The author has an hindex of 53, co-authored 87 publications receiving 7613 citations. Previous affiliations of Silvia Santamarina-Fojo include Government of the United States of America.

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Cellular localization and trafficking of the human ABCA1 transporter.

TL;DR: A complex intracellular trafficking pathway for human ABCA1 is established that may play important roles in modulatingABCA1 transporter activity and cellular cholesterol homeostasis.
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Apolipoprotein Specificity for Lipid Efflux by the Human ABCAI Transporter

TL;DR: AppoA-I and all of the other exchangeable apolipoproteins tested showed greater than a threefold increase in cholesterol and phospholipid efflux from ABCAI-GFP transfected cells compared to control cells.
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Human ATP-binding cassette transporter 1 (ABC1): Genomic organization and identification of the genetic defect in the original Tangier disease kindred

TL;DR: The genomic organization of the human ABC1 gene is reported and a frameshift mutation in the ABC2 gene of the index case of Tangier disease is identified, which will be useful in the future characterization of the structure and function of theABC1 gene and the analysis of additional ABC1 mutations in patients withTangier disease.
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The ATP binding cassette transporter A1 (ABCA1) modulates the development of aortic atherosclerosis in C57BL/6 and apoE-knockout mice.

TL;DR: It is established that, in the presence of apoE, overexpression of ABCA1 modulates HDL as well as apoB-containing lipoprotein metabolism and reduces atherosclerosis in vivo, and indicate that pharmacological agents that will increaseABCA1 expression may reduce atherogenic risk in humans.
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Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis

TL;DR: The results establish the importance of LCAT in the metabolism of both HDL and apolipoprotein B-containing lipoprotein particles with cholesterol feeding and the response to diet-induced atherosclerosis and identify LCAT as a new target for therapy to prevent atheros sclerosis.