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A more recent version of this article appeared on December 1, 2002

Papers In Press, published online ahead of print October 1, 2002
J. Lipid Res., doi:10.1194/jlr.M200279-JLR200
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Submitted on July 18, 2002
Revised on September 16, 2002
Accepted on September 17, 2002

Distinct sites on ABCA1 control distinct steps required for cellular release of phospholipids

Veronique Rigot, Yannick Hamon, Olivier Chambenoit, Melanie Alibert, Nicolas Duverger, and Giovanna Chimini

Centre d'Immunologie, INSERM CNRS de Marseille Luminy, Marseille 13288

Corresponding Author: chimini{at}ciml.univ-mrs.fr

The loss of ABCA1 function leads to Tangier dyslipidemia in humans and to a Tangier-like phenotype in mice, by impairing the transformation of nascent apoproteins into mature HDL particles. Mechanistically this ensues from the inability of cells to release membrane lipids and cholesterol. Whereas the ability of ABCA1 to promote phospholipid effluxes, surface binding of apoproteins and outward flip of membrane lipids has been documented, the relationships between this series of ABCA1-dependent events lies still elusive. Here we provide evidence that i) lipid effluxes require both flip of membrane lipids and binding of apoproteins to the cell surface ii) apoA-I binding depends on structural determinants on ABCA1 and iii) phospholipid effluxes can be modulated by engineered mutations on the structural determinants identified on ABCA1.


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