1. Academic Validation
  2. ADP-ribosylation factor (ARF)-like 7 (ARL7) is induced by cholesterol loading and participates in apolipoprotein AI-dependent cholesterol export

ADP-ribosylation factor (ARF)-like 7 (ARL7) is induced by cholesterol loading and participates in apolipoprotein AI-dependent cholesterol export

  • FEBS Lett. 2004 May 21;566(1-3):241-6. doi: 10.1016/j.febslet.2004.04.048.
Thomas Engel 1 Aloys Lueken Günther Bode Uwe Hobohm Stefan Lorkowski Bernhard Schlueter Stephan Rust Paul Cullen Michael Pech Gerd Assmann Udo Seedorf
Affiliations

Affiliation

  • 1 Institut für Arterioskleroseforschung, Westfälische Wilhelms-Universität, Domagkstr. 3, D-48149 Münster, Germany. engeltho@uni-muenster.de
Abstract

Here, we identify ADP-ribosylation factor (ARF)-like 7 (ARL7) as the only ARF- and ARL-family member whose mRNA-expression is induced by liver X-receptor/retinoid X-receptor agonists or Cholesterol loading in human macrophages. Moreover, subcellular distribution of mutant and wild type ARL7-enhanced green Fluorescent protein (EGFP) supports that ARL7 may be involved in a vesicular transport step between a perinuclear compartment and the plasma membrane. Therefore, we investigated the effect of ARL7 over-expression on the Cholesterol secretory pathway. We found that expression of wild type and dominant active ARL7-EGFP stimulated the rate of apolipoprotein AI-specific Cholesterol efflux 1.7- and 2.8-fold. In contrast, expression of the dominant negative form of ARL7-EGFP led to approximately 50% inhibition of Cholesterol efflux. This data is consistent with a model in which ARL7 is involved in transport between a perinuclear compartment and the plasma membrane apparently linked to the ABCA1-mediated Cholesterol secretion pathway.

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