| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 11022513 | Molecular Metabolism | 2018 | 12 Pages |
Abstract
By acting as an insulin-dependent retention adaptor, PID1 serves as a regulator of LRP1 function controlling the disposal of postprandial lipoproteins. PID1 inhibition provides a novel approach to lower plasma levels of pro-atherogenic TRL remnants by stimulating endocytic function of both LRP1 and LDLR in the liver.
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Authors
Alexander W. Fischer, Kirstin Albers, Lucia M. Krott, Britta Hoffzimmer, Markus Heine, Hartwig Schmale, Ludger Scheja, Philip L.S.M. Gordts, Joerg Heeren,