Frédéric Gambino, Alice Pavlowsky, Aurélie Béglé, Jean-Luc Dupont, Nadia Bahi, Raphael Courjaret, Robert Gardette, Hassen Hadjkacem, Henriette Skala, Bernard Poulain, Jamel Chelly, Nicolas Vitale, Yann Humeau
Null mutations in the IL1-receptor accessory protein-like 1 gene (IL1RAPL1) are responsible for an inherited X-linked form of cognitive impairment. IL1RAPL1 protein physically interacts with neuronal calcium sensor-1 (NCS-1), but the functional impact of the IL1RAPL1/NCS-1 interaction remains unknown. Here, we demonstrate that stable expression of IL1RAPL1 in PC12 cells induces a specific silencing of N-type voltage-gated calcium channels (N-VGCC) activity that explains a secretion deficit observed in these IL1RAPL1 cells...
May 22, 2007: Proceedings of the National Academy of Sciences of the United States of America