| First Author | He W | Year | 2014 |
| Journal | J Biol Chem | Volume | 289 |
| Issue | 30 | Pages | 20630-7 |
| PubMed ID | 24907271 | Mgi Jnum | J:216006 |
| Mgi Id | MGI:5607480 | Doi | 10.1074/jbc.M114.579862 |
| Citation | He W, et al. (2014) beta-site amyloid precursor protein cleaving enzyme 1(BACE1) regulates Notch signaling by controlling the cleavage of Jagged 1 (Jag1) and Jagged 2 (Jag2) proteins. J Biol Chem 289(30):20630-7 |
| abstractText | BACE1 is a type I transmembrane aspartyl protease that cleaves amyloid precursor protein at the beta-secretase site to initiate the release of beta-amyloid peptide. As a secretase, BACE1 also cleaves additional membrane-bound molecules by exerting various cellular functions. In this study, we showed that BACE1 can effectively shed the membrane-anchored signaling molecule Jagged 1 (Jag1).Wealso mapped the cleavage sites of Jag1 by ADAM10 and ADAM17. Although Jag1 shares a high degree of homology with Jag2 in the ectodomain region, BACE1 fails to cleave Jag2 effectively, indicating a selective cleavage of Jag1. Abolished cleavage of Jag1 in BACE1-null mice leads to enhanced astrogenesis and, concomitantly, reduced neurogenesis. This characterization provides biochemical evidence that the Jag1-Notch pathway is under the control of BACE1 activity |
