| First Author | Kizuka Y | Year | 2015 |
| Journal | FEBS Lett | Volume | 589 |
| Issue | 13 | Pages | 1418-22 |
| PubMed ID | 25957769 | Mgi Jnum | J:221641 |
| Mgi Id | MGI:5641267 | Doi | 10.1016/j.febslet.2015.04.060 |
| Citation | Kizuka Y, et al. (2015) Clec4g (LSECtin) interacts with BACE1 and suppresses Abeta generation. FEBS Lett 589(13):1418-22 |
| abstractText | beta-Site amyloid precursor protein cleaving enzyme-1 (BACE1) is a central molecule in Alzheimer's disease (AD). It cleaves amyloid precursor protein (APP) to produce the toxic amyloid-beta (Abeta) peptides. Thus, a novel BACE1 modulator could offer a new therapeutic strategy for AD. We report that C-type lectin-like domain family 4, member g (Clec4g, also designated as LSECtin) interacts with BACE1 in mouse brain and cultured cells. Overexpression of Clec4g suppressed BACE1-mediated Abeta generation, and affected the intracellular distribution of BACE1 but not its catalytic activity. These results highlight a novel role of Clec4g in negatively regulating BACE1 function. |
