Clec4g (LSECtin) interacts with BACE1 and suppresses Aβ generation. Issue 13 (7th May 2015)

• Record Type: Journal Article
• Authors: Kizuka, Yasuhiko; Kitazume, Shinobu; Sato, Keiko; Taniguchi, Naoyuki
• Is Part Of: FEBS letters. Volume 589:Issue 13(2015)
• Page Start: 1418
• Page End: 1422
• Publication Date: 2015-05-07
• Subjects: AD -- Alzheimer's disease -- APP -- amyloid precursor protein -- BACE1 -- β-site amyloid precursor protein cleaving enzyme-1 -- Clec4g -- C-type lectin-like domain containing-4g -- GlcNAc -- N-acetylglucosamine -- GnT-III -- N-acetylglucosaminyltransferase-III -- Alzheimer's disease (AD) -- β-Site amyloid precursor protein cleaving enzyme-1 (BACE1) -- Bisecting N-acetylglucosamine (GlcNAc) -- C-type lectin-like domain containing-4g (Clec4g); Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2015.04.060
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : β‐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‐β (Aβ) 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 Aβ 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. Abstract : Clec4g (LSECtin) was newly identified as a BACE1‐interacting molecule. Clec4g suppresses BACE1‐mediated Aβ generation. Clec4g affects intracellular distribution of BACE1. Clec4g might be a novel therapeutic target for Alzheimer's disease.