Clec4g (LSECtin) interacts with BACE1 and suppresses Aβ generation

FEBS Lett. 2015 Jun 4;589(13):1418-22. doi: 10.1016/j.febslet.2015.04.060. Epub 2015 May 7.


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.

Keywords: Alzheimer’s disease (AD); Bisecting N-acetylglucosamine (GlcNAc); C-type lectin-like domain containing-4g (Clec4g); β-Site amyloid precursor protein cleaving enzyme-1 (BACE1).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid Precursor Protein Secretases / genetics
  • Amyloid Precursor Protein Secretases / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Aspartic Acid Endopeptidases / genetics
  • Aspartic Acid Endopeptidases / metabolism*
  • Blotting, Western
  • Brain / metabolism*
  • Cell Line, Tumor
  • Humans
  • Lectins, C-Type / genetics
  • Lectins, C-Type / metabolism*
  • Mice, Inbred C57BL
  • Protein Binding
  • Receptors, Virus / genetics
  • Receptors, Virus / metabolism*


  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • LSECtin protein, mouse
  • Lectins, C-Type
  • Receptors, Virus
  • Amyloid Precursor Protein Secretases
  • Aspartic Acid Endopeptidases
  • Bace1 protein, mouse