BACE1 modulates filopodia-like protrusions induced by sodium channel β4 subunit

Haruko Miyazaki, Fumitaka Oyama, Hon Kit Wong, Kumi Kaneko, Takashi Sakurai, Akira Tamaoka, Nobuyuki Nukina

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


Processing of APP by BACE1 plays a crucial role in the pathogenesis of Alzheimer disease (AD). Recently, the voltage-gated sodium channel (Nav) β4 subunit (β4), an auxiliary subunit of Nav that is supposed to serve as a cell adhesion molecule, has been identified as a substrate for BACE1. However, the biological consequence of BACE1 processing of β4 remains illusive. Here, we report the biological effects of β4 processing by BACE1. Overexpression of β4 in Neuro2a cells promoted neurite extension and increased the number of F-actin rich filopodia-like protrusions. While coexpression of BACE1 together with β4 further accelerated neurite extension, the number of filopodia-like protrusions was reduced. Overexpression of C-terminal fragment of β4 that was generated by BACE1 (β4-CTF) partially recapitulated the results obtained with BACE1 overexpression. These results suggest that the processing of β4 by BACE1 regulates neurite length and filopodia-like protrusion density in neurons.

Original languageEnglish
Pages (from-to)43-48
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - Sept 14 2007
Externally publishedYes


  • BACE1
  • Filopodia-like protrusion
  • Neurite outgrowth
  • Sodium channel β4 subunit

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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