β-Site APP-cleaving enzyme 1 (BACE1) cleaves cerebellar Na+ channel β4-subunit and promotes Purkinje cell firing by slowing the decay of resurgent Na+ current

Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents

(2010) Brian W. Jarecki et al.   JOURNAL OF CLINICAL INVESTIGATION

BACE1 Deficiency Causes Altered Neuronal Activity and Neurodegeneration

(2010) X. Hu et al.   JOURNAL OF NEUROSCIENCE

BACE1-/- mice exhibit seizure activity that does not correlate with sodium channel level or axonal localization

(2010) Brian D. Hitt et al.   Molecular Neurodegeneration

Control of transient, resurgent, and persistent current by open-channel block by Na channel  4 in cultured cerebellar granule neurons

(2010) J. S. Bant et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Functional reciprocity between Na+ channel Nav1.6 and  1 subunits in the coordinated regulation of excitability and neurite outgrowth

(2010) W. J. Brackenbury et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Regulation of Persistent Na Current by Interactions between   Subunits of Voltage-Gated Na Channels

(2009) T. K. Aman et al.   JOURNAL OF NEUROSCIENCE

The Role of Amyloid Precursor Protein Processing by BACE1, the β-Secretase, in Alzheimer Disease Pathophysiology

(2008) Sarah L. Cole et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Functional properties and differential neuromodulation of Nav1.6 channels

(2008) Yuan Chen et al.   MOLECULAR AND CELLULAR NEUROSCIENCE

Non-proteolytic effect of β-site APP-cleaving enzyme 1 (BACE1) on sodium channel function

(2008) Tobias Huth et al.   NEUROBIOLOGY OF DISEASE