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International Journal of Alzheimer'S Disease|January 25, 2013
γ-Secretase-Dependent Proteolysis of Transmembrane Domain of Amyloid Precursor Protein: Successive Tri- and Tetrapeptide Release in Amyloid β-Protein ProductionMako Takami, Satoru Funamoto
Differentiation; Research in Biological Diversity|February 1, 2003
cAMP-dependent protein kinase regulates Polysphondylium pallidum developmentSatoru Funamoto, Christophe Anjard, Wolfgang Nellen, et al.
Seminars in Cell & Developmental Biology|May 2, 2020
Successive cleavage of β-amyloid precursor protein by γ-secretaseSatoru Funamoto, Shinji Tagami, Masayasu Okochi, et al.
Journal of Neurochemistry|December 30, 2016
Alanine substitutions in the GXXXG motif alter C99 cleavage by γ-secretase but not its dimerizationHidekazu Higashide, Seiko Ishihara, Mika Nobuhara, et al.
Biochemical and Biophysical Research Communications|May 23, 2018
Glycosylation status of nicastrin influences catalytic activity and substrate preference of γ-secretaseMohammad Moniruzzaman, Seiko Ishihara, Mika Nobuhara, et al.
Cell|June 14, 2002
Spatial and temporal regulation of 3-phosphoinositides by PI 3-kinase and PTEN mediates chemotaxisSatoru Funamoto, Ruedi Meili, Susan Lee, et al.
Biochemical and Biophysical Research Communications|April 24, 2021
A nontoxigenic form of Shiga toxin 2 suppresses the production of amyloid β by altering the intracellular transport of amyloid precursor protein through its receptor-binding B-subunitWaka Sato, Miho Watanabe-Takahashi, Takashi Hamabata, et al.
Biochemistry|October 20, 2004
Truncated carboxyl-terminal fragments of beta-amyloid precursor protein are processed to amyloid beta-proteins 40 and 42Satoru Funamoto, Maho Morishima-Kawashima, Yu Tanimura, et al.
The Journal of Biological Chemistry|April 6, 2006
Equimolar production of amyloid beta-protein and amyloid precursor protein intracellular domain from beta-carboxyl-terminal fragment by gamma-secretaseNobuto Kakuda, Satoru Funamoto, Sousuke Yagishita, et al.
Acta Neuropathologica Communications|November 5, 2015
The A673T mutation in the amyloid precursor protein reduces the production of β-amyloid protein from its β-carboxyl terminal fragment in cellsAsuka Kokawa, Seiko Ishihara, Hitomi Fujiwara, et al.
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