Toshiharu Suzuki

Novel cadherin-related membrane proteins, Alcadeins, enhance the X11-like protein-mediated stabilization of amyloid beta-protein precursor metabolism.

Facilitation of stress-induced phosphorylation of beta-amyloid precursor protein family members by X11-like/Mint2 protein.

Coordinated metabolism of Alcadein and amyloid beta-protein precursor regulates FE65-dependent gene transactivation.

Suppression of the caspase cleavage of beta-amyloid precursor protein by its cytoplasmic phosphorylation.

Role of 14-3-3gamma in FE65-dependent gene transactivation mediated by the amyloid beta-protein precursor cytoplasmic fragment.

Role of APP phosphorylation in FE65-dependent gene transactivation mediated by AICD.

Trafficking of Alzheimer's disease-related membrane proteins and its participation in disease pathogenesis.

Enhanced amyloidogenic metabolism of the amyloid beta-protein precursor in the X11L-deficient mouse brain.

[Novel mechanisms in signal transduction and cellular response through neural adaptor proteins].

Endoplasmic reticulum chaperones inhibit the production of amyloid-beta peptides.

Physiological mouse brain Abeta levels are not related to the phosphorylation state of threonine-668 of Alzheimer's APP.

The novel cargo Alcadein induces vesicle association of kinesin-1 motor components and activates axonal transport.

Evidence against roles for phorbol binding protein Munc13-1, ADAM adaptor Eve-1, or vesicle trafficking phosphoproteins Munc18 or NSF as phospho-state-sensitive modulators of phorbol/PKC-activated Alzheimer APP ectodomain shedding.

The X11L/X11beta/MINT2 and X11L2/X11gamma/MINT3 scaffold proteins shuttle between the nucleus and cytoplasm.

Regulation of FE65 nuclear translocation and function by amyloid beta-protein precursor in osmotically stressed cells.

Paths, elongation, and projections of ascending chick embryonic spinal commissural neurons after crossing the floor plate.

Regulation of amyloid beta-protein precursor by phosphorylation and protein interactions.

X11 proteins regulate the translocation of amyloid beta-protein precursor (APP) into detergent-resistant membrane and suppress the amyloidogenic cleavage of APP by beta-site-cleaving enzyme in brain.

Phosphorylation of the amino-terminal region of X11L regulates its interaction with APP.

Prostaglandin E2 stimulates the production of amyloid-beta peptides through internalization of the EP4 receptor.

X11-like protein deficiency is associated with impaired conflict resolution in mice.

Regulation of the physiological function and metabolism of AbetaPP by AbetaPP binding proteins.

Suppression of APP-containing vesicle trafficking and production of beta-amyloid by AID/DHHC-12 protein.

Metabolic stabilization of p53 by FE65 in the nuclear matrix of osmotically stressed cells.

Alcadein cleavages by amyloid beta-precursor protein (APP) alpha- and gamma-secretases generate small peptides, p3-Alcs, indicating Alzheimer disease-related gamma-secretase dysfunction.

Roles of the intramolecular regions of FE65 in its trans-accumulation and in p53 stabilization in the nuclear matrix of osmotically stressed cells.

Human CRB2 inhibits gamma-secretase cleavage of amyloid precursor protein by binding to the presenilin complex.

Increased amyloidogenic processing of transgenic human APP in X11-like deficient mouse brain.

IgSF molecule MDGA1 is involved in radial migration and positioning of a subset of cortical upper-layer neurons.

Expression of sorting nexin 18 (SNX18) is dynamically regulated in developing spinal motor neurons.

Suppression of Alzheimer's disease-related phenotypes by expression of heat shock protein 70 in mice.

Cysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-kappaB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis.

Alternative processing of γ-secretase substrates in common forms of mild cognitive impairment and Alzheimer's disease: evidence for γ-secretase dysfunction.

Intracellular trafficking of the amyloid β-protein precursor (APP) regulated by novel function of X11-like.

Effects of heparin and enoxaparin on APP processing and Aβ production in primary cortical neurons from Tg2576 mice.

Coordinated increase of γ-secretase reaction products in the plasma of some female Japanese sporadic Alzheimer's disease patients: quantitative analysis of p3-Alcα with a new ELISA system.

A small peptide sequence is sufficient for initiating kinesin-1 activation through part of TPR region of KLC1.

FE65 as a link between VLDLR and APP to regulate their trafficking and processing.

Membrane-microdomain localization of amyloid β-precursor protein (APP) C-terminal fragments is regulated by phosphorylation of the cytoplasmic Thr668 residue.

Multiple γ-secretase product peptides are coordinately increased in concentration in the cerebrospinal fluid of a subpopulation of sporadic Alzheimer's disease subjects.

[Alcadein].

Constitutive cleavage of the single-pass transmembrane protein alcadeinα prevents aberrant peripheral retention of Kinesin-1.

Hyperpolarization-activated cyclic nucleotide gated channels: a potential molecular link between epileptic seizures and Aβ generation in Alzheimer's disease.

Mechanism of intramembrane cleavage of alcadeins by γ-secretase.

Suppression of Alzheimer's disease-related phenotypes by geranylgeranylacetone in mice.

Simple and direct assembly of kymographs from movies using KYMOMAKER.

Increased levels of plasma p3-alcα35, a major fragment of Alcadeinα by γ-secretase cleavage, in Alzheimer's disease.

Transcriptome analysis of distinct mouse strains reveals kinesin light chain-1 splicing as an amyloid-β accumulation modifier.

Methylglyoxal produced by amyloid-β peptide-induced nitrotyrosination of triosephosphate isomerase triggers neuronal death in Alzheimer's disease.

Utility of SPM8 plus DARTEL (VSRAD) combined with magnetic resonance spectroscopy as adjunct techniques for screening and predicting dementia due to Alzheimer's disease in clinical practice.

Quantitative analysis of APP axonal transport in neurons: role of JIP1 in enhanced APP anterograde transport.

Cytoplasmic fragment of Alcadein α generated by regulated intramembrane proteolysis enhances amyloid β-protein precursor (APP) transport into the late secretory pathway and facilitates APP cleavage.

Arachidonic acid diet attenuates brain Aβ deposition in Tg2576 mice.

Stabilization of intracellular trafficking and metabolism of amyloid β-protein precursor and Alcadein β by apolipoprotein E.

Arachidonic or Docosahexaenoic Acid Diet Prevents Memory Impairment in Tg2576 Mice.

Expression and localization of X11 family proteins in neurons.

Facilitation of brain mitochondrial activity by 5-aminolevulinic acid in a mouse model of Alzheimer's disease.

Specific Triazine Herbicides Induce Amyloid-β42 Production.

Altered Cortical Dynamics and Cognitive Function upon Haploinsufficiency of the Autism-Linked Excitatory Synaptic Suppressor MDGA2.

Alternative Selection of β-Site APP-Cleaving Enzyme 1 (BACE1) Cleavage Sites in Amyloid β-Protein Precursor (APP) Harboring Protective and Pathogenic Mutations within the Aβ Sequence.

Phosphorylation of multiple sites within an acidic region of Alcadein α is required for kinesin-1 association and Golgi exit of Alcadein α cargo.

Phosphorylation of KLC1 modifies interaction with JIP1 and abolishes the enhanced fast velocity of APP transport by kinesin-1.

Induction of Amyloid-β42 Production by Fipronil and Other Pyrazole Insecticides.

The cytoplasmic region of the amyloid β-protein precursor (APP) is necessary and sufficient for the enhanced fast velocity of APP transport by kinesin-1.

Roasted Coffee Reduces β-Amyloid Production by Increasing Proteasomal β-Secretase Degradation in Human Neuroblastoma SH-SY5Y Cells.

X11 and X11-like proteins regulate the level of extrasynaptic glutamate receptors.

Novel Notch signaling inhibitor NSI‑1 suppresses nuclear translocation of the Notch intracellular domain.

RIMB-1/RIM-Binding Protein and UNC-10/RIM Redundantly Regulate Presynaptic Localization of the Voltage-Gated Calcium Channel in .

Paul Greengard, Ph.D. (1925-2019).

Decrease in p3-Alcβ37 and p3-Alcβ40, products of Alcadein β generated by γ-secretase cleavages, in aged monkeys and patients with Alzheimer's disease.

Enhanced amyloid-β generation by γ-secretase complex in DRM microdomains with reduced cholesterol levels.

γ-Secretase Activity Is Associated with Braak Senile Plaque Stages.

Generation of Transgenic Cynomolgus Monkeys Overexpressing the Gene for Amyloid-β Precursor Protein.

Amyloidogenic processing of amyloid β protein precursor (APP) is enhanced in the brains of alcadein α-deficient mice.

Cytoplasmic granule formation by FUS-R495X is attributable to arginine methylation in all Gly-rich, RGG1 and RGG2 domains.

Extracellular Release of ILEI/FAM3C and Amyloid-β Is Associated with the Activation of Distinct Synapse Subpopulations.

Dietary cis-9, trans-11-conjugated linoleic acid reduces amyloid β-protein accumulation and upregulates anti-inflammatory cytokines in an Alzheimer's disease mouse model.

Transcriptional downregulation of FAM3C/ILEI in the Alzheimer's brain.

Suppression of amyloid-β secretion from neurons by cis-9, trans-11-octadecadienoic acid, an isomer of conjugated linoleic acid.

γ-Secretase structure and activity are modified by alterations in its membrane localization and ambient environment.

Accumulation of amyloid-β in the brain of mouse models of Alzheimer's disease is modified by altered gene expression in the presence of human apoE isoforms during aging.