Bo-Jeng Wang

Tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma stimulate gamma-secretase-mediated cleavage of amyloid precursor protein through a JNK-dependent MAPK pathway.

Unnatural amino acid-substituted (hydroxyethyl)urea peptidomimetics inhibit gamma-secretase and promote the neuronal differentiation of neuroblastoma cells.

Sodium selenite inhibits gamma-secretase activity through activation of ERK.

Tumor necrosis factor-alpha-elicited stimulation of gamma-secretase is mediated by c-Jun N-terminal kinase-dependent phosphorylation of presenilin and nicastrin.

Caveolin-1 regulates γ-secretase-mediated AβPP processing by modulating spatial distribution of γ-secretase in membrane.

Autophagy: a double-edged sword in Alzheimer's disease.

Retinoic acid-elicited RARα/RXRα signaling attenuates Aβ production by directly inhibiting γ-secretase-mediated cleavage of amyloid precursor protein.

Presenilin-1 regulates the expression of p62 to govern p62-dependent tau degradation.

Aryl hydrocarbon receptor downregulates MYCN expression and promotes cell differentiation of neuroblastoma.

Calreticulin activates β1 integrin via fucosylation by fucosyltransferase 1 in J82 human bladder cancer cells.

Discovery of small molecular (D)-leucinamides as potent, Notch-sparing γ-secretase modulators.

ErbB2 regulates autophagic flux to modulate the proteostasis of APP-CTFs in Alzheimer's disease.

VEGF expression correlates with neuronal differentiation and predicts a favorable prognosis in patients with neuroblastoma.

Critical Roles of Dual-Specificity Phosphatases in Neuronal Proteostasis and Neurological Diseases.