• Publications
  • Influence
Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression
  • X. Sun, G. He, +6 authors W. Song
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences
  • 5 December 2006
The molecular mechanism underlying the pathogenesis of the majority of cases of sporadic Alzheimer's disease (AD) is unknown. A history of stroke was found to be associated with development of someExpand
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Dopamine-dependent neurotoxicity of α-synuclein: A mechanism for selective neurodegeneration in Parkinson disease
The mechanism by which dopaminergic neurons are selectively lost in Parkinson disease (PD) is unknown. Here we show that accumulation of α-synuclein in cultured human dopaminergic neurons results inExpand
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A role for the proteasome in the light response of the timeless clock protein.
The cyclic expression of the period (PER) and timeless (TIM) proteins is critical for the molecular circadian feedback loop in Drosophila. The entrainment by light of the circadian clock is mediatedExpand
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Inhibition of GSK3β-mediated BACE1 expression reduces Alzheimer-associated phenotypes.
  • P. Ly, Yili Wu, +8 authors W. Song
  • Biology, Medicine
  • The Journal of clinical investigation
  • 2 January 2013
Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the pathological hallmark of Alzheimer's disease (AD). Aβ is generated from sequential cleavages of the β-amyloidExpand
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Transcriptional regulation of BACE1, the beta-amyloid precursor protein beta-secretase, by Sp1.
Proteolytic processing of the beta-amyloid precursor protein (APP) at the beta site is essential to generate Abeta. BACE1, the major beta-secretase involved in cleaving APP, has been identified as aExpand
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Oxidative stress potentiates BACE1 gene expression and Aβ generation
Summary.Alzheimer’s Disease (AD) is the most common neurodegenerative disorder leading to dementia and its prevalence increases with age. The pathological features of AD are characterized by theExpand
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BACE2, as a novel APP θ‐secretase, is not responsible for the pathogenesis of Alzheimer's disease in Down syndrome
  • X. Sun, G. He, W. Song
  • Biology, Medicine
  • FASEB journal : official publication of the…
  • 1 July 2006
Amyloid β protein (Aβ), the major component of neuritic plaques in Alzheimer's disease (AD), is derived from APP by sequential cleavages of β‐ and y‐secretases. Beta‐site APP cleaving enzyme 1Expand
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Presenilins are required for γ-secretase cleavage of β-APP and transmembrane cleavage of Notch-1
Presenilins are required for γ -secretase cleavage of β -APP and transmembrane cleavage of Notch-1
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Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease.
Elevated levels of β-site APP cleaving enzyme 1 (BACE1) were found in the brain of some sporadic Alzheimer's disease (AD) patients; however, the underlying mechanism is unknown. BACE1 cleavesExpand
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Degradation of BACE by the ubiquitin‐proteasome pathway
The amyloid β protein (Aβ) is derived from β‐amyloid precursor protein (APP). Cleavage of APP by β‐secretase generates a C‐terminal fragment (APPCTFβ or C99), which is subsequently cleaved byExpand
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