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The cytoplasmic nuclear shuttling of Beclin 1 in neurons with Alzheimer's disease-like injury.

Neuroscience letters (2017-10-02)
Li Wang, Xiao-Bin Xu, Wen-Wen You, Xiao-Xia Lin, Cheng-Tan Li, Hao-Ran Qian, Li-Hui Zhang, Yi Yang
ABSTRACT

The abnormal expression of the autophagy-related protein Beclin 1 has been implicated in Alzheimer's disease (AD) brains, whereas the precise involvement of Caspase-mediated Beclin 1 cleavage in AD neurons has not yet been fully clarified. In this study, we investigated the distribution of Beclin 1 fragments in neurons with AD-like injury. Our results demonstrated that Beclin 1 was expressed in neurons but not in astrocytes in both neuron-glia co-cultures and in cortical tissue slices. The full length and C-terminal fragments of human Beclin 1 was mainly expressed in cytoplasm, while the N-terminal fragment of Beclin 1 was predominantly localized in nucleus. Compared to amyloid-β (Aβ)

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Poly-D-lysine hydrobromide, average mol wt 30,000-70,000, lyophilized powder, γ-irradiated, BioReagent, suitable for cell culture
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N-Acetyl-Asp-Glu-Val-Asp-al, ≥95%, powder