BETA AMYLOID PEPTIDE 25-35 INDUCES Tau PROTEIN HYPERPHOSPHORYLATION IN CORTICAL NEURONS THROUGH JNK/p38 MAPK PATH IN RAT EMBRYO

Acta Anatomica Sinica ›› 2007, Vol. 38 ›› Issue (5) : 532-536.

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Acta Anatomica Sinica ›› 2007, Vol. 38 ›› Issue (5) : 532-536.
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BETA AMYLOID PEPTIDE 25-35 INDUCES Tau PROTEIN HYPERPHOSPHORYLATION IN CORTICAL NEURONS THROUGH JNK/p38 MAPK PATH IN RAT EMBRYO

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Abstract

Objective To investigate the effect and the molecular mechanism of aggregated beta-amyloid peptide 25-35 (Aβ SUB>25-35/SUB>) on the level of Tau protein phosphorylation in rat embryo cortical neurons. Methods Western blotting and immunocytochemical stain were performed to observe the Tau protein phosphorylation and the expression of JNK/p38 MAPK Results The level of Tau protein phosphorylation in the sites of SerSUP>396/SUP>, SerSUP> 199/202/SUP> and ThrSUP>205/SUP> increased after Aβ SUB>25-35/SUB> of 20μmol/L was exposed to cortical neurons, meanwhile the level of JNK/p38 MAPK also increased after treatment with Aβ25-35 for 12 hours. Pretreatment with specific inhibitor of JNK/p38 MAPK markedly attenuated Tau pr

Key words

Beta-amyloid peptide 25-35 / JNK/p38 MAPK / Tau protein / Alzheimer disease / Western blotting / Immunocytochemical / Rat

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BETA AMYLOID PEPTIDE 25-35 INDUCES Tau PROTEIN HYPERPHOSPHORYLATION IN CORTICAL NEURONS THROUGH JNK/p38 MAPK PATH IN RAT EMBRYO[J]. Acta Anatomica Sinica. 2007, 38(5): 532-536

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