Polypeptide for inhibiting glycogen synthase kinase-3[beta] acetylation, coding gene of polypeptide and application of polypeptide and coding gene

Abstract

The invention relates to the technical field of genetic engineering, and discloses a polypeptide for inhibiting glycogen synthase kinase-3[beta] acetylation, and a coding gene of polypeptide and application of polypeptide and coding gene. The sequence of the polypeptide is shown as SEQ.ID.NO:1. The polypeptide for inhibiting glycogen synthase kinase-3[beta] acetylation can block the combination of tau protein and glycogen synthase kinase-3[beta] in the whole level of cells and animals, and can block the acetylation and activation effects of the tau protein on the glycogen synthase kinase-3[beta]; and the morphology and function of cells are improved, and the learning and memory ability of mice is improved. The polypeptide provided by the invention can play a role in preventing and treating glycogen synthase kinase-3[beta] activation related diseases such as Alzheimer's disease and the like.

Description

technical field [0001] The invention relates to the technical field of genetic engineering, in particular to a polypeptide for inhibiting the acetylation of glycogen synthase kinase-3β, its coding gene and their application. Background technique [0002] Glycogen synthase kinase-3β (GSK-3β) is highly expressed in the central nervous system, and the overactivation of GSK-3β plays a key role in neuropsychiatric diseases such as Alzheimer's disease (AD) and metabolic diseases such as diabetes. In the brain and plasma of AD patients and in the plasma of diabetic patients, the activity of GSK-3β was significantly increased. For two characteristic pathologies observed in AD brains, GSK-3β promotes β-amyloid (Aβ) production by upregulating β-amyloid-cleaving enzyme-1 (BACE1) and presenilin-1 (PS1), And mediate the toxicity of Aβ. Upregulation of GSK-3β also induces hyperphosphorylation of tau protein, impairs neuronal synaptic plasticity, and leads to impairment of spatial memory...

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Problems solved by technology

It was also found that GSK-3βK15 acetylation aggravated synaptic damage, neuroinflammation, tau protein hyperphosphorylation and Aβ production on the basis of wild-type GSK-3β, and finally caused cognitive dysfunction in mice

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