编码小分子伴侣蛋白质MOG1基因的突变体及其应用
By using the E50K MOG1 mutant, the problem of high dose and poor effect of wild-type MOG1 in increasing cardiac sodium current has been solved, enabling more efficient gene therapy, especially for the treatment of Brugada syndrome, arrhythmia and dilated cardiomyopathy.
Patent Information
- Authority / Receiving Office
- CN · China
- Patent Type
- Patents(China)
- Current Assignee / Owner
- HUAZHONG UNIV OF SCI & TECH
- Filing Date
- 2022-04-21
- Publication Date
- 2026-07-17
AI Technical Summary
In existing technologies, wild-type MOG1 protein requires high doses and is not very effective in increasing cardiac sodium current, which limits its application in gene therapy, especially its effectiveness in treating diseases such as Brugada syndrome, arrhythmia, and dilated cardiomyopathy.
By employing the E50K mutant encoding the small molecule chaperone protein MOG1, the binding strength to Ran is reduced and the stability is improved, thereby enhancing the effect of myocardial sodium current and developing a more efficient gene therapy.
The E50K MOG1 mutant significantly increased myocardial sodium current density, reduced the viral dose required for gene therapy, and enhanced the therapeutic effect on arrhythmias and cardiomyopathy caused by SCN5A mutations.
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Abstract
Citation Information
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