Post-translational Modifications of the p53 Protein and the Impact in Alzheimer's Disease: A Review of the Literature

被引:18
|
作者
Clark, James S. [1 ]
Kayed, Rakez [2 ,3 ]
Abate, Giulia [4 ]
Uberti, Daniela [5 ]
Kinnon, Paul [1 ]
Piccirella, Simona [1 ]
机构
[1] Diadem srl, Brescia, Italy
[2] Univ Texas Med Branch, Mitchell Ctr Neurodegenerat Dis, Galveston, TX USA
[3] Univ Texas Med Branch, Dept Neurol Neurosci & Cell Biol, Galveston, TX USA
[4] Univ Brescia, Dept Mol & Translat Med, Div Pharmacol, Brescia, Italy
[5] Univ Brescia, Dept Mol & Translat Med, Brescia, Italy
来源
关键词
p53; Alzheimer's disease (AD); post translational modification (PTM); review; TP53; MILD COGNITIVE IMPAIRMENT; AMYLOID PRECURSOR PROTEIN; OXIDATIVE STRESS; TAU PHOSPHORYLATION; UNFOLDED P53; CELL-DEATH; BETA; MECHANISMS; PROMOTES; KINASE;
D O I
10.3389/fnagi.2022.835288
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Our understanding of Alzheimer's disease (AD) pathogenesis has developed with several hypotheses over the last 40 years, including the Amyloid and Tau hypotheses. More recently, the p53 protein, well-known as a genome guardian, has gained attention for its potential role in the early evolution of AD. This is due to the central involvement of p53's in the control of oxidative stress and potential involvement in the Amyloid and Tau pathways. p53 is commonly regulated by post-translational modifications (PTMs), which affect its conformation, increasing its capacity to adopt multiple structural and functional states, including those that can affect brain processes, thus contributing to AD development. The following review will explore the impact of p53 PTMs on its function and consequential involvement in AD pathogenesis. The greater understanding of the role of p53 in the pathogenesis of AD could result in more targeted therapies benefiting the many patients of this debilitating disease.
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页数:11
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