Laboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, pr. Stachki 194/1, 344090 Rostov-on-Don, Russia.
Neuroscience Center HiLife, University of Helsinki, Haartmaninkatu 8, P.O. Box 63, 00014 Helsinki, Finland.
Int J Mol Sci. 2021 Jul 26;22(15):7947. doi: 10.3390/ijms22157947.
Histone deacetylase (HDAC) and histone acetyltransferase (HAT) regulate transcription and the most important functions of cells by acetylating/deacetylating histones and non-histone proteins. These proteins are involved in cell survival and death, replication, DNA repair, the cell cycle, and cell responses to stress and aging. HDAC/HAT balance in cells affects gene expression and cell signaling. There are very few studies on the effects of stroke on non-histone protein acetylation/deacetylation in brain cells. HDAC inhibitors have been shown to be effective in protecting the brain from ischemic damage. However, the role of different HDAC isoforms in the survival and death of brain cells after stroke is still controversial. HAT/HDAC activity depends on the acetylation site and the acetylation/deacetylation of the main proteins (c-Myc, E2F1, p53, ERK1/2, Akt) considered in this review, that are involved in the regulation of cell fate decisions. Our review aims to analyze the possible role of the acetylation/deacetylation of transcription factors and signaling proteins involved in the regulation of survival and death in cerebral ischemia.
组蛋白去乙酰化酶 (HDAC) 和组蛋白乙酰转移酶 (HAT) 通过乙酰化/去乙酰化组蛋白和非组蛋白蛋白来调节转录和细胞的最重要功能。这些蛋白质参与细胞存活和死亡、复制、DNA 修复、细胞周期以及细胞对应激和衰老的反应。细胞中的 HDAC/HAT 平衡会影响基因表达和细胞信号转导。关于卒中对脑细胞中非组蛋白蛋白乙酰化/去乙酰化的影响,研究甚少。HDAC 抑制剂已被证明可有效保护大脑免受缺血性损伤。然而,不同 HDAC 同工酶在卒中后脑细胞存活和死亡中的作用仍存在争议。HAT/HDAC 的活性取决于乙酰化位点和本文综述中考虑的主要蛋白质(c-Myc、E2F1、p53、ERK1/2、Akt)的乙酰化/去乙酰化,这些蛋白质参与细胞命运决定的调控。我们的综述旨在分析参与脑缺血中存活和死亡调控的转录因子和信号蛋白的乙酰化/去乙酰化的可能作用。