Affiliations
- Laboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, 194/1 Stachki ave., Rostov-on-Don, 344090, Russia.
- Department of General and Clinical Biochemistry no.2, Rostov State Medical University, Nakhichevansky lane, Rostov-on-Don, 344022, Russia.
- State Key Laboratory of Functions and Applications of Medicinal Plants, Engineering Research Center for the Development and Application of Ethnic Medicine and TCM (Ministry of Education), Guizhou Provincial Key Laboratory of Pharmaceutics, School of Pharmacy, Guizhou Medical University, Guiyang, 550004, China.
PMID: 37580538 DOI: 10.1007/s12975-023-01183-z
Abstract
Background: The role of histone acetylation and deacetylation in non-histone proteins like p53 during post-stroke recovery is not well understood. This study identified key enzymes affecting p53's acetylation and activity in ischemic penumbra neurons.
Results: Acetylation of p53 at lysine 320, regulated by PCAF, HDAC1, and HDAC6, promotes neuronal survival. p53 acetylation at this site favors its cytoplasmic distribution, suggesting potential therapeutic strategies targeting PCAF and HDACs for stroke recovery.
Conclusion: Modulating p53 acetylation through acetyltransferases and deacetylases may provide neuroprotective benefits in post-stroke therapy.
Keywords
Acetylated p53; Apoptosis; Histone acetyltransferase; Histone deacetylase; Stroke recovery; p53.
