Histone acetylation at H4K16 as one of the outcomes of ischemia in in vitro model

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Dr. R. Dmitriev and Prof. D. Papkovsky are the authors of the new research article (communication) published in FEBS Letters journal (Dec. 2014).

The paper entitled "In vitro ischemia decreases histone H4K16 acetylation in neural cells" reveals that oxygen and glucose deprivation of cultured cells (commonly used model of brain and heart ischemia) leads to transient decrease of acetylation status of histone H4 at residue K16 (H4K16). This epigenetic mark is involved in variety of cellular processes such as general chromatin decompaction or cell cycle arrest, if impaired, and is essential for survival of animal cell. This observation is expected to facilitate future progress in the area of stroke and help to develop better therapies.

The full-text can be found here.

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