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p38丝裂原活化蛋白激酶参与食物厌恶学习表观遗传机制的调控。

p38 МАРK is Involved in Regulation of Epigenetic Mechanisms of Food Aversion Learning.

作者信息

Grinkevich L N

机构信息

I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.

出版信息

Bull Exp Biol Med. 2017 Aug;163(4):412-414. doi: 10.1007/s10517-017-3816-9. Epub 2017 Aug 29.

Abstract

Consolidation of the conditioned food aversion response in Helix lucorum was associated with induction of histone H3 acetylation and methylation. We hypothesized that not only activatory, but also inhibitory p38 MARK-mediated pathways are involved in these processes. To assess the contribution of p38 MAPK to epigenetic processes, we studied the effect p38 MAPK inhibitor SB203580 on acetylation of histone H3 during training of Helix lucorum. Administration of SB203580 decreased learning-induced enhancement of histone H3 acetylation in the CNS of Helix lucorum, which was accompanied by long-term memory impairment. Thus, p38 MAPK is involved in the regulation of epigenetic mechanisms of long-term memory.

摘要

福寿螺中条件性食物厌恶反应的巩固与组蛋白H3乙酰化和甲基化的诱导有关。我们推测,不仅激活型,而且抑制型p38丝裂原活化蛋白激酶(MARK)介导的信号通路都参与了这些过程。为了评估p38丝裂原活化蛋白激酶(MAPK)对表观遗传过程的作用,我们研究了p38丝裂原活化蛋白激酶抑制剂SB203580在福寿螺训练过程中对组蛋白H3乙酰化的影响。给予SB203580可降低福寿螺中枢神经系统中学习诱导的组蛋白H3乙酰化增强,这伴随着长期记忆损伤。因此,p38丝裂原活化蛋白激酶参与了长期记忆表观遗传机制的调控。

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