熱烈慶祝華中科技大學同濟醫學院基礎醫學院魯老師課題組裴磊老師 使用武漢百意欣生物FITC標記多肽 新文章發表

再接再厲，再創佳績

Abstract

Synaptic spine loss is one of the major preceding consequences of stroke damages, but its underlying molecular mechanisms

remain unknown. Here, we report that a direct interaction of DAPK1 with Tau causes spine loss and subsequently neuronal

death in a mouse model with stroke.We found that DAPK1 phosphorylates Tau protein at Ser262 (pS262) in cortical neurons of

stroke mice. Either genetic deletion of DAPK1 kinase domain (KD) in mice (DAPK1-KD?/?) or blocking DAPK1-Tau interaction by

systematic application of a membrane permeable peptide protects spine damages and improves neurological functions against

stroke insults. Thus, disruption of DAPK1-Tau interaction is a promising strategy in clinical management of stroke.