热烈庆祝华中科技大学同济医学院基础医学院鲁老师课题组裴磊老师 使用武汉百意欣生物FITC标记多肽 新文章发表

再接再厉，再创佳绩

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.