报告题目：Molecular Mechanism of Glutamate Receptor Trafficking

报告人：Victor Anggono，Queensland Brain Institute , The University of Queensland,Australia
    

主持人：孙坚原研究员
   

时间： 2017年10月24日 下午2:00
   

地点：9408会议室
   

摘要：
The ability of neurons to modulate the strength of their connections, termed synaptic plasticity, is determined in part by the number of these receptors at synapses. Dysregulation of AMPA receptor trafficking results in an imbalance in neuronal excitation and inhibition, which often results in the memory impairment and cognitive deficits associated with various neurological disorders, such as Alzheimer’s disease, schizophrenia, bipolar disorders and autism. The major aim of the our group is to understand the detailed molecular mechanisms regulating AMPA receptor trafficking, synaptic plasticity, learning and memory.
In 2015, we discovered that all four AMPA receptor subunits (GluA1-4) undergo post-translational ubiquitination in an activity-dependent manner. They mapped the sites of ubiquitination to specific lysine residues in the carboxyl-terminal tails of GluA1 and GluA2 subunits. Mutation of these lysine residues inhibits AMPA receptor ubiquitination, subsequently leading to mis-sorting of AMPA receptors from late- to recycling-endosomes. As a consequence, these mutant AMPA receptors escape the degradation pathway and are more stable in neurons.