Regulatory mechanism for spine morphogenesis by a small G-protein Rheb

点击翻译按钮获取中文摘要

An activity-regulated small G-protein Rheb is activated in tuberous sclerosis, which is accompanied with dendritic spine dysmorphogenesis. We have investigated the underlying mechanism and have clarified that mitochondria is increased in dendrites of tuberous sclerosis neurons and that impaired spinogenesis in tuberous sclerosis is caused by an increase in RBP levels, not due to mTORC1 activation. These findings may lead to development of a new treatment for tuberous sclerosis associated with epilepsy, mental retardation or autism.