The fragile X mutation impairs homeostatic plasticity in human neurons by blocking synaptic retinoic acid signaling
Zhenjie Zhang(Stanford Medicine), Samuele Marro(California Institute for Regenerative Medicine), Yingsha Zhang(Stanford University), Kristin L. Arendt(Stanford Medicine), Christopher Patzke(Stanford University), Bo Zhou(Stanford University), Tyler Fair(California Institute for Regenerative Medicine), Nan Yang(California Institute for Regenerative Medicine), Thomas C. Südhof(Howard Hughes Medical Institute), Marius Wernig(California Institute for Regenerative Medicine), Lu Chen(Stanford Medicine)
Cited by 121
Abstract
mutations that might contribute to neuronal dysfunction in FXS. In addition, our results suggest that FXS patient iPS cell-derived neurons might be useful for studying the mechanisms mediating functional abnormalities in FXS.
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