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Division Chief
  • 02-2789-9174 (Lab) (Room No: N703)
  • 02-2652-3523 (Office)

  • Translational Control/ RNA 轉譯調控
  • Cap modification/ RNA-cap 修飾調控
  • Molecular & Cellular Neuroscience/ 分子與細胞神經生物學

Education and Positions:
  • Ph.D. University of Texas Southwestern Medical Center at Dallas

Highlight Detail

Calpain 2 activated through the NMDA receptor signaling cleaves CPEB3 and abrogates CPEB3-repressed translation in neurons.

Dr. Huang, Yi-Shuian
MCB, Jun 18, 2012

Long-term memory requires the activity-dependent reorganization of synaptic proteome to modulate synaptic efficacy and consequently consolidate memory. Activity-regulated RNA translation can change the protein composition at the stimulated synapse. CPEB3 is a sequence-specific RNA-binding protein that represses translation of its target mRNAs in neurons, while activation of NMDA receptors alleviates this repression. Although recent research has revealed the mechanism of CPEB3-inhibited translation, how NMDA receptor signaling modulates the translational activity of CPEB3 remains unclear.