Genetic and Acute CPEB Depletion Ameliorate Fragile X Pathophysiology

@inproceedings{Udagawa2013GeneticAA,
  title={Genetic and Acute CPEB Depletion Ameliorate Fragile X Pathophysiology},
  author={Tsuyoshi Udagawa and Natalie G. Farny and Mira Jakovcevski and Hanoch Kaphzan and Juan Marcos Alarc{\'o}n and Shobha Rani Anilkumar and Maria P. Ivshina and Jessica A. Hurt and Kentaro Nagaoka and Vijayalaxmi C. Nalavadi and Lori J. Lorenz and Gary Jonathan Bassell and Schahram Akbarian and Sumantra Chattarji and Eric Klann and Joel D. Richter},
  booktitle={Nature Medicine},
  year={2013}
}
Fragile X syndrome (FXS), the most common cause of inherited mental retardation and autism, is caused by transcriptional silencing of FMR1, which encodes the translational repressor fragile X mental retardation protein (FMRP). FMRP and cytoplasmic polyadenylation element–binding protein (CPEB), an activator of translation, are present in neuronal dendrites, are predicted to bind many of the same mRNAs and may mediate a translational homeostasis that, when imbalanced, results in FXS. Consistent… CONTINUE READING
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