Raptor-Mediated Proteasomal Degradation of Deamidated 4E-BP2 Regulates Postnatal Neuronal Translation and NF-κB Activity

Stella Kouloulia, Erik I. Hallin, Konstanze Simbriger, Inês S. Amorim, Gilliard Lach, Theoklitos Amvrosiadis, Kleanthi Chalkiadaki, Agniete Kampaite, Vinh Tai Truong, Mehdi Hooshmandi, Seyed Mehdi Jafarnejad, Paul Skehel, Petri Kursula, Arkady Khoutorsky, Christos G. Gkogkas

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Abstract

Kouloulia et al. demonstrate that, during early postnatal brain development, deamidation of the translation initiation factor 4E-BP2 renders it susceptible to ubiquitination and proteasomal degradation via enhanced binding to the Raptor-CUL4B complex. mTORC1 or glutamate receptor inhibition stabilizes deamidated 4E-BP2. Moreover, deamidated 4E-BP2 regulates the translation of specific mRNAs and NF-κB activity.
Original languageEnglish
Pages (from-to)3620-3635.e7
JournalCell Reports
Volume29
Issue number11
DOIs
Publication statusPublished - 10 Dec 2019

Keywords

  • 4E-BP2
  • CUL4B
  • NF-κB
  • Raptor
  • asparagine deamidation
  • mTORC1
  • postnatal brain
  • proteasome
  • translational control

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