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 language | English |
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Pages (from-to) | 3620-3635.e7 |
Journal | Cell Reports |
Volume | 29 |
Issue number | 11 |
DOIs | |
Publication status | Published - 10 Dec 2019 |
Keywords
- 4E-BP2
- CUL4B
- NF-κB
- Raptor
- asparagine deamidation
- mTORC1
- postnatal brain
- proteasome
- translational control