Lost in Translation: Cul3-Dependent Pathological Mechanisms in Psychiatric Disorders

In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic tra...

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Bibliographic Details
Published in:Neuron (Cambridge, Mass.) Mass.), 2020-02, Vol.105 (3), p.398-399
Main Authors: Chen, Huei-Ying, Maher, Brady J.
Format: Article
Language:English
Subjects:
Anxiety
Autism
Behavior
Cullin Proteins
Excitability
Genes
Glutamatergic transmission
Humans
Mental Disorders
Morphology
Mutation
Neurons
Physiology
Protein biosynthesis
Proteins
Translation
Ubiquitin
Ubiquitin-protein ligase
Ubiquitin-Protein Ligases
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Summary:In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety. In this issue of Neuron, Dong et al. (2020) finds that deficiency of the psychiatric risk gene Cul3, which encodes an E3 ubiquitin ligase, leads to an upregulation of Cap-dependent protein translation. The resulting imbalance in protein synthesis and degradation is found to disrupt glutamatergic transmission and excitability in networks that underlie sociability and anxiety.
ISSN:0896-6273
1097-4199
DOI:10.1016/j.neuron.2020.01.010