DEPDC5 regulates the strength of excitatory synaptic transmission by interacting with ubiquitin-specific protease 46

Cerullo MS
Center for Synaptic Neuroscience and Technology, Genova
June 2, 2025
Neurobiol Dis
https://pubmed.ncbi.nlm.nih.gov/40467011/

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/40467011/

Research summary

This study identifies DEPDC5 as a key regulator of excitatory synaptic strength via its interaction with USP46. Using a mouse model, the authors demonstrate that DEPDC5 loss leads to increased AMPA receptor activity and excitatory synaptic transmission.

Key outcome of the study

Loss of Depdc5 enhances excitatory synaptic transmission through dysregulated AMPA receptor expression, implicating its role in epilepsy and neurodevelopmental disorders.

Model

Depdc5 conditional Knockout mouse model (using Cre-loxP system for neuron-specific deletion, such as CamKIIa-Cre or Nestin-Cre)

TARGET:
Depdc5
DEP domain containing 5

Keywords

Epilepsy, Synaptic plasticity, Neurodevelopment, mTOR pathway

Technical specifications

Conditional Knockout, Cre-loxP, Brain-specific deletion, Synaptic regulation

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Tissue-specific KO mouse

Use tissue- or cell-specific conditional Knockout mouse models to bypass embryonic lethality, compensatory mechanisms, complex phenotypes, etc.