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.
Loss of Depdc5 enhances excitatory synaptic transmission through dysregulated AMPA receptor expression, implicating its role in epilepsy and neurodevelopmental disorders.
Depdc5 conditional Knockout mouse model (using Cre-loxP system for neuron-specific deletion, such as CamKIIa-Cre or Nestin-Cre)
Epilepsy, Synaptic plasticity, Neurodevelopment, mTOR pathway
Conditional Knockout, Cre-loxP, Brain-specific deletion, Synaptic regulation
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
