Our laboratory focuses on understanding the molecular mechanisms which underlie the synaptic plasticity, activity dependent formation of neuronal circuitry, and learning and memory. We generate knockout mice and inducible knockout mice of signal transduction molecules including the glutamate receptors and Rho family GTPases. We have recently applied proteomics analysis to these mice. We also try to generate murine models for human genetic diseases.
- Saito et al. Comprehensive analysis of a novel mouse model of the 22q11.2 deletion syndrome: a model with the most common 3.0-Mb deletion at the human 22q11.2 locus. Transl Psychiatry, 10, 35, 2020.
- Nakao et al. mGluR1 in cerebellar Purkinje cells is essential for the formation but not expression of associative eyeblink memory. Sci Rep, 9, 7353, 2019.
- Sakai et al. Hyperactivation of mTORC1 disrupts cellular homeostasis in cerebellar Purkinje cells. Sci Rep, 9, 2799, 2019.
- Nakao et al. A possible aid in targeted insertion of large DNA elements by CRISPR/ Cas in mouse zygotes. Genesis, 54, 65-77, 2016.
- Uesaka et al. Retrograde Semaphorin Signaling Regulates Synapse Elimination in the Developing Mouse Brain. Science, 344, 1020-1023, 2014.
- Kassai et al. Selective Activation of mTORC1 Signaling Recapitulates Microcephaly, Tuberous Sclerosis, and Neurodegenerative Diseases. Cell Rep, 7, 1626-1639, 2014.