G2C::Press Releases

TNiK and cognitive function

In a paper published in Journal of Neuroscience, led by University of Edinburgh with collaborators at Cambridge University and University of California Los Angeles, we report the first in vivo evidence for the role of TNiK, Traf2 and NcK interacting Kinase in synaptic plasticity, neuronal development and specific aspects of higher order cognitive processing. By engineering a specific knockout mutation of TNiK in mice, we found that loss of TNiK leads to dysregulation of key synaptic and nuclear signalling mechanisms. We identified complexes of proteins associated with TNiK in the postsynaptic density and the nucleus and show that the TNiK mutation impacts regulation of GSK3Β and phosphorylation of proteins within the complexes. Our data shows that TNiK is a multifunctional protein that plays a role in multiple cognitive functions through both synaptic and nuclear signalling pathways. These findings provide insight into the mechanisms of psychiatric diseases since TNiK and its interacting proteins have been implicated in schizophrenia, autism and intellectual disability.


TNiK paper and resources

© G2C 2014. The Genes to Cognition Programme received funding from The Wellcome Trust and the EU FP7 Framework Programmes:
EUROSPIN (FP7-HEALTH-241498), SynSys (FP7-HEALTH-242167) and GENCODYS (FP7-HEALTH-241995).

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