Journal
MOLECULAR PSYCHIATRY
Volume 16, Issue 10, Pages 1006-1023Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2010.87
Keywords
DISC1; schizophrenia; synapse; TNIK
Funding
- MRC [G0600765] Funding Source: UKRI
- Medical Research Council [G0600765] Funding Source: researchfish
- Medical Research Council [G0600765] Funding Source: Medline
- NINDS NIH HHS [R01 NS035527-08A1, R01 NS035527-10, R01 NS035527-09, R01 NS035527, R01 NS035527-11, R01 NS035527-12] Funding Source: Medline
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Disrupted in schizophrenia 1 (DISC1), a genetic risk factor for multiple serious psychiatric diseases including schizophrenia, bipolar disorder and autism, is a key regulator of multiple neuronal functions linked to both normal development and disease processes. As these diseases are thought to share a common deficit in synaptic function and architecture, we have analyzed the role of DISC1 using an approach that focuses on understanding the protein-protein interactions of DISC1 specifically at synapses. We identify the Traf2 and Nck-interacting kinase (TNIK), an emerging risk factor itself for disease, as a key synaptic partner for DISC1, and provide evidence that the DISC1-TNIK interaction regulates synaptic composition and activity by stabilizing the levels of key postsynaptic density proteins. Understanding the novel DISC1-TNIK interaction is likely to provide insights into the etiology and underlying synaptic deficits found in major psychiatric diseases. Molecular Psychiatry (2011) 16, 1006-1023; doi: 10.1038/mp.2010.87; published online 14 September 2010
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