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WANG, Q; CHARYCH, E. L; TAYLOR, N; XIE, Y; PAUSCH, M; HAYASHI-TAKAG I, A; ISHIZUKA, K; SESHADRI, S; BATES, B; KARIYA, K; SAWA, A; WEINBERG, R. J; PULITO, V. L; MOSS, S. J; HOUSLAY, M. D; YAN, Z; BRANDON, N. J; LEE, J. B; GRAZIANE, N. M; CROZIER, R. A; REVILLA-SANCHEZ, R; KELLY, M. P; DUNLOP, A. J; MURDOCH, H
Molecular psychiatry, 10/2011, Letnik: 16, Številka: 10Journal Article
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.
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