@article{oai:repo.qst.go.jp:00046878,
 author = {Takao, Keizo and Kobayashi, Katsunori and Hagihara, Hideo and Ohira, Koji and Shoji, Hirotaka and Hattori, Satoko and Koshimizu, Hisatsugu and Umemori, Juzoh and Toyama, Keiko and K, Nakamura Hironori and Kuroiwa, Mahomi and Maeda, Jun and Atsuzawa, Kimie and Esaki, Kayoko and Yamaguchi, Shun and Furuya, Shigeki and Takagi, Tsuyoshi and M, Walton Noah and Hayashi, Nobuhiro and Suzuki, Hidenori and Higuchi, Makoto and Usuda, Nobuteru and Suhara, Tetsuya and Nishi, Akinori and Matsumoto, Mitsuyuki and Ishii, Shunsuke and Miyakawa, Tsuyoshi and 前田 純 and 樋口 真人 and 須原 哲也},
 issue = {8},
 journal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
 month = {Feb},
 note = {Schnurri-2 (Shn-2), an nuclear factor-κB site-binding protein, tightly binds to the enhancers of major histocompatibility complex class I genes and inflammatory cytokines, which have been shown to harbor common variant single-nucleotide polymorphisms associated with schizophrenia. Although genes related to immunity are implicated in schizophrenia, there has been no study showing that their mutation or knockout (KO) results in schizophrenia. Here, we show that Shn-2 KO mice have behavioral abnormalities that resemble those of schizophrenics. The mutant brain demonstrated multiple schizophrenia-related phenotypes, including transcriptome/proteome changes similar to those of postmortem schizophrenia patients, decreased parvalbumin and GAD67 levels, increased theta power on electroencephalograms, and a thinner cortex. Dentate gyrus granule cells failed to mature in mutants, a previously proposed endophenotype of schizophrenia. Shn-2 KO mice also exhibited mild chronic inflammation of the brain, as evidenced by increased inflammation markers (including GFAP and NADH/NADPH oxidase p22 phox), and genome-wide gene expression patterns similar to various inflammatory conditions. Chronic administration of anti-inflammatory drugs reduced hippocampal GFAP expression, and reversed deficits in working memory and nest-building behaviors in Shn-2 KO mice. These results suggest that genetically induced changes in immune system can be a predisposing factor in schizophrenia.},
 pages = {1409--1425},
 title = {Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.},
 volume = {38},
 year = {2013}
}