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It is therefore possible that TBR1 controls the expression of other autism risk factors. The downstream genes of TBR1 have been identified using microarray and promoter analyses. In this study, we annotated individual genes downstream of TBR1 and investigated any associations with ASDs through extensive literature searches. Of 124 TBR1 target genes, 23 were reported to be associated with ASDs. In addition, one gene, <jats:italic>Kiaa0319<\/jats:italic>, is a known causative gene for dyslexia, a disorder frequently associated with autism. A change in expression level in 10 of these 24 genes has been previously confirmed. We further validated the alteration of RNA expression levels of <jats:italic>Kiaa0319, Baiap2<\/jats:italic>, and <jats:italic>Gad1<\/jats:italic> in <jats:italic>Tbr1<\/jats:italic> deficient mice. Among these 24 genes, four transcription factors <jats:italic>Auts2, Nfia, Nr4a2<\/jats:italic>, and <jats:italic>Sox5<\/jats:italic> were found, suggesting that TBR1 controls a transcriptional cascade relevant to autism pathogenesis. A further five of the 24 genes (<jats:italic>Cd44, Cdh8, Cntn6, Gpc6<\/jats:italic>, and <jats:italic>Ntng1<\/jats:italic>) encode membrane proteins that regulate cell adhesion and axonal outgrowth. These genes likely contribute to the role of TBR1 in regulation of neuronal migration and axonal extension. Besides, decreases in <jats:italic>Grin2b<\/jats:italic> expression and increases in <jats:italic>Gad1<\/jats:italic> expression imply that neuronal activity may be aberrant in <jats:italic>Tbr1<\/jats:italic> deficient mice. These analyses provide direction for future experiments to reveal the pathogenic mechanism of autism. <jats:bold><jats:italic>Autism Res<\/jats:italic><\/jats:bold> <jats:italic>2015, 8: 412\u2013426<\/jats:italic>. \u00a9 2015 International Society for Autism Research, Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/aur.1456","type":"journal-article","created":{"date-parts":[[2015,1,20]],"date-time":"2015-01-20T11:27:11Z","timestamp":1421753231000},"page":"412-426","source":"Crossref","is-referenced-by-count":54,"title":["T\u2010Brain\u20101 \u2013 A Potential Master Regulator in Autism Spectrum Disorders"],"prefix":"10.1002","volume":"8","author":[{"given":"Hsiu\u2010Chun","family":"Chuang","sequence":"first","affiliation":[{"name":"Graduate Institute of Life Sciences, National Defense Medical Center"},{"name":"Institute of Molecular Biology, Academia Sinica Taipei 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