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BCPs have a particular domain, the bromodomain (Brd), which was originally identified as specifically binding acetyl-lysine residues at the N-terminus of histone proteins<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>. Other domains of BCPs are responsible for binding partner proteins to form regulatory complexes. Once these complexes are assembled, BCPs alter chromosomal states and regulate gene expression. Some BCP complexes bind nucleosomes, are involved in basal transcription regulation, and influence the transcription of many genes. However, most BCPs are involved in targeting. For example, some BCPs function as a recruitment platform or scaffold through their Brds-binding targeting sites. Others are recruited to form a complex to bind the targeting sites of their partners. The regulation mediated by these proteins is especially critical during normal and abnormal development. Mutant BCPs or dysfunctional BCP-containing complexes are implicated in the initiation and development of neurodevelopmental disorders. However, the pathogenic molecular mechanisms are not fully understood. In this review, we focus on the roles of regulatory BCPs associated with neurodevelopmental disorders, including mental retardation, Fragile X syndrome (FRX), Williams syndrome (WS), Rett syndrome and Rubinstein-Taybi syndrome (RTS). A better understanding of the molecular pathogenesis, based upon the roles of BCPs, will lead to screening of targets for the treatment of neurodevelopmental disorders.<\/jats:p>","DOI":"10.1186\/1866-1955-5-4","type":"journal-article","created":{"date-parts":[[2013,2,20]],"date-time":"2013-02-20T22:38:16Z","timestamp":1361399896000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Development of neurodevelopmental disorders: a regulatory mechanism involving bromodomain-containing proteins"],"prefix":"10.1186","volume":"5","author":[{"given":"Junlin","family":"Li","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guifang","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaocai","family":"Gao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2013,2,20]]},"reference":[{"key":"29_CR1","doi-asserted-by":"publisher","first-page":"150","DOI":"10.1007\/s11689-009-9018-7","volume":"1","author":"AJ Silva","year":"2009","unstructured":"Silva AJ, Ehninger D: Adult reversal of cognitive phenotypes in neurodevelopmental disorders. 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