[1] Rosenfeld JA, Ballif BC, Lucas A, Spence EJ, Powell C, Aylsworth AS, Torchia BA, Shaffer LG. Small deletions of SATB2 cause some of the clinical features of the 2q33.1 microdeletion syndrome. PLoS One, 2009, 4(8): e6568.[2] Brugmann SA, Powder KE, Young NM, Goodnough LH, Hahn SM, James AW, Helms JA, Lovett M. Comparative gene expression analysis of avian embryonic facial structures reveals new candidates for human craniofacial disorders. Hum Mol Genet, 2010, 19(5): 920-930.[3] Depew MJ, Compagnucci C. Tweaking the hinge and caps: testing a model of the organization of jaw. J Exp Zool B Mol Dev Evol, 2008, 310B(4): 315-335.[4] Ahn HJ, Park Y, Kim S, Park HC, Seo SK, Yeo SY, Geum D. The expression profile and function of Satb2 in zebrafish embryonic development. Mol Cells, 2010, 30(4): 377-382[5] Dobreva G, Dambacher J, Grosschedl R. SUMO modification of a novel MAR-binding protein, SATB2, modulates immunoglobulin μ gene expression. Genes Dev, 2003, 17(24): 3048-3061.[6] Hassan MQ, Gordon JAR, Beloti MM, Croce CM, van Wijnen AJ, Stein JL, Stein GS, Lian JB. A network connecting Runx2, SATB2, and the miR-23a~27a~24-2 cluster regulates the osteoblast differentiation program. Proc Natl Acad Sci USA, 2010, 107(46): 19879-19884.[7] Dobreva G, Chahrour M, Dautzenberg M, Chirivella L, Kanzler B, Fariñas I, Karsenty G, Grosschedl R. SATB2 is a multifunctional determinant of craniofacial patterning and osteoblast differentiation. Cell, 2006, 125(5): 971-986.[8] Mao XY, Tang SJ. Effects of phenytoin on Satb2 and Hoxa2 gene expressions in mouse embryonic craniofacial tissue. Biochem Cell Biol, 2010, 88(4): 731-735.[9] Ellies DL, Krumlauf R. Bone formation: The nuclear matrix reloaded. Cell, 2006, 125(5): 840-842.[10] Yu VWC, Akhouayri O, St-Arnaud R. FIAT is co-expressed with its dimerization target ATF4 in early osteoblasts, but not in osteocytes. Gene Expr Patterns, 2009, 9(5): 335-340.[11] Britanova O, Depew MJ, Schwark M, Thomas BL, Miletich I, Sharpe P, Tarabykin V. Satb2 haploinsufficiency phenocopies 2q32-q33 deletions, whereas loss suggests a fundamental role in the coordination of jaw development. Am J Hum Genet, 2006, 79(4): 668-678.[12] Fitzpatrick DR, Carr IM, McLaren L, Leek JP, Wightman P, Williamson K, Gautier P, McGill N, Hayward C, Firth H, Markham AF, Fantes JA, Bonthron DT. Identification of SATB2 as the cleft palate gene on 2q32-q33. Hum Mol Genet, 2003, 12(19): 2491-2501.[13] Vieira AR, Avila JR, Daack-Hirsch S, Dragan E, Félix TM, Rahimov F, Harrington J, Schultz RR, Watanabe Y, Johnson M, Fang J, O'Brien SE, Orioli IM, Castilla EE, FitzPatrick DR, Jiang RL, Marazita ML, Murray JC. Medical sequencing of candidate genes for nonsyndromic cleft lip and palate. PLoS Genet, 2005, 1(6): e64.[14] van Buggenhout G, van Ravenswaaij-Arts C, Mc Maas N, Thoelen R, Vogels A, Smeets D, Salden I, Matthijs G, Fryns JP, Vermeesch JR. The del(2)(q32.2q33) deletion syndrome de?ned by clinical and molecular characterization of four pa-tients. Eur J Med Genet, 2005, 48(3): 276-289.[15] Carter TC, Molloy AM, Pangilinan F, Troendle JF, Kirke PN, Conley MR, Orr DJA, Earley M, McKiernan E, Lynn EC, Doyle A, Scott JM, Brody LC, Mills JL. Testing reported associations of genetic risk factors for oral clefts in a large Irish study population. Birth Defects Res A Clin Mol Teratol, 2010, 88(2): 84-93.[16] Urquhart J, Black GCM, Clayton-Smith J. 4.5 Mb microdeletion in chromosome band 2q33.1 associated with learning disability and cleft palate. Eur J Med Genet, 2009, 52(6): 454-457.[17] Beaty TH, Hetmanski JB, Fallin MD, Park JW, Sull JW, McIntosh I, Liang KY, VanderKolk CA, Redett RJ, Boyadjiev SA, Jabs EW, Chong SS, Cheah FSH, Wu-Chou YH, Chen PK, Chiu YF, Yeow |