Ausgewählte Publikationen der letzten 5 Jahre

Barrionuevo, F., Naumann, A., Bagheri-Fam, S., Taketo, M.M., Scherer, G., and Neubüser, A.: Sox9 is required for invagination and survival of the otic placode in mice. Dev. Biol. (in press).

Hargus, G., Kist, R., Kramer, J., Gerstel, D., Neitz, A., Scherer, G., and Rohwedel, J.: Loss of Sox9 function results in defective chondrocyte differentiation of mouse embryonic stem cells in vitro. Int. J. Dev. Biol. (in press).

Bagheri-Fam, S., Sim, H., Bernard, P., Jayakody, I., Taketo, M.M., Scherer, G., and Harley, V.R.: Loss of Fgfr2 leads to partial XY sex reversal. Dev. Biol. 314, 71-83 (2008).

Seymour, P.A., Freude, K.K., Tran, M.N., Mayes, E.E., Jensen, J., Kist, R., Scherer, G., and Sander, M.: SOX9 is required for maintenance of the pancreatic progenitor cell pool. Proc. Natl. Acad. Sci. USA 104, 1865-1870 (2007).

Bastide, P., Darido, C., Pannequin, J., Kist, R., Robine, S., Marty-Double, C., Bibeau, F., Scherer, G., Joubert, D., Hollande, F., Blache, P., and Jay, P.: Sox9 regulates cell proliferation and is required for Paneth cell differentiation in the intestinal epithelium. J. Cell Biol. 178, 635-648 (2007).

Temel, S.G., Gulten, T., Yakut, T., Saglam, H., Kilic, N., Bausch, E., Jin, W.J., Leipoldt, M., and Scherer, G.: Extended pedigree with multiple cases of XX sex reversal in the absence of SRY and of a mutation at the SOX9 locus. Sex. Dev. 1, 24-34 (2007).

Leipoldt, M., Erdel, M., Bien-Willner, G.A., Smyk, M., Theurl, M., Yatsenko, S., Lupski, J.R., Lane, A.H., Shanske, A.L., Stankiewicz, P., and Scherer, G.: Two novel translocation breakpoints upstream of SOX9 define borders of the proximal and distal breakpoint cluster region in campomelic dysplasia. Clin. Genet. 71, 67-75 (2007).

Barrionuevo, F., Bagheri-Fam, S., Klattig, J., Kist, R., Taketo, M.M., Englert, C., and Scherer, G.: Homozygous inactivation of Sox9 causes complete XY sex reversal in mice. Biol. Reprod. 74, 195-201 (2006).

Barrionuevo, F., Taketo, M.M., Scherer, G., and Kispert, A.: Sox9 is required for notochord maintenance in mice. Dev. Biol. 295, 128-140 (2006).

Bagheri-Fam, S., Barrionuevo, F., Dohrmann, U., Günther, T., Schüle, R., Kemler, R., Mallo, M., Kanzler, B., and Scherer, G.: Long range upstream and downstream enhancers control distinct subsets of the complex spatiotemporal Sox9 expression pattern. Dev. Biol. 291, 382-397 (2006).

Pop, R., Zaragoza, M.V., Gaudette M., Dohrmann, U., and Scherer, G.: A homozygous nonsense mutation in SOX9 in the dominant disorder campomelic dysplasia: a case of mitotic gene conversion. Hum. Genet. 117, 43-53 (2005).

Pop, R., Conz, C., Lindenberg, K.S., Blesson, S., Schmalenberger, B., Briault, S., Pfeifer, D., and Scherer, G.: Screening of the 1 Mb SOX9 5’ control region by array CGH identifies a large deletion in a case of campomelic dysplasia with XY sex reversal. J. Med. Genet. 41, e47 (2004).

Sock, E., Pagon, R.A., Keymolen, K., Lissens, W., Wegner, M., and Scherer, G.: Loss of DNA-dependent dimerization of the transcription factor SOX9 as a cause for campomelic dysplasia. Hum. Mol. Genet. 12, 1439-1447 (2003).