Expression of the SOX10 gene during human development

[1]  M. Wegner,et al.  Mutation of the Sry-related Sox10 gene in Dominant megacolon, a mouse model for human Hirschsprung disease. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[2]  Giovanni Romeo,et al.  SOX10 mutations in patients with Waardenburg-Hirschsprung disease , 1998, Nature Genetics.

[3]  P. Corvol,et al.  Ontogeny of endothelins-1 and -3, their receptors, and endothelin converting enzyme-1 in the early human embryo. , 1998, The Journal of clinical investigation.

[4]  M. Wegner,et al.  Sox10, a Novel Transcriptional Modulator in Glial Cells , 1998, The Journal of Neuroscience.

[5]  L. Leatherbury,et al.  Role of cardiac neural crest cells in cardiovascular development. , 1998, Annual review of physiology.

[6]  W. Pavan,et al.  SOX10 mutation disrupts neural crest development in Dom Hirschsprung mouse model , 1998, Nature Genetics.

[7]  S. Taviaux,et al.  SOX22 is a new member of the SOX gene family, mainly expressed in human nervous tissue. , 1997, Human molecular genetics.

[8]  J. Osinga,et al.  Mutations in Hirschsprung Disease: When Does a Mutation Contribute to the Phenotype , 1997, European journal of human genetics : EJHG.

[9]  R. Lovell-Badge,et al.  Sox genes find their feet. , 1997, Current opinion in genetics & development.

[10]  Y. Kanai,et al.  Identification of two Sox17 messenger RNA isoforms, with and without the high mobility group box region, and their differential expression in mouse spermatogenesis , 1996, The Journal of cell biology.

[11]  A. Chakravarti.  Endothelin receptor-mediated signaling in hirschsprung disease. , 1996, Human molecular genetics.

[12]  J. W. Foster,et al.  Mutations in SOX9, the gene responsible for Campomelic dysplasia and autosomal sex reversal. , 1995, American journal of human genetics.

[13]  N. Tommerup,et al.  Autosomal sex reversal and campomelic dysplasia are caused by mutations in and around the SRY-related gene SOX9 , 1994, Cell.

[14]  Sahar Mansour,et al.  Campomelic dysplasia and autosomal sex reversal caused by mutations in an SRY-related gene , 1994, Nature.

[15]  M. Bronner‐Fraser.  Neural crest cell formation and migration in the developing embryo , 1994, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[16]  J. Mallet,et al.  Nucleus basalis magnocellularis and hippocampus are the major sites of FMR-1 expression in the human fetal brain , 1993, Nature Genetics.

[17]  H. Clevers,et al.  Ancestry and diversity of the HMG box superfamily. , 1993, Nucleic acids research.

[18]  P. Koopman,et al.  Seven new members of the Sox gene family expressed during mouse development. , 1993, Nucleic acids research.

[19]  P N Goodfellow,et al.  SRY and sex determination in mammals. , 1993, Annual review of genetics.

[20]  A. Ashworth,et al.  A conserved family of genes related to the testis determining gene, SRY. , 1992, Nucleic acids research.

[21]  A. Sinclair,et al.  Genetic evidence equating SRY and the testis-determining factor , 1990, Nature.

[22]  Peter Goodfellow,et al.  A gene mapping to the sex-determining region of the mouse Y chromosome is a member of a novel family of embryonically expressed genes , 1990, Nature.

[23]  Robin Lovell-Badge,et al.  A gene from the human sex-determining region encodes a protein with homology to a conserved DNA-binding motif , 1990, Nature.

[24]  R. Bolande.  The neurocristopathies: A unifying concept of disease arising in neural crest maldevelopment , 1974 .