Pairing SOX off: with partners in the regulation of embryonic development.
By Y. Kamachi, M. Uchikawa, H. Kondoh. Trends in Genetics, 2000
684 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Genetics
View Paper: https://www.semanticscholar.org/paper/c67cb02988c6a3eb993e82ad7a7a7e875db7a825
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In Cellular and Molecular Neuroscience
In Genetics
Citations in the corpus
- SOX9 is an intestine crypt transcription factor, is regulated by the Wnt pathway, and represses the CDX2 and MUC2 genes (2004, background): “Similarly to TCFs, SOX proteins have been widely implicated in the establishment of cell multipotency (Avilion et al., 2003; Kim et al., 2003), cell commitment (Mori-Akiyama et al., 2003; Stolt et al., 2003), and differentiation (Kamachi et al., 2000; Stolt et al., 2002).”
- Terminal differentiation of myelin-forming oligodendrocytes depends on the transcription factor Sox10. (2002, background): “Sox proteins depend on cooperating transcription factors for full activity (Wegner 1999; Kamachi et al. 2000).”
- Strategies and new developments in the generation of patient-specific pluripotent stem cells. (2007, background): “Sox proteins, in general, regulate their target genes by associating with specific partner factors (Kamachi et al., 2000; Wilson and Koopman, 2002).”
- Sox2 deficiency causes neurodegeneration and impaired neurogenesis in the adult mouse brain (2004, background): “These genes are also involved in hereditary diseases in man (Kamachi et al., 2000).”
- Sox17 and β-catenin cooperate to regulate the transcription of endodermal genes (2004, background): “The prevailing idea is that interacting protein partners are key determinants of Sox protein specificity and activity (Kamachi et al., 2000; Wilson and Koopman, 2002), but in the case of Sox17, its interacting transcriptional co-factors were previously unknown.”