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SOX6  -  SRY (sex determining region Y)-box 6

Homo sapiens

Synonyms: HSSOX6, SOXD, Transcription factor SOX-6
 
 
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Disease relevance of SOX6

  • Expression of a transcriptional factor, SOX6, in human gliomas [1].
  • Immunohistochemical analysis of SOX6 expression in human brain tumors [2].
  • The reverse transcription-polymerase chain reaction (RT-PCR) revealed that the SOX6 gene was more highly expressed in glioma tissues and fetal brain than in normal adult brain and other cancer cells, except melanoma cells [1].
  • In contrast, ependymal tumors (ependymoma and subependymoma), meningioma, and schwannoma, which are all well differentiated tumors, showed either no staining or only faint staining for SOX6 [2].
  • Immunohistochemical analysis revealed that astrocytic and oligodendroglial tumors expressed SOX6; neuronal-glial cell tumors (central neurocytoma) and embryonal tumors (medulloblastoma), which arise from multipotential stem cell precursors, also showed a high intensity of SOX6 staining [2].
 

High impact information on SOX6

  • Here we show that SRY and the Sox protein SOX6 colocalize with splicing factors in the nucleus and are dynamically redistributed following the blockage of splicing in living cells [3].
  • We also demonstrate a decrease in mRNA levels of the transcriptional co-activators L-Sox5 and Sox6 upon ROCK inhibition and cytochalasin D [4].
  • Identification of a human glioma antigen, SOX6, recognized by patients' sera [5].
  • SOX6 is a transcriptional factor that is specifically expressed in the developing central nervous system and in the early stages of chondrogenesis in mouse embryos [5].
  • RT-PCR and Northern blot analysis revealed that the SOX6 gene was more highly expressed in glioma tissues than in normal adult tissues, except testis [5].
 

Biological context of SOX6

 

Anatomical context of SOX6

  • Northern blot analysis revealed that SOX6 is expressed in a wide variety of tissues, most abundantly in skeletal muscle, suggesting an important role for SOX6 in muscle [6].
  • To test the validity of this proposition, we analyzed the expression of SOX6 in various human central nervous system (CNS) tumors [2].
  • SOX6 may be a useful marker for the diagnosis of tumors arising from immature bipotential cells that may differentiate into neuronal and glial cells [2].
  • Immunohistochemical analysis with the anti-SOX6 antibody showed that all the glioma tissues analysed expressed SOX6 in tumor cells, but only a few SOX6-positive cells were detected in non-neoplastic tissues from the cerebral cortex [5].
  • L-Sox5 and Sox6 are respectively induced coincident and after the expression of Bmpr1b in the prechondrogenic aggregate, and their activation correlates with the induction of Type II Collagen and Aggrecan genes in the differentiating cartilages [8].
 

Associations of SOX6 with chemical compounds

  • SOX6 attenuates glucose-stimulated insulin secretion by repressing PDX1 transcriptional activity [9].
 

Other interactions of SOX6

  • In this report, we show that SOX6 is modified in vitro and in vivo by small ubiquitin-related modifier (SUMO) on two distinct sites [10].
  • These results show that SOX6 can recruit CtBP2 to repress transcription from the Fgf-3 promoter [7].
  • In turn, BMPs in concert with Sox9, Sox6, and L-Sox5 would be responsible for the execution and maintenance of the cartilage differentiation program [8].
  • The L-SOX5 gene contains 18 exons and shows similar genomic structure to SOX6 [11].
  • Balanced translocation in a patient with craniosynostosis disrupts the SOX6 gene and an evolutionarily conserved non-transcribed region [12].
 

Analytical, diagnostic and therapeutic context of SOX6

  • Western blot analysis with an anti-SOX6 antibody demonstrated that the SOX6 protein was expressed in glioma tissues, but not in normal adult brain tissue [5].

References

  1. Expression of a transcriptional factor, SOX6, in human gliomas. Ueda, R., Yoshida, K., Kawakami, Y., Kawase, T., Toda, M. Brain tumor pathology. (2004) [Pubmed]
  2. Immunohistochemical analysis of SOX6 expression in human brain tumors. Ueda, R., Yoshida, K., Kawakami, Y., Kawase, T., Toda, M. Brain tumor pathology. (2004) [Pubmed]
  3. A direct role of SRY and SOX proteins in pre-mRNA splicing. Ohe, K., Lalli, E., Sassone-Corsi, P. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  4. RhoA/ROCK Signaling Regulates Chondrogenesis in a Context-dependent Manner. Woods, A., Beier, F. J. Biol. Chem. (2006) [Pubmed]
  5. Identification of a human glioma antigen, SOX6, recognized by patients' sera. Ueda, R., Iizuka, Y., Yoshida, K., Kawase, T., Kawakami, Y., Toda, M. Oncogene (2004) [Pubmed]
  6. Cloning, characterization and chromosome mapping of the human SOX6 gene. Cohen-Barak, O., Hagiwara, N., Arlt, M.F., Horton, J.P., Brilliant, M.H. Gene (2001) [Pubmed]
  7. SOX6 binds CtBP2 to repress transcription from the Fgf-3 promoter. Murakami, A., Ishida, S., Thurlow, J., Revest, J.M., Dickson, C. Nucleic Acids Res. (2001) [Pubmed]
  8. Analysis of the molecular cascade responsible for mesodermal limb chondrogenesis: Sox genes and BMP signaling. Chimal-Monroy, J., Rodriguez-Leon, J., Montero, J.A., Gañan, Y., Macias, D., Merino, R., Hurle, J.M. Dev. Biol. (2003) [Pubmed]
  9. SOX6 attenuates glucose-stimulated insulin secretion by repressing PDX1 transcriptional activity. Iguchi, H., Sakai, J. Nippon Yakurigaku Zasshi (2006) [Pubmed]
  10. Repression of SOX6 transcriptional activity by SUMO modification. Fernández-Lloris, R., Osses, N., Jaffray, E., Shen, L.N., Vaughan, O.A., Girwood, D., Bartrons, R., Rosa, J.L., Hay, R.T., Ventura, F. FEBS Lett. (2006) [Pubmed]
  11. Identification and characterization of the human long form of Sox5 (L-SOX5) gene. Ikeda, T., Zhang, J., Chano, T., Mabuchi, A., Fukuda, A., Kawaguchi, H., Nakamura, K., Ikegawa, S. Gene (2002) [Pubmed]
  12. Balanced translocation in a patient with craniosynostosis disrupts the SOX6 gene and an evolutionarily conserved non-transcribed region. Tagariello, A., Heller, R., Greven, A., Kalscheuer, V.M., Molter, T., Rauch, A., Kress, W., Winterpacht, A. J. Med. Genet. (2006) [Pubmed]
 
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