Transcription factor SOX-6 is a protein that in humans is encoded by the SOX6 gene.[5][6]

SOX6
Identifiers
AliasesSOX6, HSSOXD, SRY-box 6, SRY-box transcription factor 6, TOLCAS
External IDsOMIM: 607257; MGI: 98368; HomoloGene: 22631; GeneCards: SOX6; OMA:SOX6 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)Chr 11: 15.97 – 16.74 MbChr 7: 115.47 – 116.04 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

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The SOX gene family encodes a group of transcription factors defined by the conserved high mobility group (HMG) DNA-binding domain. Unlike most transcription factors, SOX transcription factors bind to the minor groove of DNA, causing a 70- to 85-degree bend and introducing local conformational changes.[supplied by OMIM][6]

Interactions

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SOX6 has been shown to interact with CTBP2[7] and CENPK.[8]

It has also been demonstrated that SOX6 protein accumulates in the differentiating human erythrocytes, and then is able to downregulate its own transcription, by directly binding to an evolutionarily conserved consensus sequences located near SOX6 transcriptional start site.[9]

Sox6 appears to have a crucial role in the transcriptional regulation of globin genes, and in directing the terminal differentiation of red blood cells.[10] In addition, SOX6 may have a role in tumor growth of Ewing sarcoma.[11] A new role of Sox6 in renin and prorenin regulation was studied using a Sox KO mouse model in which Sox6 is only knockout in renin expressing cells. This study showed that renin promoter possesses the binding site for Sox6. The highlight of the study was that Sox6 is one of the key regulators of renin and prorenin regulation and JG cell expansion during low salt and dehydration in mice. PMID 31760770; DOI: 10.1152/ajprenal.00095.2019

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000110693Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000051910Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Cohen-Barak O, Hagiwara N, Arlt MF, Horton JP, Brilliant MH (March 2001). "Cloning, characterization and chromosome mapping of the human SOX6 gene". Gene. 265 (1–2): 157–164. doi:10.1016/S0378-1119(01)00346-8. PMID 11255018.
  6. ^ a b "Entrez Gene: SOX6 SRY (sex determining region Y)-box 6".
  7. ^ Murakami A, Ishida S, Thurlow J, Revest JM, Dickson C (August 2001). "SOX6 binds CtBP2 to repress transcription from the Fgf-3 promoter". Nucleic Acids Research. 29 (16): 3347–3355. doi:10.1093/nar/29.16.3347. PMC 55854. PMID 11504872.
  8. ^ Yamashita A, Ito M, Takamatsu N, Shiba T (September 2000). "Characterization of Solt, a novel SoxLZ/Sox6 binding protein expressed in adult mouse testis". FEBS Letters. 481 (2): 147–151. Bibcode:2000FEBSL.481..147Y. doi:10.1016/S0014-5793(00)01987-6. PMID 10996314. S2CID 20831354.
  9. ^ Cantu' C, Grande V, Alborelli I, Cassinelli L, Cantu' I, Colzani MT, et al. (January 2011). "A highly conserved SOX6 double binding site mediates SOX6 gene downregulation in erythroid cells". Nucleic Acids Research. 39 (2): 486–501. doi:10.1093/nar/gkq819. PMC 3025548. PMID 20852263.
  10. ^ Cantù C, Ierardi R, Alborelli I, Fugazza C, Cassinelli L, Piconese S, et al. (March 2011). "Sox6 enhances erythroid differentiation in human erythroid progenitors". Blood. 117 (13): 3669–3679. doi:10.1182/blood-2010-04-282350. PMID 21263153.
  11. ^ Marchetto A, Ohmura S, Orth MF, Knott MM, Colombo MV, Arrigoni C, et al. (May 2020). "Oncogenic hijacking of a developmental transcription factor evokes vulnerability toward oxidative stress in Ewing sarcoma". Nature Communications. 11 (1): 2423. Bibcode:2020NatCo..11.2423M. doi:10.1038/s41467-020-16244-2. PMC 7228971. PMID 32415069.

Further reading

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This article incorporates text from the United States National Library of Medicine, which is in the public domain.