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SUPT7L

Introduction

STAGA complex 65 subunit gamma is a protein that in humans is encoded by the SUPT7L gene.[1][2][3]

Model organisms

Model organisms

Model organisms have been used in the study of SUPT7L function. A conditional knockout mouse line, called Supt7ltm1a(EUCOMM)Wtsi[9][10] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[11][12][13]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[7][14] Twenty four tests were carried out on mutant mice and two significant abnormalities were observed.[7] No homozygous mutant embryos were identified during gestation, and therefore none survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice but no further abnormalities were observed.[7]

Interactions

Interactions

SUPT7L has been shown to interact with TAF9[2] and Transcription initiation protein SPT3 homolog.[2]

References

References

  1. ↑ Nagase T, Ishikawa K, Suyama M, Kikuno R, Miyajima N, Tanaka A, Kotani H, Nomura N, Ohara O (October 1998). “Prediction of the coding sequences of unidentified human genes. XI. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro”. DNA Research. 5 (5): 277–86. doi:10.1093/dnares/5.5.277. PMID 9872452.
  2. ↑ 2.0 2.1 2.2 Martinez E, Palhan VB, Tjernberg A, Lymar ES, Gamper AM, Kundu TK, Chait BT, Roeder RG (October 2001). “Human STAGA complex is a chromatin-acetylating transcription coactivator that interacts with pre-mRNA splicing and DNA damage-binding factors in vivo”. Molecular and Cellular Biology. 21 (20): 6782–95. doi:10.1128/MCB.21.20.6782-6795.2001. PMC 99856. PMID 11564863.
  3. ↑ “Entrez Gene: SUPT7L suppressor of Ty 7 (S. cerevisiae)-like”.
  4. ↑ “Dysmorphology data for Supt7l”. Wellcome Trust Sanger Institute.
  5. ↑ “Salmonella infection data for Supt7l”. Wellcome Trust Sanger Institute.
  6. ↑ “Citrobacter infection data for Supt7l”. Wellcome Trust Sanger Institute.
  7. ↑ 7.0 7.1 7.2 7.3 Gerdin AK (2010). “The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice”. Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  8. ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  9. ↑ “International Knockout Mouse Consortium”.
  10. ↑ “Mouse Genome Informatics”.
  11. ↑ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (June 2011). “A conditional knockout resource for the genome-wide study of mouse gene function”. Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  12. ↑ Dolgin E (June 2011). “Mouse library set to be knockout”. Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  13. ↑ Collins FS, Rossant J, Wurst W (January 2007). “A mouse for all reasons”. Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  14. ↑ van der Weyden L, White JK, Adams DJ, Logan DW (2011). “The mouse genetics toolkit: revealing function and mechanism”. Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.
Further reading

Further reading