DIP2B

DIP2 disco-interacting protein 2 homolog B (Drosophila) is a protein that in humans is encoded by the DIP2B gene.[1] A member of the disco-interacting protein homolog 2 protein family, it contains a binding site for the transcriptional regulator DNA methyltransferase 1 associated protein 1, as well as AMP-binding sites. The presence of these sites suggests that DIP2B may participate in DNA methylation. This gene is located near a folate-sensitive fragile site.[1][2]

Model organisms

Model organisms have been used in the study of DIP2B function. A conditional knockout mouse line, called Dip2btm1a(EUCOMM)Wtsi[8][9] 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.[10][11][12]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[6][13] Twenty five tests were carried out on mutant mice and three significant abnormalities were observed.[6] Few homozygous mutant mice survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice; abnormal fertility and decreased mean corpuscular haemoglobin levels were observed in these animals.[6]

References

  1. 1 2 "DIP2 disco-interacting protein 2 homolog B (Drosophila)". Retrieved 2011-12-05.
  2. ↑ Winnepenninckx, B.; Debacker, K.; Ramsay, J.; Smeets, D.; Smits, A.; Fitzpatrick, D. R.; Kooy, R. F. (2007). "CGG-Repeat Expansion in the DIP2B Gene is Associated with the Fragile Site FRA12A on Chromosome 12q13.1". The American Journal of Human Genetics. 80 (2): 221–231. doi:10.1086/510800. PMC 1785358Freely accessible. PMID 17236128.
  3. ↑ "Haematology data for Dip2b". Wellcome Trust Sanger Institute.
  4. ↑ "Salmonella infection data for Dip2b". Wellcome Trust Sanger Institute.
  5. ↑ "Citrobacter infection data for Dip2b". Wellcome Trust Sanger Institute.
  6. 1 2 3 4 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.
  7. ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  8. ↑ "International Knockout Mouse Consortium".
  9. ↑ "Mouse Genome Informatics".
  10. ↑ Skarnes, W. C.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M.; Harrow, J.; Cox, T.; Jackson, D.; Severin, J.; Biggs, P.; Fu, J.; Nefedov, M.; De Jong, P. J.; Stewart, A. F.; Bradley, A. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–342. doi:10.1038/nature10163. PMC 3572410Freely accessible. PMID 21677750.
  11. ↑ Dolgin E (2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  12. ↑ Collins FS, Rossant J, Wurst W (2007). "A Mouse for All Reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  13. ↑ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism.". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837Freely accessible. PMID 21722353.

Further reading

  • Houlston, R. S.; Cheadle, J.; Dobbins, S. E.; Tenesa, A.; Jones, A. M.; Howarth, K.; Spain, S. L.; Broderick, P.; Domingo, E.; Farrington, S.; Prendergast, J. G. D.; Pittman, A. M.; Theodoratou, E.; Smith, C. G.; Olver, B.; Walther, A.; Barnetson, R. A.; Churchman, M.; Jaeger, E. E. M.; Penegar, S.; Barclay, E.; Martin, L.; Gorman, M.; Mager, R.; Johnstone, E.; Midgley, R.; Niittymäki, I.; Tuupanen, S.; Colley, J.; Idziaszczyk, S. (2010). "Meta-analysis of three genome-wide association studies identifies susceptibility loci for colorectal cancer at 1q41, 3q26.2, 12q13.13 and 20q13.33". Nature Genetics. 42 (11): 973–977. doi:10.1038/ng.670. PMID 20972440. 


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