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Gene Review

E2f2  -  E2F transcription factor 2

Mus musculus

Synonyms: 9230110J10, E130207A07, E2F-2, Transcription factor E2F2
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Disease relevance of E2f2


High impact information on E2f2


Biological context of E2f2

  • Our studies of mice deficient for the E2F1 and E2F2 transcription factors have revealed essential roles for these proteins in the cell cycle control of pancreatic exocrine cells and the regulation of pancreatic beta cell maintenance [6].
  • Furthermore, mice deficient for both E2F1 and E2F2 develop nonautoimmune, insulin-dependent diabetes with high penetrance [6].
  • Induction of cell cycle entry and cell death in postmitotic lens fiber cells by overexpression of E2F1 or E2F2 [7].
  • Importantly, hematopoietic defects observed in E2F1/E2F2 double-knockout (DKO) mice appear to result from impeded S phase progression in hematopoietic progenitor cells [1].
  • Consistent with these observations, E2F1/E2F2 mutant mice are highly predisposed to the development of tumors, and some mice exhibit signs of autoimmunity [8].

Anatomical context of E2f2

  • The development of diabetes in E2f1/E2f2 mutant mice reveals important roles for bone marrow-derived cells in preventing islet cell loss [6].
  • We now demonstrate that E2f1, E2f2, and E2f3 are also required for oncogene-mediated transformation of mouse embryonic fibroblasts [9].
  • In non-neuronal tissues, high E2F-4 transcript levels are present in regions corresponding to proliferative chondrocytes, whereas E2F-2 and E2F-4 transcripts are very abundant in the thymic cortex, which contains immature thymocytes [10].
  • E2F-1, E2F-2 and E2F-5 are first detected in the 9.5 days post-coitus (dpc) forebrain [10].
  • E2F1/E2F2 compound-mutant mice develop nonautoimmune insulin-deficient diabetes and exocrine pancreatic dysfunction characterized by endocrine and exocrine cell dysplasia, a reduction in the number and size of acini and islets, and their replacement by ductal structures and adipose tissue [5].

Associations of E2f2 with chemical compounds

  • As opposed to UVB-exposed skin, UVB-induced tumors showed elevated levels of E2F1, but these were reduced in silibinin-treated tumors without any effect on E2F2 and E2F3 [11].

Other interactions of E2f2

  • In 12.5 dpc embryos, E2F-1, E2F-2 and E2F-5 are highly expressed in proliferating, undifferentiated neuronal precursors [10].

Analytical, diagnostic and therapeutic context of E2f2

  • Quantitative real time PCR revealed that E2F1, E2F2, E2F3, and E2F4 alleviate G0 arrest by induction of cyclinA and E cyclins [2].


  1. Defective gene expression, S phase progression, and maturation during hematopoiesis in E2F1/E2F2 mutant mice. Li, F.X., Zhu, J.W., Hogan, C.J., DeGregori, J. Mol. Cell. Biol. (2003) [Pubmed]
  2. Divergent siblings: E2F2 and E2F4 but not E2F1 and E2F3 induce DNA synthesis in cardiomyocytes without activation of apoptosis. Ebelt, H., Hufnagel, N., Neuhaus, P., Neuhaus, H., Gajawada, P., Simm, A., Müller-Werdan, U., Werdan, K., Braun, T. Circ. Res. (2005) [Pubmed]
  3. High incidence of thymic epithelial tumors in E2F2 transgenic mice. Scheijen, B., Bronk, M., van der Meer, T., De Jong, D., Bernards, R. J. Biol. Chem. (2004) [Pubmed]
  4. Mutation of E2F2 in mice causes enhanced T lymphocyte proliferation, leading to the development of autoimmunity. Murga, M., Fernández-Capetillo, O., Field, S.J., Moreno, B., Borlado, L.R., Fujiwara, Y., Balomenos, D., Vicario, A., Carrera, A.C., Orkin, S.H., Greenberg, M.E., Zubiaga, A.M. Immunity (2001) [Pubmed]
  5. Diabetes and exocrine pancreatic insufficiency in E2F1/E2F2 double-mutant mice. Iglesias, A., Murga, M., Laresgoiti, U., Skoudy, A., Bernales, I., Fullaondo, A., Moreno, B., Lloreta, J., Field, S.J., Real, F.X., Zubiaga, A.M. J. Clin. Invest. (2004) [Pubmed]
  6. The development of diabetes in E2f1/E2f2 mutant mice reveals important roles for bone marrow-derived cells in preventing islet cell loss. Li, F.X., Zhu, J.W., Tessem, J.S., Beilke, J., Varella-Garcia, M., Jensen, J., Hogan, C.J., DeGregori, J. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  7. Induction of cell cycle entry and cell death in postmitotic lens fiber cells by overexpression of E2F1 or E2F2. Chen, Q., Hung, F.C., Fromm, L., Overbeek, P.A. Invest. Ophthalmol. Vis. Sci. (2000) [Pubmed]
  8. E2F1 and E2F2 determine thresholds for antigen-induced T-cell proliferation and suppress tumorigenesis. Zhu, J.W., Field, S.J., Gore, L., Thompson, M., Yang, H., Fujiwara, Y., Cardiff, R.D., Greenberg, M., Orkin, S.H., DeGregori, J. Mol. Cell. Biol. (2001) [Pubmed]
  9. Control of the p53-p21CIP1 Axis by E2f1, E2f2, and E2f3 Is Essential for G1/S Progression and Cellular Transformation. Sharma, N., Timmers, C., Trikha, P., Saavedra, H.I., Obery, A., Leone, G. J. Biol. Chem. (2006) [Pubmed]
  10. Expression patterns of the E2F family of transcription factors during mouse nervous system development. Dagnino, L., Fry, C.J., Bartley, S.M., Farnham, P., Gallie, B.L., Phillips, R.A. Mech. Dev. (1997) [Pubmed]
  11. Differential effect of silibinin on E2F transcription factors and associated biological events in chronically UVB-exposed skin versus tumors in SKH-1 hairless mice. Gu, M., Singh, R.P., Dhanalakshmi, S., Mohan, S., Agarwal, R. Mol. Cancer Ther. (2006) [Pubmed]
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