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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Myc-mediated proliferation and lymphomagenesis, but not apoptosis, are compromised by E2f1 loss.

Myc and E2f1 promote cell cycle progression, but overexpression of either can trigger p53-dependent apoptosis. Mice expressing an Emu-Myc transgene in B lymphocytes develop lymphomas, the majority of which sustain mutations of either the Arf or p53 tumor suppressors. Emu-Myc transgenic mice lacking one or both E2f1 alleles exhibited a slower onset of lymphoma development associated with increased expression of the cyclin-dependent kinase inhibitor p27(Kip1) and a reduced S phase fraction in precancerous B cells. In contrast, Myc- induced apoptosis and the frequency of Arf and p53 mutations in lymphomas were unaffected by E2f1 loss. Therefore, Myc does not require E2f1 to induce Arf, p53, or apoptosis in B cells, but depends upon E2f1 to accelerate cell cycle progression and downregulate p27(Kip1).[1]

References

  1. Myc-mediated proliferation and lymphomagenesis, but not apoptosis, are compromised by E2f1 loss. Baudino, T.A., Maclean, K.H., Brennan, J., Parganas, E., Yang, C., Aslanian, A., Lees, J.A., Sherr, C.J., Roussel, M.F., Cleveland, J.L. Mol. Cell (2003) [Pubmed]
 
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