E2F4 and E2F5 play an essential role in pocket protein-mediated G1 control.


Journal Article

E2F transcription factors are major regulators of cell proliferation. The diversity of the E2F family suggests that individual members perform distinct functions in cell cycle control. E2F4 and E2F5 constitute a defined subset of the family. Until now, there has been little understanding of their individual biochemical and biological functions. Here, we report that simultaneous inactivation of E2F4 and E2F5 in mice results in neonatal lethality, suggesting that they perform overlapping functions during mouse development. Embryonic fibroblasts isolated from these mice proliferated normally and reentered from Go with normal kinetics compared to wild-type cells. However, they failed to arrest in G1 in response to p16INK4a. Thus, E2F4 and E2F5 are dispensable for cell cycle progression but necessary for pocket protein-mediated G1 arrest of cycling cells.

Full Text

Cited Authors

  • Gaubatz, S; Lindeman, GJ; Ishida, S; Jakoi, L; Nevins, JR; Livingston, DM; Rempel, RE

Published Date

  • September 2000

Published In

Volume / Issue

  • 6 / 3

Start / End Page

  • 729 - 735

PubMed ID

  • 11030352

Pubmed Central ID

  • 11030352

Electronic International Standard Serial Number (EISSN)

  • 1097-4164

International Standard Serial Number (ISSN)

  • 1097-2765

Digital Object Identifier (DOI)

  • 10.1016/s1097-2765(00)00071-x


  • eng