E2F - at the crossroads of life and death

Shirley Polager, Doron Ginsberg

Research output: Contribution to journalReview articlepeer-review

252 Scopus citations

Abstract

The retinoblastoma tumor suppressor, pRb, restricts cell-cycle progression mainly by regulating members of the E2F-transcription-factor family. The Rb pathway is often inactivated in human tumors, resulting in deregulated-E2F activity that promotes proliferation or cell death, depending on the cellular context. Specifically, the outcome of deregulated-E2F activity is determined by integration of signals coming from the cellular DNA and the external environment. Alterations in cell proliferation and cell-death pathways are key features of transformed cells and, therefore, an understanding of the variables that determine the outcome of E2F activation is pivotal for cancer research and treatment. In this review, we discuss recent studies that have elucidated some of the signals affecting E2F activity and that have revealed additional E2F targets and functions, thereby enriching the understanding of this versatile transcription-factor family.

Original languageEnglish
Pages (from-to)528-535
Number of pages8
JournalTrends in Cell Biology
Volume18
Issue number11
DOIs
StatePublished - Nov 2008

Bibliographical note

Funding Information:
We apologize to colleagues whose work could not be cited owing to space limitations. Work in the laboratory of D.G. is supported by grants from the Israel Science Foundation (ISF), the Israel Cancer Association and the Israeli Ministry of Health.

Funding

We apologize to colleagues whose work could not be cited owing to space limitations. Work in the laboratory of D.G. is supported by grants from the Israel Science Foundation (ISF), the Israel Cancer Association and the Israeli Ministry of Health.

FundersFunder number
Israel Cancer Association
Israel Science Foundation
Ministry of Health, State of Israel

    Fingerprint

    Dive into the research topics of 'E2F - at the crossroads of life and death'. Together they form a unique fingerprint.

    Cite this