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Literature DB >> 11230146

E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryos.

Abstract

The E2F transcription factors are thought to be key downstream targets of the retinoblastoma protein (pRB) tumor suppressor. It is widely believed that E2F1, E2F2, and E2F3 can all activate cellular proliferation but that E2F1 is the specific inducer of apoptosis. Here we show that the E2f3 mutation completely suppresses both the inappropriate proliferation and the p53-dependent apoptosis arising in the Rb mutant embryos. Through the analysis of Rb(-/-);E2f3(+/-) embryos, we have been able to separate E2F3's role in the induction of apoptosis from its ability to induce proliferation. Thus, contrary to the prevailing view of E2F action, E2F3 makes a major contribution to the apoptosis resulting from pRB loss.

Entities: Disease Gene

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Year: 2001 PMID： 11230146 PMCID： PMC312633 DOI： 10.1101/gad.858801

Source DB: PubMed Journal: Genes Dev ISSN： 0890-9369 Impact factor: 11.361

22 in total

E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryos.

1. CDC25A phosphatase is a target of E2F and is required for efficient E2F-induced S phase.

2. Surfing the p53 network.

3. Effects of an Rb mutation in the mouse.

4. E2f3 is critical for normal cellular proliferation.

Review 5. The retinoblastoma gene and gene product.

6. Role for the p53 homologue p73 in E2F-1-induced apoptosis.

7. A common E2F-1 and p73 pathway mediates cell death induced by TCR activation.

8. Requirement for a functional Rb-1 gene in murine development.

9. Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis.

10. Heterozygous Rb-1 delta 20/+mice are predisposed to tumors of the pituitary gland with a nearly complete penetrance.

1. E2F1 and E2F2 determine thresholds for antigen-induced T-cell proliferation and suppress tumorigenesis.

2. Selective induction of E2F1 in response to DNA damage, mediated by ATM-dependent phosphorylation.

3. Telencephalon-specific Rb knockouts reveal enhanced neurogenesis, survival and abnormal cortical development.

4. Rb function in extraembryonic lineages suppresses apoptosis in the CNS of Rb-deficient mice.

5. Inactivation of E2F3 results in centrosome amplification.

6. Defective gene expression, S phase progression, and maturation during hematopoiesis in E2F1/E2F2 mutant mice.

7. Conditional mutation of Rb causes cell cycle defects without apoptosis in the central nervous system.

8. Specificity in the activation and control of transcription factor E2F-dependent apoptosis.

9. E2F1 induces phosphorylation of p53 that is coincident with p53 accumulation and apoptosis.

10. Combinatorial gene control involving E2F and E Box family members.