Cited by 221Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsSignaling Pathways in Disease

The DOI matches its Crossref record; 19 of the 20 references it cites were found in a registry or an index.

Identification and Characterization of E2F7, a Novel Mammalian E2F Family Member Capable of Blocking Cellular Proliferation

Open access

Abstract

The mammalian E2F family of transcription factors plays a crucial role in the regulation of cellular proliferation, apoptosis, and differentiation. Consistent with its biological role in a number of important cellular processes, E2F regulates the expression of genes involved in cell cycle, DNA replication, DNA repair, and mitosis. It has proven difficult, however, to determine the specific roles played by the various known family members in these cellular processes. The work presented here now extends the complexity of this family even further by the identification of a novel E2F family member, which we now term E2F7. Like the expression of the known E2F activators, E2F1, E2F2, and E2F3, the expression of E2F7 is growth-regulated, at least in part, through E2F binding elements on its promoter, and its protein product is localized to the nucleus and associates with DNA E2F recognition sites with high affinity. A number of salient features, however, make this member unique among the E2F family. First, the E2F7 gene encodes a protein that possesses two distinct DNA-binding domains and that lacks a dimerization domain as well as a transcriptional activation and a retinoblastoma-binding domain. In contrast to the E2F activators, E2F7 can block the E2F-dependent activation of a subset of E2F target genes as well as mitigate cellular proliferation of mouse embryo fibroblasts. These findings identify E2F7 as a novel member of the mammalian E2F transcription factor family that has properties of a transcriptional repressor capable of negatively influencing cellular proliferation.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1074/jbc.m308105200

Cites

19 of 19 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 20 references

Research works printed but not linked: 1

  1. Nevins, 1998, Cell Growth Differ., 9, 585

Cited by

Sorted by citations

See all 221

Metadata

Authors
de Bruin, A., Maiti, B., Jakoi, L., Timmers, C., Buerki, R., & Leone, G.
Affiliations
  • The Ohio State University (US)
  • Howard Hughes Medical Institute (US)
Corresponding author
Leone, Gustavo
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2003-10
Volume
278
Issue
43
Pages
42041-42049
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2122511750
Cited by
221
References
20
Citations by year
2026: 4 · 2025: 3 · 2024: 9 · 2023: 4 · 2022: 5 · 2021: 9 · 2020: 10 · 2019: 7 · 2018: 9 · 2017: 3 · 2016: 10 · 2015: 6 · 2014: 2 · 2013: 9 · 2012: 6
FWCI
10.07
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
E2F7, E2F transcription factors, transcriptional repressor, cell proliferation, growth inhibition, DNA-binding domain, E2F target genes, mouse embryonic fibroblasts, cell cycle regulation
MeSH terms
Animals, Binding Sites, Cell Division, Cloning, Molecular, DNA, Embryo, Mammalian, Fibroblasts, Gene Expression Regulation, Promoter Regions, Genetic, Repressor Proteins, Transfection, Protein Structure, Tertiary, DNA, Complementary, Response Elements, Peptide Elongation Factor 2, E2F7 Transcription Factor, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review