Evidence map›Paper›PMID 21310950›Full record

ArticleThe Journal of biological chemistry2011

Genome-wide analysis of transcription factor E2F1 mutant proteins reveals that N- and C-terminal protein interaction domains do not participate in targeting E2F1 to the human genome.

Alina R Cao, Roman Rabinovich, Maoxiong Xu, Xiaoqin Xu, Victor X Jin, Peggy J Farnham

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. DNA G-Quadruplex in NRP1 Promoter Facilitates SARS-CoV-2 Infection.International journal of molecular sciences · 2024
    Article
  4. Article
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  6. Bioinformatic-based mechanism identification ofJournal of gastrointestinal oncology · 2022
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  7. Article
  8. Article
  9. Therapeutic Targeting ofAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019
    Article
  10. Article
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  19. Article
  20. Leveraging biological replicates to improve analysis in ChIP-seq experiments.Computational and structural biotechnology journal · 2014
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Alina R CaoGenome Center, University of California, Davis, California 95616, USA.
Roman Rabinovich
Maoxiong Xu
Xiaoqin Xu
Victor X Jin
Peggy J Farnham
University of California, Davis · USThe Ohio State University · USUniversity of Southern California · US

Funding

Production Center for Global Mapping of Regulatory ElementsU54HG004558 · NHGRI · YALE UNIVERSITY · PI SNYDER, MICHAEL P. · 2007 to 2011
$15.4M
UC Davis MCB T32 Administrative Supplement to Recognize Excellence in Diversity, Equity, Inclusion, and Accessibility (DEIA) MentorshipT32GM007377 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI CHEDIN, FREDERIC LOUIS · 1985 to 2023
$9.9M
TRANSCRIPTIONAL REGULATION OF GROWTH-RELATED GENESR01CA045240 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI FARNHAM, PEGGY J · 1992 to 2011
$3.4M
TRANSCRIPTIONAL REGULATION OF GROWTH-RELATED GENESR29CA045240 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI FARNHAM, PEGGY J · 1987 to 1991
–
NCI NIH HHS CA45240NCI NIH HHS R01 CA045240NHGRI NIH HHS HG004558NHGRI NIH HHS U54 HG004558NIGMS NIH HHS GM007377NIGMS NIH HHS T32 GM007377
6 · The paper itself

Abstract

Previous studies of E2F family members have suggested that protein-protein interactions may be the mechanism by which E2F proteins are recruited to specific genomic regions. We have addressed this hypothesis on a genome-wide scale using ChIP-seq analysis of MCF7 cell lines that express tagged wild type and mutant E2F1 proteins. First, we performed ChIP-seq for tagged WT E2F1. Then, we analyzed E2F1 proteins that lacked the N-terminal SP1 and cyclin A binding domains, the C-terminal transactivation and pocket protein binding domains, and the internal marked box domain. Surprisingly, we found that the ChIP-seq patterns of the mutant proteins were identical to that of WT E2F1. However, mutation of the DNA binding domain abrogated all E2F1 binding to the genome. These results suggested that the interaction between the E2F1 DNA binding domain and a consensus motif may be the primary determinant of E2F1 recruitment. To address this possibility, we analyzed the in vivo binding sites for the in vitro-derived consensus E2F1 motif (TTTSSCGC) and also performed de novo motif analysis. We found that only 12% of the ChIP-seq peaks contained the TTTSSCGC motif. De novo motif analysis indicated that most of the in vivo sites lacked the 5' half of the in vitro-derived consensus, having instead the in vivo consensus of CGCGC. In summary, our findings do not provide support for the model that protein-protein interactions are involved in recruiting E2F1 to the genome, but rather suggest that recognition of a motif found at most human promoters is the critical determinant.

Indexed as

Cell Line, TumorChromatin ImmunoprecipitationE2F1 Transcription FactorGenome, HumanHumansMutationProtein Structure, TertiaryE2F1 Transcription Factor

Identifiers

PMID21310950
PMCPMC3069401
OpenAlexW1966276188

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.