Evidence map›Paper›PMID 14627987›Full record

ArticleOncogene2003

PARP-1 binds E2F-1 independently of its DNA binding and catalytic domains, and acts as a novel coactivator of E2F-1-mediated transcription during re-entry of quiescent cells into S phase.

Cynthia M Simbulan-Rosenthal, Dean S Rosenthal, RuiBai Luo, Raed Samara, Luis A Espinoza, Paul O Hassa, Michael O Hottiger, Mark E Smulson

Abstract read
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In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
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  16. Molecular signatures of aggressive pediatric liver cancer.Archives of stem cell and therapy · 2021
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9 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Cynthia M Simbulan-RosenthalDepartment of Biochemistry and Molecular Biology, Georgetown University School of Medicine, Washington, DC 20007, USA. simbulac@georgetown.edu
Dean S Rosenthal
RuiBai Luo
Raed Samara
Luis A Espinoza
Paul O Hassa
Michael O Hottiger
Mark E Smulson
Georgetown University · USUniversity of Zurich · CH

Funding

THYMIDINE KINASE AND BRAIN TUMOR RADIATION RESISTANCEP01CA074175 · NCI · GEORGETOWN UNIVERSITY · PI DRITSCHILO, ANATOLY · 1997 to 2006
$13.2M
NCI NIH HHS CA25344NCI NIH HHS P01 CA74175
6 · The paper itself

Abstract

The transcription factor E2F-1 is implicated in the activation of S-phase genes as well as induction of apoptosis, and is regulated by interactions with Rb and by cell cycle-dependent alterations in E2F-1 abundance. We earlier demonstrated a pivotal role for poly(ADP-ribose) polymerase-1 (PARP-1) in the regulation of E2F-1 expression and promoter activity during S-phase re-entry when quiescent cells re-enter the cell cycle. We now investigate the putative mechanism(s) by which PARP-1 may upregulate E2F-1 promoter activity during S-phase re-entry. DNase-1 footprint assays with purified PARP-1 showed that PARP-1 did not directly bind the E2F-1 promoter in a sequence-specific manner. In contrast to p53, a positive acceptor in poly(ADP-ribosyl)ation reactions, E2F-1 was not poly(ADP-ribosyl)ated by wild-type PARP-1 in vitro, indicating that PARP-1 does not exert a dual effect on E2F-1 transcriptional activation. Protein-binding reactions and coimmunoprecipitation experiments with purified PARP-1 and E2F-1, however, revealed that PARP-1 binds to E2F-1 in vitro. More significantly, physical association of PARP-1 and E2F-1 in vivo also occurred in wild-type fibroblasts 5 h after re-entry into S phase, coincident with the increase in E2F-1 promoter activity and expression of E2F-1-responsive S-phase genes cyclin A and c-Myc. Mapping of the interaction domains revealed that full-length PARP-1 as well as PARP-1 mutants lacking either the catalytic active site or the DNA-binding domain equally bind E2F-1, whereas a PARP-1 mutant lacking the automodification domain does not, suggesting that the protein interaction site is located in this central domain. Finally, gel shift analysis with end-blocked E2F-1 promoter sequence probes verified that the binding of PARP-1 to E2F-1 enhances binding to the E2F-1 promoter, indicating that PARP-1 acts as a positive cofactor of E2F-1-mediated transcription.

Indexed as

Cell Cycle ProteinsDNA-Binding ProteinsTranscription, GeneticAnimalsBinding SitesCyclin AE2F1 Transcription FactorE2F Transcription FactorsGenes, mycHumansPoly(ADP-ribose) PolymerasesPrecipitin TestsS PhaseTranscription FactorsCell Cycle ProteinsCyclin ADNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorE2F Transcription FactorsPoly(ADP-ribose) PolymerasesTranscription Factors

Identifiers

PMID14627987
OpenAlexW2035398180

What OpenQuestion holds

Textmetadata
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.