Evidence map›Paper›PMID 8382609›Full record

ArticleThe EMBO journal1993

Heterodimer formation of cJun and ATF-2 is responsible for induction of c-jun by the 243 amino acid adenovirus E1A protein.

H van Dam, M Duyndam, R Rottier, A Bosch, L de Vries-Smits, P Herrlich, A Zantema, P Angel, A J van der Eb

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed
20.4field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 379 citations in OpenAlex.

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83 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

9 authors at 1 institution in 1 country.

H van DamLaboratory for Molecular Carcinogenesis, Sylvius Laboratories, University of Leiden, The Netherlands.
M Duyndam
R Rottier
A Bosch
L de Vries-Smits
P Herrlich
A Zantema
P Angel
A J van der Eb
FZI Research Center for Information Technology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adenovirus E1A proteins differentially regulate AP-1-responsive genes. Collagenase and stromelysin are repressed by E1A, whereas the expression of c-jun is elevated. Inhibition of collagenase has been found to be exerted through the consensus AP-1 binding site TGAGTCA. Here we show that the distal AP-1 binding site in the c-jun promoter, the jun2TRE (TTACCTCA), is the decisive element of this promoter in mediating the positive response to the 243 amino acid E1A product. In vitro binding studies revealed that, in contrast to the consensus AP-1 site which is preferentially targeted by dimers composed of the Jun and Fos families, the jun2TRE binds heterodimers composed of cJun and ATF-2(-like) proteins. Since stimulation of c-jun transcription is a function of the transforming domain of E1A encoded by conserved region 1, cJun--ATF-2 may be one of the effector factors involved in transformation. The data further suggest that E1A can distinguish between cJun--cJun and cJun--ATF-2 in imposing opposite states of activity.

Indexed as

Genes, jun3T3 CellsActivating Transcription FactorsAdenovirus E1A ProteinsAnimalsBase SequenceBinding SitesBlood ProteinsCyclic AMPHeLa CellsHumansMiceMolecular Sequence DataOligonucleotidesProto-Oncogene Proteins c-junTranscription FactorsActivating Transcription FactorsAdenovirus E1A ProteinsBlood ProteinsCyclic AMPOligonucleotidesProto-Oncogene Proteins c-junTranscription Factors

Identifiers

PMID8382609
PMCPMC413231
OpenAlexW1692197226

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.