Evidence map›Paper›PMID 10777209›Full record

ArticleOncogene2000

B-ATF functions as a negative regulator of AP-1 mediated transcription and blocks cellular transformation by Ras and Fos.

D R Echlin, H J Tae, N Mitin, E J Taparowsky

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

64 citing papers in PubMed, 123 citations in OpenAlex.

  1. Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026
    Review
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  10. Genetically targeting the BATF family transcription factors BATF and BATF3 in the mouse abrogates effector T cell activities and enables long-term heart allograft survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Article
  11. Article
  12. Review
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  18. Investigating the Role of BATF3 in Grass Carp (International journal of molecular sciences · 2019
    Article
  19. Article
  20. Article

4 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

4 authors at 2 institutions in 1 country.

D R EchlinDepartment of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392, USA.
H J Tae
N Mitin
E J Taparowsky
Purdue University West Lafayette · USLG Chem (South Korea)

Funding

BATF in Blood Cell Growth, Development and MalignanciesR01CA078264 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI TAPAROWSKY, ELIZABETH J · 1998 to 2006
$1.7M
NCI NIH HHS CA-78264
6 · The paper itself

Abstract

B-ATF is a nuclear basic leucine zipper protein that belongs to the AP-1/ATF superfamily of transcription factors. Northern blot analysis reveals that the human B-ATF gene is expressed most highly in hematopoietic tissues. Interaction studies in vitro and in vivo show that the leucine zipper of B-ATF mediates dimerization with members of the Jun family of proteins. Chimeric proteins consisting of portions of B-ATF and the DNA binding domain of the yeast activator GAL4 do not stimulate reporter gene expression in mammalian cells, indicating that B-ATF does not contain a conventional transcription activation domain. Jun/B-ATF dimers display similar DNA binding profiles as Jun/Fos dimers, with a bias toward binding TRE (12-O-tetradecanolyphorbol-13-acetate-response element) over CRE (cyclic AMP-response element) DNA sites. B-ATF inhibits transcriptional activation of a reporter gene containing TRE sites in a dose-dependent manner, presumably by competing with Fos for Jun and forming transcriptionally inert Jun/B-ATF heterodimers. Stable expression of B-ATF in C3H10T1/2 cells does not reduce cell viability, but does result in a reduced cellular growth rate when compared to controls. This effect is dominant in the presence of the growth promoting effects of the H-Ras or the v-Fos oncoproteins, since expression of B-ATF restricts the efficiency of focus formation by these transforming agents. These findings demonstrate that B-ATF is a tissue-specific transcription factor with the potential to function as a dominant-negative to AP-1.

Indexed as

Cell Transformation, NeoplasticDNA-Binding ProteinsLeucine ZippersTranscriptional ActivationTranscription, GeneticAdultAnimalsBasic-Leucine Zipper Transcription FactorsBinding SitesCell LineConsensus SequenceDimerizationGene ExpressionHematopoietic SystemHumansMiceBasic-Leucine Zipper Transcription FactorsBATF protein, humanDNA-Binding ProteinsNuclear ProteinsOncogene Protein p21(ras)Oncogene Proteins v-fosProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junRecombinant Fusion ProteinsRepressor ProteinsRNA, MessengerTranscription Factor AP-1Transcription Factors

Identifiers

PMID10777209
OpenAlexW1977330771

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.