Evidence map›Paper›PMID 10523647›Full record

ArticleMolecular and cellular biology1999

CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins.

M Ubeda, M Vallejo, J F Habener

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

63 citing papers in PubMed, 140 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
  6. Article
  7. Advances in the study of death receptor 5.Frontiers in pharmacology · 2025
    Review
  8. Endoplasmic reticulum stress enhances the expression of TLR3-induced TSLP by airway epithelium.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. CHOP and c-JUN up-regulate the mutant Z αThe Journal of biological chemistry · 2020
    Article
  14. Review
  15. Article
  16. Article
  17. Inducible Intestine-Specific Expression of krasNeoplasia (New York, N.Y.) · 2018
    Article
  18. Article
  19. Article
  20. Article

3 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

3 authors at 3 institutions in 2 countries.

M UbedaLaboratory of Molecular Endocrinology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
M Vallejo
J F Habener
Harvard University · USHoward Hughes Medical Institute · USLaboratory of Molecular Genetics · PL

Funding

SOMATOSTATIN: ENDOCRINE &PARACRINE BIOSYNTHESISR01DK030457 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HABENER, JOEL F · 1986 to 1991
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SOMATOSTATIN: ENDOCRINE AND PARACRINE BIOSYNTHESISR37DK030457 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HABENER, JOEL F · 1992 to 1999
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NIDDK NIH HHS DK30457
6 · The paper itself

Abstract

The transcription factor CHOP (C/EBP homologous protein 10) is a bZIP protein induced by a variety of stimuli that evoke cellular stress responses and has been shown to arrest cell growth and to promote programmed cell death. CHOP cannot form homodimers but forms stable heterodimers with the C/EBP family of activating transcription factors. Although initially characterized as a dominant negative inhibitor of C/EBPs in the activation of gene transcription, CHOP-C/EBP can activate certain target genes. Here we show that CHOP interacts with members of the immediate-early response, growth-promoting AP-1 transcription factor family, JunD, c-Jun, and c-Fos, to activate promoter elements in the somatostatin, JunD, and collagenase genes. The leucine zipper dimerization domain is required for interactions with AP-1 proteins and transactivation of transcription. Analyses by electrophoretic mobility shift assays and by an in vivo mammalian two-hybrid system for protein-protein interactions indicate that CHOP interacts with AP-1 proteins inside cells and suggest that it is recruited to the AP-1 complex by a tethering mechanism rather than by direct binding of DNA. Thus, CHOP not only is a negative or a positive regulator of C/EBP target genes but also, when tethered to AP-1 factors, can activate AP-1 target genes. These findings establish the existence of a new mechanism by which CHOP regulates gene expression when cells are exposed to cellular stress.

Indexed as

CCAAT-Enhancer-Binding ProteinsTranscriptional ActivationBasic-Leucine Zipper Transcription FactorsCollagenasesDimerizationDNA-Binding ProteinsG-Box Binding FactorsMacromolecular SubstancesModels, GeneticPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junResponse ElementsTranscription Factor AP-1Transcription Factor CHOPBasic-Leucine Zipper Transcription FactorsCCAAT-Enhancer-Binding ProteinsCollagenasesDNA-Binding ProteinsG-Box Binding FactorsMacromolecular SubstancesProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTranscription Factor AP-1Transcription Factor CHOPTranscription Factors

Identifiers

PMID10523647
PMCPMC84780
OpenAlexW2122399381

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.