Evidence map›Paper›PMID 15316101›Full record

ArticleNucleic acids research2004

MAGE-A1 interacts with adaptor SKIP and the deacetylase HDAC1 to repress transcription.

Sandra Laduron, Rachel Deplus, Sifang Zhou, Olga Kholmanskikh, Danièle Godelaine, Charles De Smet, S Diane Hayward, François Fuks, Thierry Boon, Etienne De Plaen

Open access · greenAbstract read
In one paragraph

Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Cancer regression and neurological toxicity following anti-MAGE-A3 TCR gene therapy.Journal of immunotherapy (Hagerstown, Md. : 1997) · 2013
    Trial
  3. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. SKIP Silencing Decreased Disease Resistance AgainstFrontiers in plant science · 2020
    Article
  13. Review
  14. PLAC1: biology and potential application in cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2019
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

Sandra LaduronLudwig Institute for Cancer Research, Brussels branch, and Cellular Genetics Unit, Université Catholique de Louvain, Brussels B1200, Belgium.
Rachel Deplus
Sifang Zhou
Olga Kholmanskikh
Danièle Godelaine
Charles De Smet
S Diane Hayward
François Fuks
Thierry Boon
Etienne De Plaen
Ludwig Cancer Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MAGE-A1 belongs to a family of 12 genes that are active in various types of tumors and silent in normal tissues except in male germ-line cells. The MAGE-encoded antigens recognized by T cells are highly tumor-specific targets for T cell-oriented cancer immunotherapy. The function of MAGE-A1 is currently unknown. To analyze it, we attempted to identify protein partners of MAGE-A1. Using yeast two-hybrid screening, we detected an interaction between MAGE-A1 and Ski Interacting Protein (SKIP). SKIP is a transcriptional regulator that connects DNA-binding proteins to proteins that either activate or repress transcription. We show that MAGE-A1 inhibits the activity of a SKIP-interacting transactivator, namely the intracellular part of Notch1. Deletion analysis indicated that this inhibition requires the binding of MAGE-A1 to SKIP. Moreover, MAGE-A1 was found to actively repress transcription by binding and recruiting histone deacetylase 1 (HDAC1). Our results indicate that by binding to SKIP and by recruiting HDACs, MAGE-A1 can act as a potent transcriptional repressor. MAGE-A1 could therefore participate in the setting of specific gene expression patterns for tumor cell growth or spermatogenesis.

Indexed as

Gene SilencingTranscription FactorsAnimalsAntigens, NeoplasmChlorocebus aethiopsCOS CellsHeLa CellsHistone Deacetylase 1Histone DeacetylasesHumansMelanoma-Specific AntigensNeoplasm ProteinsNuclear ProteinsNuclear Receptor CoactivatorsReceptor, Notch1Receptors, Cell SurfaceAntigens, NeoplasmHDAC1 protein, humanHistone Deacetylase 1Histone DeacetylasesMelanoma-Specific AntigensNeoplasm ProteinsNOTCH1 protein, humanNuclear ProteinsNuclear Receptor CoactivatorsReceptor, Notch1Receptors, Cell SurfaceRepressor ProteinsSNW1 protein, humanTranscription Factors

Identifiers

PMID15316101
PMCPMC514365
OpenAlexW1975522366

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.