Evidence map›Paper›PMID 12697811›Full record

ArticleMolecular and cellular biology2003

Histone deacetylase 1/mSin3A disrupts gamma interferon-induced CIITA function and major histocompatibility complex class II enhanceosome formation.

Eleni Zika, Susanna F Greer, Xin-Sheng Zhu, Jenny P-Y Ting

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Chromatin-Remodeling Factor BRG1 Is a Negative Modulator ofFrontiers in cellular and infection microbiology · 2022
    Article
  5. Article
  6. Histone deacetylase inhibition promotes intratumoral CD8Cancer immunology, immunotherapy : CII · 2019
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. The Journal of biological chemistry · 2017
    Article
  12. Metastatic melanoma cells evade immune detection by silencing STAT1.International journal of molecular sciences · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

4 authors at 3 institutions in 2 countries.

Eleni ZikaCurriculum in Genetics and Molecular Biology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
Susanna F Greer
Xin-Sheng Zhu
Jenny P-Y Ting
UNC Lineberger Comprehensive Cancer CenterSegeberger Kliniken · DEUniversity of North Carolina at Chapel Hill · US

Funding

PHS HHS 29564PHS HHS 41751PHS HHS 45580
6 · The paper itself

Abstract

The class II transactivator (CIITA) is a master transcriptional regulator of major histocompatibility complex class II (MHC-II) promoters. CIITA does not bind DNA, but it interacts with the transcription factors RFX5, NF-Y, and CREB and associated chromatin-modifying enzymes to form an enhanceosome. This report examines the effects of histone deacetylases 1 and 2 (HDAC1/HDAC2) on MHC-II gene induction by gamma interferon (IFN-gamma) and CIITA. The results show that an inhibitor of HDACs, trichostatin A, enhances IFN-gamma-induced MHC-II expression, while HDAC1/HDAC2 inhibits IFN-gamma- and CIITA-induced MHC-II gene expression. mSin3A, a corepressor of HDAC1/HDAC2, is important for this inhibition, while NcoR, a corepressor of HDAC3, is not. The effect of this inhibition is directed at CIITA, since HDAC1/HDAC2 reduces transactivation by a GAL4-CIITA fusion protein. CIITA binds to overexpressed and endogenous HDAC1, suggesting that HDAC and CIITA may affect each other by direct or indirect association. Inhibition of HDAC activity dramatically increases the association of NF-YB and RFX5 with CIITA, the assembly of CIITA, NF-YB, and RFX5 enhanceosome, and the extent of H3 acetylation at the MHC-II promoter. These results suggest a model where HDAC1/HDAC2 affect the function of CIITA through a disruption of MHC-II enhanceosome and relevant coactivator-transcription factor association and provide evidence that CIITA may act as a molecular switch to modulate MHC-II transcription by coordinating the functions of both histone acetylases and HDACs.

Indexed as

AcetylationAnimalsCCAAT-Binding FactorCells, CulturedCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsEnzyme InhibitorsGene Expression RegulationGenes, MHC Class IIHistocompatibility Antigens Class IIHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansCCAAT-Binding FactorCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsEnzyme InhibitorsHDAC1 protein, humanHistocompatibility Antigens Class IIHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsInterferon-gammaMacromolecular SubstancesMHC class II transactivator proteinNCOR1 protein, humanNuclear ProteinsNuclear Receptor Co-Repressor 1Recombinant Fusion ProteinsRegulatory Factor X Transcription FactorsRepressor ProteinsRFX5 protein, humanSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTrans-ActivatorsTranscription Factorstrichostatin A

Identifiers

PMID12697811
PMCPMC153210
OpenAlexW2141661046

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.