Evidence map›Paper›PMID 23235109›Full record

ArticleEpigenetics2013

DNA demethylation and histone H3K9 acetylation determine the active transcription of the NKG2D gene in human CD8+ T and NK cells.

Alba Fernández-Sánchez, Aroa Baragaño Raneros, Reyes Carvajal Palao, Ana B Sanz, Alberto Ortiz, Francisco Ortega, Beatriz Suárez-Álvarez, Carlos López-Larrea

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.4field-weighted citation impact, top 20% 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, 63 citations in OpenAlex.

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  4. Killing the killers: Natural killer cell therapy targeting glioma stem cells in high-grade glioma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  12. What nature has to offer: Opportunities for immuno-oncology.Journal of food and drug analysis · 2023
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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

8 authors at 3 institutions in 1 country.

Alba Fernández-SánchezDepartment of Immunology, Hospital Universitario Central de Asturias, Oviedo, Spain.
Aroa Baragaño Raneros
Reyes Carvajal Palao
Ana B Sanz
Alberto Ortiz
Francisco Ortega
Beatriz Suárez-Álvarez
Carlos López-Larrea
Hospital Universitario Central de Asturias · ESFundación Renal Española · ESHospital Universitario La Paz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human activating receptor NKG2D is mainly expressed by NK, NKT, γδ T and CD8(+) T cells and, under certain conditions, by CD4(+) T cells. This receptor recognizes a diverse family of ligands (MICA, MICB and ULBPs 1-6) leading to the activation of effector cells and triggering the lysis of target cells. The NKG2D receptor-ligand system plays an important role in the immune response to infections, tumors, transplanted graft and autoantigens. Elucidation of the regulatory mechanisms of NKG2D is therefore essential for therapeutic purposes. In this study, we speculate whether epigenetic mechanisms, such as DNA methylation and histone acetylation, participate in NKG2D gene regulation in T lymphocytes and NK cells. DNA methylation in the NKG2D gene was observed in CD4(+) T lymphocytes and T cell lines (Jurkat and HUT78), while this gene was unmethylated in NKG2D-positive cells (CD8(+) T lymphocytes, NK cells and NKL cell line) and associated with high levels of histone H3 lysine 9 acetylation (H3K9Ac). Treatment with the histone acetyltransferase (HAT) inhibitor curcumin reduces H3K9Ac levels in the NKG2D gene, downregulates NKG2D transcription and leads to a marked reduction in the lytic capacity of NKG2D-mediated NKL cells. These findings suggest that differential NKG2D expression in the different cell subsets is regulated by epigenetic mechanisms and that its modulation by epigenetic treatments might provide a new strategy for treating several pathologies.

Indexed as

Transcription, GeneticAcetylationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell DegranulationCurcuminCytotoxicity, ImmunologicDNA MethylationDown-RegulationEnzyme InhibitorsHistone Deacetylase InhibitorsHistonesHumansInterferon-gammaJurkat CellsKiller Cells, NaturalCurcuminEnzyme InhibitorsHistone Deacetylase InhibitorsHistonesInterferon-gammaKLRK1 protein, humanLysineNK Cell Lectin-Like Receptor Subfamily KcurcumincytotoxicityDNA methylationH3K9 acetylationKLRK1geneNKG2D receptor

Identifiers

PMID23235109
PMCPMC3549882
OpenAlexW1990889144

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.