Evidence map›Paper›PMID 15179560›Full record

ArticleJournal of human genetics2004

Association between genetic variation in the gene for death-associated protein-3 (DAP3) and adult asthma.

Tomomitsu Hirota, Kazuhiko Obara, Akira Matsuda, Mitsuteru Akahoshi, Kazuko Nakashima, Koichi Hasegawa, Naomi Takahashi, Makiko Shimizu, Hiroshi Sekiguchi, Miki Kokubo and 11 more

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In one paragraph

Article in Journal of human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. 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

21 authors at 10 institutions in 1 country.

Tomomitsu HirotaLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Kazuhiko ObaraLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Akira MatsudaLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Mitsuteru AkahoshiLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Kazuko NakashimaDepartment of Health Promotion and Human Behavior, Kyoto University Graduate School of Public Health, Kyoto, Japan.
Koichi HasegawaDepartment of Health Promotion and Human Behavior, Kyoto University Graduate School of Public Health, Kyoto, Japan.
Naomi TakahashiLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Makiko ShimizuLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Hiroshi SekiguchiLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Miki KokuboLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Satoru DoiOsaka Prefectural Habikino Hospital, Osaka, Japan.
Hiroshi FujiwaraOsaka Prefectural Habikino Hospital, Osaka, Japan.
Akihiko MiyatakeMiyatake Asthma Clinic, Osaka, Japan.
Kimie FujitaCollege of Nursing, University of Shiga, Shiga, Japan.
Tadao EnomotoWakayama Medical Center, Japanese Red Cross Society, Wakayama, Japan.
Fumio KishiDepartment of Microbiology and Immunology, Kagoshima University Dental School, Kagoshima, Japan.
Yoichi SuzukiDepartment of Medical Genetics, Tohoku University School of Medicine, Sendai, Japan.
Hirohisa SaitoDepartment of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
Yusuke NakamuraLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Taro ShirakawaLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan.
Mayumi TamariLaboratory for Genetics of Allergic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa 230-0045, Japan. tamari@src.riken.go.jp.
RIKEN · JPKyoto University · JPOsaka Prefectural Makino high school · JPRIKEN Center for Integrative Medical Sciences · JPJapanese Red Cross Society Wakayama Medical Center · JPKagoshima University · JPNational Center For Child Health and Development · JPShiga University · JPThe University of Tokyo · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung epithelium plays a central role in modulation of the lung inflammatory response, and lung repair and airway epithelial cells are targets in asthma and viral infection. Activated T lymphocytes release cytokines such as interferon-gamma (IFN-gamma) that induce apoptosis, or programmed cell death, of damaged epithelial cells. Death-associated protein-3 (DAP3) is involved in mediating IFN-gamma-induced cell death. To assess the possible involvement of genetic variants of DAP3 with asthma, we searched for single-nucleotide polymorphisms (SNPs) in the gene and conducted a case-control study with 1,341 subjects. We found a strong association between bronchial asthma (BA) in adults (P=0.0051, odds ratio=1.87, 95% CI=1.20-2.92), whereas no association was found with childhood asthma. The tendency was more prominent in patients with higher serum total immunoglobulin E (IgE) (>250 IU/ml) (P=0.00061, odds ratio=2.40, 95% CI=1.44-4.00). DAP3 was expressed in normal bronchial epithelial cells, and the expression was induced by IFN-gamma. These results indicated that specific variants of the DAP3 gene might be associated with the mechanisms responsible for adult BA and contribute to airway inflammation and remodeling.

Indexed as

Genetic VariationAdolescentAdultAgedAged, 80 and overAllelesApoptosisApoptosis Regulatory ProteinsAsthmaCase-Control StudiesCell DeathChildChild, PreschoolEpithelial CellsFemaleGene FrequencyApoptosis Regulatory ProteinsDAP3 protein, humanImmunoglobulin EInterferon-gammaProteinsRibosomal ProteinsRNA-Binding Proteins

Identifiers

PMID15179560
OpenAlexW2062038151

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.