ArticleGenes and immunity2009
Human V-ATPase gene can protect or predispose the host to pulmonary tuberculosis.
Article in Genes and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026Review
- Discovery of a Small-Molecule Probe for V-ATPase Function.Journal of the American Chemical Society · 2015Article
- Epiregulin (EREG) and human V-ATPase (TCIRG1): genetic variation, ethnicity and pulmonary tuberculosis susceptibility in Guinea-Bissau and The Gambia.Genes and immunity · 2014Article
- PA1b inhibitor binding to subunits c and e of the vacuolar ATPase reveals its insecticidal mechanism.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients (305 patients with pulmonary tuberculosis) and controls (290 household genetically unrelated contacts) were tested by polymerase chain reaction (PCR) for polymorphisms in the intron 15 and the 5' untranslated region of the gene coding for the a3 isoform of the human ATPase gene. Diagnosis of pulmonary tuberculosis was based on chest radiography and sputum smear examination and confirmed by PCR and bacteriological tests. Alleles (two at each site) segregated in the form of four haplotype pairs: 13, 14 (very rare), 23, and 24. The 13/24 (double heterozygous) patients were protected against tuberculosis (OR: 0.15; P: 10(-8); CI: 0.08-0.3). The 13/13 vs 13/24 and 23/23 vs 23/24 (double homozygous) patients were susceptible to the disease (OR. 5.8; P: 6 x 10(-7); CI: 2.8-11.9; OR: 4.5; P: 5 x 10(-7); CI: 2.5-8.4, respectively).
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Registered trials
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