ArticleJournal of human genetics2008
Association study of the C3 gene with adult and childhood asthma.
Article in Journal of human genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Study on the Interaction Between C3 Gene Polymorphism and Environment in Patients with Type 2 Diabetes Combined with Coronary Artery Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Trial
- Proteomic Profile Differences in Immune-Related Diseases in Pediatric Patients Under Five Years Old: Asthma and IgE-Dependent Allergies-A Pilot Study.International journal of molecular sciences · 2026Article
- Complement's involvement in allergic Th2 immunity: a cross-barrier perspective.The Journal of clinical investigation · 2025Review
- Genetic contributions to pain modulation in sickle cell: A focus on single nucleotide polymorphisms.Gene reports · 2024Article
- Complement C1q essential for aeroallergen sensitization via CSF1RThe Journal of allergy and clinical immunology · 2023Article
- C3a is required for ILC2 function in allergic airway inflammation.Mucosal immunology · 2018Article
- Genes associated with RSV lower respiratory tract infection and asthma: the application of genetic epidemiological methods to understand causality.Future virology · 2015Article
- Genome-wide association study for serum complement C3 and C4 levels in healthy Chinese subjects.PLoS genetics · 2012Article
- Is asthma related to choroidal neovascularization?PloS one · 2012Article
- Adjuvant effects of ambient particulate matter monitored by proteomics of bronchoalveolar lavage fluid.Proteomics · 2010Article
- The heritability and genetics of complement C3 expression in UK SLE families.Genes and immunity · 2009Article
- An imbalance in C/EBPs and increased mitochondrial activity in asthmatic airway smooth muscle cells: novel targets in asthma therapy?British journal of pharmacology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchial asthma (BA) is a multifactorial disorder, the development of which is affected by both environmental and genetic factors. The complement system plays an important role in immunological response against invading microorganisms. It has been shown that complement-C3-deficient mice have reduced inflammation of asthmatic airways. Previously, we reported the association of four single nuclear proteins (SNPs) in the exons of the C3 gene with childhood and adult BA. The C3 gene, however, is a large gene, and functional SNPs associated with susceptibility to BA have not yet been identified. We analyzed 26 SNPs in the C3 gene and its promoter region to narrow down the regions showing association with childhood and adult BA. Childhood and adult atopic BA patients and healthy child and adult controls were recruited from urban cities in Japan and genotyped. In SNP analysis, an SNP (SNP24, rs11569562) located in intron 31 of the C3 gene was associated with adult BA [corrected P (Pcor) = 0.030]. In linkage disequilibrium (LD) block 4 spanning exons 24-41, the frequency of the CCC haplotype in adult BA was significantly higher than that in adult controls (Pcor = 0.038). Neither the SNP nor the haplotype showing association with adult BA demonstrated a significant association with serum total immunoglobulin E (IgE) level in BA patients and controls. Our results suggest that LD block 4 confers susceptibility to adult BA with mechanisms relevant to the effector phase of allergic inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.