ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2005
Mapping and identifying genes for asthma and psoriasis.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled 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.
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
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.
- Chronic Inflammation as the Underlying Mechanism of the Development of Lung Diseases in Psoriasis: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Association between psoriasis and asthma risk: A meta-analysis.Allergy and asthma proceedings · 2018Pooled it
- Co-Occurrence of Psoriasis and Asthma in the Pediatric Population: A Systematic Review and Meta-Analysis.Journal of clinical medicine · 2024Review
- Genome‑wide association study and polygenic risk scores predict psoriasis and its shared phenotypes in Taiwan.Molecular medicine reports · 2024Article
- Cancer-predicting transcriptomic and epigenetic signatures revealed for ulcerative colitis in patient-derived epithelial organoids.Oncotarget · 2018Article
- Psoriasis and Respiratory Comorbidities: The Added Value of Fraction of Exhaled Nitric Oxide as a New Method to Detect, Evaluate, and Monitor Psoriatic Systemic Involvement and Therapeutic Efficacy.BioMed research international · 2018Review
- Different genetic associations of the IgE production among fetus, infancy and childhood.PloS one · 2013Article
- The role of neuropeptide S and neuropeptide S receptor 1 in regulation of respiratory function in mice.Peptides · 2011Article
- Polymorphisms and haplotype analysis of IL-4Ralpha Q576R and I75V in patients with penicillin allergy.European journal of clinical pharmacology · 2009Article
- Global expression profiling in atopic eczema reveals reciprocal expression of inflammatory and lipid genes.PloS one · 2008Article
- Introduction: genetic variation and human health.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Susceptibility genes for complex diseases are characterized by reduced penetrance, caused by the influence of other genes, the environment or stochastic events. Recently, positional cloning efforts have yielded several candidate susceptibility genes in different complex disorders such as Crohn's disease and asthma. Within a genetic locus, however, the identification of the effector gene may pose further challenges and require functional studies. I review two examples of such challenges: the cloning of GPR154 (GPRA) and AAA1 on chromosome 7p14 at a susceptibility locus for atopy and asthma, and the study of HLA-Cw6, CCHCR1 (HCR) and CDSN on chromosome 6p21 at PSORS1, the major susceptibility locus for psoriasis. The susceptibility locus for atopy and asthma contains two genes and only one of them is protein coding. We studied its isoform-specific expression in bronchial biopsies and in a mouse model of ovalbumin-induced inflammation of bronchial epithelia. In the PSORS1 locus, strong linkage disequilibrium between genes has made it difficult to distinguish the effects of the three nearby genes. We engineered transgenic mice with either a HCR non-risk allele or the HCR*WWCC risk allele controlled by the cytokeratin-14 promoter. The results suggested that the overexpression of HCR in mouse skin was insufficient to induce a psoriasiform phenotype, but it appeared to induce allele-specific gene expression changes that were similar to those observed in psoriatic skin.
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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.