Hui Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Hui Wang has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Adaikalavan Ramasamy
Respiratory Epidemiology and Public Health Group, National Heart and Lung Institute, Imperial College London, London, UK
1 shared publication - Alexessander Couto Alves
School of Human Development and Health, Faculty of Medicine, University of Southampton, Southampton SO17 1BJ, UK
1 shared publication - Fredrik Barrenas
The Center for Individualized Medication, Linköping University Hospital, 58185, Linköping, Sweden
1 shared publication - Gary L. Rogers
Department of Electrical Engineering and Computer Science, University of Tennessee, Knoxville, TN 37996, USA
1 shared publication - Lachlan J. M. Coin
Department of Microbiology and Immunology, The University of Melbourne, at the Peter Doherty Institute for Infection and Immunity
1 shared publication - Marjo-Riitta Järvelin
Research Unit of Population Health, Faculty of Medicine, University of Oulu, Oulu, Finland
1 shared publication
Latest Publications
- Open Access
- 15 June 2012
- Published by Springer Nature in Genome Biology
- Vol. 13 (6) , R46
Highly interconnected genes in disease-specific networks are enriched for disease-associated polymorphisms
Background: Complex diseases are associated with altered interactions between thousands of genes. We developed a novel method to identify and prioritize disease genes, which was generally applicable to complex diseases. Results: We identified modules of highly interconnected genes in disease-specific networks derived from integrating gene-expression and protein interaction data. We examined if those modules were enriched for disease-associated SNPs, and could be used to find novel genes for functional studies. First, we analyzed publicly available gene expression microarray and genome-wide association study (GWAS) data from 13, highly diverse, complex diseases. In each disease, highly interconnected genes formed modules, which were significantly enriched for genes harboring disease-associated SNPs. To test if such modules could be used to find novel genes for functional studies, we repeated the analyses using our own gene expression microarray and GWAS data from seasonal allergic rhinitis. We identified a novel gene, FGF2, whose relevance was supported by functional studies using combined small interfering RNA-mediated knock-down and gene expression microarrays. The modules in the 13 complex diseases analyzed here tended to overlap and were enriched for pathways related to oncological, metabolic and inflammatory diseases. This suggested that this union of the modules would be associated with a general increase in susceptibility for complex diseases. Indeed, we found that this union was enriched with GWAS genes for 145 other complex diseases. Conclusions: Modules of highly interconnected complex disease genes were enriched for disease-associated SNPs, and could be used to find novel genes for functional studies.
- 15 June 2012
- Published by Springer Nature in Genome Biology
- Vol. 13 (6) , R46
Open AccessHighly interconnected genes in disease-specific networks are enriched for disease-associated polymorphisms
Background: Complex diseases are associated with altered interactions between thousands of genes. We developed a novel method to identify and prioritize disease genes, which was generally applicable to complex diseases. Results: We identified modules of highly interconnected genes in disease-specific networks derived from integrating gene-expression and protein interaction data. We examined if those modules were enriched for disease-associated SNPs, and could be used to find novel genes for functional studies. First, we analyzed publicly available gene expression microarray and genome-wide association study (GWAS) data from 13, highly diverse, complex diseases. In each disease, highly interconnected genes formed modules, which were significantly enriched for genes harboring disease-associated SNPs. To test if such modules could be used to find novel genes for functional studies, we repeated the analyses using our own gene expression microarray and GWAS data from seasonal allergic rhinitis. We identified a novel gene, FGF2, whose relevance was supported by functional studies using combined small interfering RNA-mediated knock-down and gene expression microarrays. The modules in the 13 complex diseases analyzed here tended to overlap and were enriched for pathways related to oncological, metabolic and inflammatory diseases. This suggested that this union of the modules would be associated with a general increase in susceptibility for complex diseases. Indeed, we found that this union was enriched with GWAS genes for 145 other complex diseases. Conclusions: Modules of highly interconnected complex disease genes were enriched for disease-associated SNPs, and could be used to find novel genes for functional studies.