1. A disease module in the interactome explains disease heterogeneity, drug response and captures novel pathways and genes in asthma.

    Human Molecular Genetics 24(11):3005 (2015) PMID 25586491 PMCID PMC4447811

    Recent advances in genetics have spurred rapid progress towards the systematic identification of genes involved in complex diseases. Still, the detailed understanding of the molecular and physiological mechanisms through which these genes affect disease phenotypes remains a major challenge. Here...
  2. Human gene-centered transcription factor networks for enhancers and disease variants.

    Cell 161(3):661 (2015) PMID 25910213 PMCID PMC4409666

    Gene regulatory networks (GRNs) comprising interactions between transcription factors (TFs) and regulatory loci control development and physiology. Numerous disease-associated mutations have been identified, the vast majority residing in non-coding regions of the genome. As current GRN mapping m...
  3. Widespread macromolecular interaction perturbations in human genetic disorders.

    Cell 161(3):647 (2015) PMID 25910212 PMCID PMC4441215

    How disease-associated mutations impair protein activities in the context of biological networks remains mostly undetermined. Although a few renowned alleles are well characterized, functional information is missing for over 100,000 disease-associated variants. Here we functionally profile sever...
  4. Protein domain-level landscape of cancer-type-specific somatic mutations.

    PLoS computational biology 11(3):e1004147 (2015) PMID 25794154 PMCID PMC4368709

    Identifying driver mutations and their functional consequences is critical to our understanding of cancer. Towards this goal, and because domains are the functional units of a protein, we explored the protein domain-level landscape of cancer-type-specific somatic mutations. Specifically, we syst...
  5. Disease networks. Uncovering disease-disease relationships through the incomplete interactome.

    Science 347(6224):1257601 (2015) PMID 25700523 PMCID PMC4435741

    According to the disease module hypothesis, the cellular components associated with a disease segregate in the same neighborhood of the human interactome, the map of biologically relevant molecular interactions. Yet, given the incompleteness of the interactome and the limited knowledge of diseas...
  6. Uncovering disease-disease relationships through the incomplete interactome.

    Science 347(6224) (2015) PMID 25700523

    According to the disease module hypothesis, the cellular components associated with a disease segregate in the same neighborhood of the human interactome, the map of biologically relevant molecular interactions. Yet, given the incompleteness of the interactome and the limited knowledge of diseas...
  7. Disease networks. Uncovering disease-disease relationships through the incomplete interactome.

    Science 347(6224):1257601 (2015) PMID 25700523

    According to the disease module hypothesis, the cellular components associated with a disease segregate in the same neighborhood of the human interactome, the map of biologically relevant molecular interactions. Yet, given the incompleteness of the interactome and the limited knowledge of diseas...
  8. Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases.

    Neuron 85(4):742 (2015) PMID 25695269 PMCID PMC4335356

    The psychiatric disorders autism and schizophrenia have a strong genetic component, and copy number variants (CNVs) are firmly implicated. Recurrent deletions and duplications of chromosome 16p11.2 confer a high risk for both diseases, but the pathways disrupted by this CNV are poorly defined. H...
  9. Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases.

    Neuron 85(4):742 (2015) PMID 25695269

    The psychiatric disorders autism and schizophrenia have a strong genetic component, and copy number variants (CNVs) are firmly implicated. Recurrent deletions and duplications of chromosome 16p11.2 confer a high risk for both diseases, but the pathways disrupted by this CNV are poorly defined. H...
  10. Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases.

    Neuron 85(4):742 (2015) PMID 25695269 PMCID PMC4335356

    The psychiatric disorders autism and schizophrenia have a strong genetic component, and copy number variants (CNVs) are firmly implicated. Recurrent deletions and duplications of chromosome 16p11.2 confer a high risk for both diseases, but the pathways disrupted by this CNV are poorly defined. H...
  11. Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases.

    Neuron 85(4):742 (2015) PMID 25695269

    The psychiatric disorders autism and schizophrenia have a strong genetic component, and copy number variants (CNVs) are firmly implicated. Recurrent deletions and duplications of chromosome 16p11.2 confer a high risk for both diseases, but the pathways disrupted by this CNV are poorly defined. H...
  12. Selecting causal genes from genome-wide association studies via functionally coherent subnetworks.

    Nature Methods 12(2):154 (2015) PMID 25532137 PMCID PMC4480866

    Genome-wide association (GWA) studies have linked thousands of loci to human diseases, but the causal genes and variants at these loci generally remain unknown. Although investigators typically focus on genes closest to the associated polymorphisms, the causal gene is often more distal. Reliance...
  13. Selecting causal genes from genome-wide association studies via functionally coherent subnetworks.

    Nature Methods 12(2):154 (2015) PMID 25532137

    Genome-wide association (GWA) studies have linked thousands of loci to human diseases, but the causal genes and variants at these loci generally remain unknown. Although investigators typically focus on genes closest to the associated polymorphisms, the causal gene is often more distal. Reliance...
  14. Selecting causal genes from genome-wide association studies via functionally coherent subnetworks.

    Nature Methods 12(2):154 (2015) PMID 25532137

    Genome-wide association (GWA) studies have linked thousands of loci to human diseases, but the causal genes and variants at these loci generally remain unknown. Although investigators typically focus on genes closest to the associated polymorphisms, the causal gene is often more distal. Reliance...
  15. The yeast two-hybrid assay: still finding connections after 25 years.

    Nature Methods 11(12):1203 (2014) PMID 25584376

  16. The yeast two-hybrid assay: still finding connections after 25 years.

    Nature Methods 11(12):1203 (2014) PMID 25584376

  17. The yeast two-hybrid assay: still finding connections after 25 years.

    Nature Methods 11(12):1203 (2014) PMID 25584376

  18. Multiplex single-molecule interaction profiling of DNA-barcoded proteins.

    Nature 515(7528):554 (2014) PMID 25252978 PMCID PMC4246050

    In contrast with advances in massively parallel DNA sequencing, high-throughput protein analyses are often limited by ensemble measurements, individual analyte purification and hence compromised quality and cost-effectiveness. Single-molecule protein detection using optical methods is limited by...
  19. Multiplex single-molecule interaction profiling of DNA-barcoded proteins.

    Nature 515(7528):554 (2014) PMID 25252978 PMCID PMC4246050

    In contrast with advances in massively parallel DNA sequencing, high-throughput protein analyses are often limited by ensemble measurements, individual analyte purification and hence compromised quality and cost-effectiveness. Single-molecule protein detection using optical methods is limited by...
  20. Multiplex single-molecule interaction profiling of DNA-barcoded proteins.

    Nature 515(7528):554 (2014) PMID 25252978 PMCID PMC4246050

    In contrast with advances in massively parallel DNA sequencing, high-throughput protein analyses are often limited by ensemble measurements, individual analyte purification and hence compromised quality and cost-effectiveness. Single-molecule protein detection using optical methods is limited by...