DISNOR is a new resource that aims at exploiting the explosion of data on the identification of diseaseassociated genes to assemble inferred disease pathways. This may help dissecting the signaling events whose disruption causes the pathological phenotypes and may contribute to build a platform for precision medicine. To this end we combine the genedisease association (GDA) data annotated in the DisGeNET resource with a new curation effort aimed at populating the SIGNOR database with causal interactions related to disease genes with the highest possible coverage. DISNOR can be freely accessed at http://DISNOR.uniroma2.it/where >3700 disease-networks, linking similar to 2600 disease genes, can be explored. For each disease curated in DisGeNET, DISNOR links disease genes by manually annotated causal relationships and offers an intuitive visualization of the inferred 'patho-pathways' at different complexity levels. User- defined gene lists are also accepted in the query pipeline. In addition, for each list of query genes-either annotated in DisGeNET or user-defined-DISNOR performs a gene set enrichment analysis on KEGG-defined pathways or on the lists of proteins associated with the inferred disease pathways. This function offers additional information on disease- associated cellular pathways and disease similarity.

Lo Surdo, P., Calderone, A., Iannuccelli, M., Licata, L., Peluso, D., Castagnoli, L., et al. (2018). DISNOR: A disease network open resource. NUCLEIC ACIDS RESEARCH, 46(D1), D527-D534 [10.1093/nar/gkx876].

DISNOR: A disease network open resource

Calderone A.;Iannuccelli M.;Licata L.;Castagnoli L.;Cesareni G.;Perfetto L.
2018-01-04

Abstract

DISNOR is a new resource that aims at exploiting the explosion of data on the identification of diseaseassociated genes to assemble inferred disease pathways. This may help dissecting the signaling events whose disruption causes the pathological phenotypes and may contribute to build a platform for precision medicine. To this end we combine the genedisease association (GDA) data annotated in the DisGeNET resource with a new curation effort aimed at populating the SIGNOR database with causal interactions related to disease genes with the highest possible coverage. DISNOR can be freely accessed at http://DISNOR.uniroma2.it/where >3700 disease-networks, linking similar to 2600 disease genes, can be explored. For each disease curated in DisGeNET, DISNOR links disease genes by manually annotated causal relationships and offers an intuitive visualization of the inferred 'patho-pathways' at different complexity levels. User- defined gene lists are also accepted in the query pipeline. In addition, for each list of query genes-either annotated in DisGeNET or user-defined-DISNOR performs a gene set enrichment analysis on KEGG-defined pathways or on the lists of proteins associated with the inferred disease pathways. This function offers additional information on disease- associated cellular pathways and disease similarity.
4-gen-2018
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/18 - GENETICA
English
Data Curation; Disease; Gene Regulatory Networks; Genetic Association Studies; Humans; Internet; Mutation; Polymorphism, Single Nucleotide; Search Engine; Signal Transduction; Software; User-Computer Interface; Databases, Genetic
Lo Surdo, P., Calderone, A., Iannuccelli, M., Licata, L., Peluso, D., Castagnoli, L., et al. (2018). DISNOR: A disease network open resource. NUCLEIC ACIDS RESEARCH, 46(D1), D527-D534 [10.1093/nar/gkx876].
Lo Surdo, P; Calderone, A; Iannuccelli, M; Licata, L; Peluso, D; Castagnoli, L; Cesareni, G; Perfetto, L
Articolo su rivista
File in questo prodotto:
File Dimensione Formato  
DISNOR2018.pdf

solo utenti autorizzati

Descrizione: articolo preincipale
Licenza: Copyright dell'editore
Dimensione 2.2 MB
Formato Adobe PDF
2.2 MB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/234331
Citazioni
  • ???jsp.display-item.citation.pmc??? 24
  • Scopus 33
  • ???jsp.display-item.citation.isi??? 28
social impact