LincSNP: a database of linking disease-associated SNPs to human large intergenic non-coding RNAs

BMC Bioinformatics. 2014 May 20:15:152. doi: 10.1186/1471-2105-15-152.

Abstract

Background: Genome-wide association studies (GWAS) have successfully identified a large number of single nucleotide polymorphisms (SNPs) that are associated with a wide range of human diseases. However, many of these disease-associated SNPs are located in non-coding regions and have remained largely unexplained. Recent findings indicate that disease-associated SNPs in human large intergenic non-coding RNA (lincRNA) may lead to susceptibility to diseases through their effects on lincRNA expression. There is, therefore, a need to specifically record these SNPs and annotate them as potential candidates for disease.

Description: We have built LincSNP, an integrated database, to identify and annotate disease-associated SNPs in human lincRNAs. The current release of LincSNP contains approximately 140,000 disease-associated SNPs (or linkage disequilibrium SNPs), which can be mapped to around 5,000 human lincRNAs, together with their comprehensive functional annotations. The database also contains annotated, experimentally supported SNP-lincRNA-disease associations and disease-associated lincRNAs. It provides flexible search options for data extraction and searches can be performed by disease/phenotype name, SNP ID, lincRNA name and chromosome region. In addition, we provide users with a link to download all the data from LincSNP and have developed a web interface for the submission of novel identified SNP-lincRNA-disease associations.

Conclusions: The LincSNP database aims to integrate disease-associated SNPs and human lincRNAs, which will be an important resource for the investigation of the functions and mechanisms of lincRNAs in human disease. The database is available at http://bioinfo.hrbmu.edu.cn/LincSNP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Databases, Nucleic Acid*
  • Disease / genetics*
  • Genome-Wide Association Study
  • Humans
  • Linkage Disequilibrium
  • Phenotype
  • Polymorphism, Single Nucleotide*
  • RNA, Long Noncoding / genetics*
  • Software

Substances

  • RNA, Long Noncoding