%0 Journal Article
%T miRdSNP: a database of disease-associated SNPs and microRNA target sites on 3'UTRs of human genes
%A Andrew E Bruno
%A Li Li
%A James L Kalabus
%A Yuzhuo Pan
%A Aiming Yu
%A Zihua Hu
%J BMC Genomics
%D 2012
%I BioMed Central
%R 10.1186/1471-2164-13-44
%X miRdSNP provides a unique database of dSNPs on the 3'UTRs of human genes manually curated from PubMed. The current release includes 786 dSNP-disease associations for 630 unique dSNPs and 204 disease types. miRdSNP annotates genes with experimentally confirmed targeting by miRNAs and indexes miRNA target sites predicted by TargetScan and PicTar as well as potential miRNA target sites newly generated by dSNPs. A robust web interface and search tools are provided for studying the proximity of miRNA binding sites to dSNPs in relation to human diseases. Searches can be dynamically filtered by gene name, miRBase ID, target prediction algorithm, disease, and any nucleotide distance between dSNPs and miRNA target sites. Results can be viewed at the sequence level showing the annotated locations for miRNA target sites and dSNPs on the entire 3'UTR sequences. The integration of dSNPs with the UCSC Genome browser is also supported.miRdSNP provides a comprehensive data source of dSNPs and robust tools for exploring their distance from miRNA target sites on the 3'UTRs of human genes. miRdSNP enables researchers to further explore the molecular mechanism of gene dysregulation for dSNPs at posttranscriptional level. miRdSNP is freely available on the web at http://mirdsnp.ccr.buffalo.edu webcite.Single nucleotide polymorphisms (SNPs) underlie disease susceptibility through their effects on protein function and gene expression. Most identified mutations are non-synonymous SNPs that result in amino acid changes in proteins. It is well known that non-coding disease-associated SNPs (dSNPs) within regulatory regions of the genome can result in gene dysregulation at either transcriptional or posttranscriptional level. One potential source for the latter is SNPs which create, destroy, or modify the efficiency of miRNA binding to the 3'UTR of a gene. Supporting this idea, SNPs within the miRNA target sites of genes have been implicated in hippocampal sclerosis [1], parkinson disease [2],
%U http://www.biomedcentral.com/1471-2164/13/44