Disease-miRNAdb: a manually-curated database for the investigation of the microRNA-human disease relationship

Authors
Shin, Jae MoonLim, WooyoungLee, Kyung-MiWon, Jung ImJung, Da WoonNho, Chu WonKang, Kui DongYoon, Jee HeeCho, Yoon Shin
Issue Date
2017-12
Publisher
SPRINGER
Citation
GENES & GENOMICS, v.39, no.12, pp.1419 - 1424
Abstract
MicroRNAs (miRNA) of approximately 22 nucleotides are fundamental molecules in cellular biology that act by modulating target gene expression. As a post-transcriptional/translational regulator, the role of miRNAs in human disease is highly expected. Recently, a rising number of miRNAs that are associated with a variety of human diseases have been reported in the literature. Aiming to provide a comprehensive of resource of miRNAs that are related to the human disease, we built the Disease miRNA Database (Disease-miRNAdb). MiRNAs from three groups of diseases including kidney disease, cancer, and metabolic disease were manually curated in the current version of database located on a user-friendly online website (http://disease-miRNAdb.hallym.ac.kr). In addition, this database also includes information regarding single nucleotide polymorphisms (SNPs) located in pre-miRNAs, miRNA flanking regions, and 3'-UTRs of miRNA target genes. The generation of genetic variation in these regions may result in a loss or gain of miRNA-target gene interactions, which may influence the development of disease. Thus, information regarding miRNA-related SNPs will be useful in the discovery of disease-associated miRNAs in human populations by employing SNP association analysis for the disease of interest. Disease-miRNAdb will be continually maintained with up-to-date information to provide a current and valuable resource for investigating the roles of miRNAs in human disease.
Keywords
ASSOCIATION; ASSOCIATION; MicroRNA; MicroRNA target gene; Diseases; Database; Single nucleotide polymorphism
ISSN
1976-9571
URI
https://pubs.kist.re.kr/handle/201004/122007
DOI
10.1007/s13258-017-0628-2
Appears in Collections:
KIST Article > 2017
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