MicroRNA regulation of key biological and developmental pathways is a rapidly expanding area of research, accompanied by vast amounts of experimental data. This data, however, is not widely available in bioinformatic resources, making it difficult for researchers to find and analyze microRNA-related experimental data and define further research projects. We are addressing this problem by providing two new bioinformatics data sets that contain experimentally verified functional information for mammalian microRNAs involved in cardiovascular-relevant, and other, processes. To date, our resource provides over 4400 Gene Ontology annotations associated with over 500 microRNAs from human, mouse, and rat and over 2400 experimentally validated microRNA:target interactions. We illustrate how this resource can be used to create microRNA-focused interaction networks with a biological context using the known biological role of microRNAs and the mRNAs they regulate, enabling discovery of associations between gene products, biological pathways and, ultimately, diseases. This data will be crucial in advancing the field of microRNA bioinformatics and will establish consistent data sets for reproducible functional analysis of microRNAs across all biological research areas.
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http://dx.doi.org/10.1261/rna.065565.118 | DOI Listing |
J Mol Histol
January 2025
Department of Structural and Functional Biology, University of Campinas (UNICAMP), Campinas, SP, Brazil.
This study investigated tempol action on genes and miRNAs related to NFκB pathway in androgen dependent or independent cell lines and in TRAMP model in the early and late-stages of cancer progression. A bioinformatic search was conducted to select the miRNAs to be measured based on the genes of interest from NFκB pathway. The miR-let-7c-5p, miR-26a-5p and miR-155-5p and five target genes (BCL2, BCL2L1, RELA, TNF, PTGS2) were chosen for RT-PCR and gene enrichment analyses.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Shandong Trauma Center, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, Shandong, 250014, People's Republic of China.
Background: Posttraumatic elbow stiffness is a complex complication with two characteristics of capsular contracture and heterotopic ossification. Currently, genomic mechanisms and pathogenesis of posttraumatic elbow stiffness remain inadequately understood. This study aims to identify differentially expressed genes (DEGs) and elucidate molecular networks of posttraumatic elbow stiffness, providing novel insights into disease mechanisms at transcriptome level.
View Article and Find Full Text PDFBiochem Biophys Rep
March 2025
Center for Medical Laboratory Science, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, 533000, China.
Background: Intrauterine exposure to gestational diabetes mellitus (GDM) poses significant risks to fetal development and future metabolic health. Despite its clinical importance, the role of microRNAs (miRNAs) in fetoplacental vascular endothelial cell (VEC) programming in the context of GDM remains elusive. This study aims to identify signature miRNA genes involved in this process using bioinformatics analysis via multiple algorithms.
View Article and Find Full Text PDFHere, we have discussed the molecular mechanisms of p53-responsive microRNAs dysregulation in response to genotoxic stress in diffuse large B-cell lymphoma (DLBCL) patients. The role of micro ribonucleic acids (microRNAs) in p53-signaling cellular stress has been studied. MicroRNAs are the small non-coding RNAs, which regulate genes expression at post-transcriptional level.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
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