biostudies-otherUnknownCarole ProctorScientific Reportshttps://www.ebi.ac.uk/biostudies/studies/MODEL1704110001biostudies-other10.1038/s41598-017-12538-6Carole ProctorfalseProctor2017 - Identifying microRNA for muscle regeneration during ageing (Mir181_in_muscle)<notes xmlns="http://www.sbml.org/sbml/level2/version4"> <body xmlns="http://www.w3.org/1999/xhtml"> <div class="dc:title">Proctor2017 - Identifying microRNA for muscleregeneration during ageing (Mir181_in_muscle)</div><div class="dc:bibliographicCitation"> <p>This model is described in the article:</p> <div class="bibo:title"> <a href="http://identifiers.org/doi/10.1038/s41598-017-12538-6" title="Access to this publication">Using computer simulation models to investigate the most promising microRNAs to improve muscle regeneration during ageing</a> </div> <div class="bibo:authorList">Carole J. Proctor & Katarzyna Goljanek-Whysall</div> <div class="bibo:Journal">Scientific Reports</div> <p>Abstract:</p> <div class="bibo:abstract"> <p>MicroRNAs (miRNAs) regulate gene expression through interactions with target sites within mRNAs, leading to enhanced degradation of the mRNA or inhibition of translation. Skeletal muscle expresses many different miRNAs with important roles in adulthood myogenesis (regeneration) and myofibre hypertrophy and atrophy, processes associated with muscle ageing. However, the large number of miRNAs and their targets mean that a complex network of pathways exists, making it difficult to predict the effect of selected miRNAs on age-related muscle wasting. Computational modelling has the potential to aid this process as it is possible to combine models of individual miRNA:target interactions to form an integrated network. As yet, no models of these interactions in muscle exist. We created the first model of miRNA:target interactions in myogenesis based on experimental evidence of individual miRNAs which were next validated and used to make testable predictions. Our model confirms that miRNAs regulate key interactions during myogenesis and can act by promoting the switch between quiescent/proliferating/differentiating myoblasts and by maintaining the differentiation process. We propose that a threshold level of miR-1 acts in the initial switch to differentiation, with miR-181 keeping the switch on and miR-378 maintaining the differentiation and miR-143 inhibiting myogenesis.</p> </div></div><div class="dc:publisher"> <p>This model is hosted on <a href="http://www.ebi.ac.uk/biomodels/">BioModels Database</a> and identified by: <a href="http://identifiers.org/biomodels.db/MODEL1704110001">MODEL1704110001</a>.</p> <p>To cite BioModels Database, please use: <a href="http://identifiers.org/pubmed/25414348" target="_blank">Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8</a>.</p></div><div class="dc:license"> <p>To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to <a href="http://creativecommons.org/publicdomain/zero/1.0/" title="Access to: CC0 1.0 Universal (CC0 1.0), Public Domain Dedication">CC0 Public Domain Dedication</a> for more information.</p></div></body> </notes>2017-04-11T00:00:00Z2025-07-14T17:55:04.639Z2025-03-30T22:39:38.621ZMODEL1704110001MAMO_000004610.1038/s41598-017-12538-6