http://researchonline.federation.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13721 Wed 07 Apr 2021 14:01:49 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13680 Wed 07 Apr 2021 14:01:47 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:11958 Wed 07 Apr 2021 13:57:15 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10451 Wed 07 Apr 2021 13:55:49 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5379 Wed 07 Apr 2021 13:45:01 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4790 1.1) were differentially expressed between HHR and NHR (n=16). We then performed an in silico analysis to predict the miRNAs that are able to bind to the 3′ untranslated region of Endog mRNA, and therefore could regulate Endog levels. We discovered that the miRNAs let-7b, miR-338 and miR-347 are predicted to bind to Endog mRNA. Functional studies are being undertaken to determine whether these miRNAs can regulate Endog mRNA levels in vitro and their role in the pathological processes leading to cardiac hypertrophy. These miRNAs could be a new target for the prevention and treatment of cardiac hypertrophy in humans]]> Wed 07 Apr 2021 13:44:20 AEST ]]>