Gene Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 Biomarker disease BEFREE miR-499 released during myocardial infarction causes endothelial injury by targeting α7-nAchR. 31270949 2019
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 AlteredExpression disease BEFREE NPY deletion increased miR-499 expression and decreased FoxO4 expression in MI <i>in vivo</i> and <i>in vitro</i>. 31708788 2019
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 GeneticVariation disease BEFREE The multivariate Cox proportional hazard analysis (relative risk [RR]; 95% confidence interval [CI]) revealed that miR-208b-3p (1.225; 1.092-1.375), miR-34a-5p (0.963; 0.935-0.992), and miR-499-5p (0.077; 0.025-0.239) were independently associated with risk of CVD/MI/CIE, as well as risk of each event. 29350392 2018
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 Biomarker disease BEFREE This is the first report to highlight the biological significance of this polymorphism on the maturation of miR-499-5p and its antiapoptotic role during MI. 30102014 2018
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 Biomarker disease BEFREE MiR-499 (for the inhibition of cardiomyocyte apoptosis) and plasmid encoding vascular endothelial growth factor (for the promotion of angiogenesis) are sequentially delivered for systemic treatment of MI. 29920798 2018
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 GeneticVariation disease BEFREE These findings indicate that miR-499 rs3746444 and miR-146a rs2910164 may represent novel markers of MI susceptibility. 24850191 2014
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 Biomarker disease BEFREE Discrimination of MI was accurate for miR-208b (AUC = 0.82) and miR-499-5p (AUC = 0.79) but considerable lower than for Troponin T (AUC = 0.95). 23448306 2013
Entrez Id: 574501
Gene Symbol: MIR499A
MIR499A
0.080 AlteredExpression disease BEFREE Our data reveal a role for miR-499 in regulating the mitochondrial fission machinery and we suggest that modulation of miR-499 levels may provide a therapeutic approach for treating myocardial infarction. 21186368 2011