Basic Information

Symbol
hsa-mir-223
RNA class
miRNA miRNA hairpin
Alias
MIR223 MicroRNA 223 Hsa-MiR-223-5p Hsa-MiR-223-3p Hsa-Mir-223 MIRN223 Hsa-Mir-223_pre MIMAT0000280 MIMAT0004570 MI0000300 MiRNA223 Mir-223
Location (GRCh38)
Forensic tag(s)
Tissue/body fluid identification Wound age identification Sudden cardiac death diagnosis

Sequence & Structure

Transcript ID
hsa-mir-223
Sequence length
110 nt
GC content
0.5364

Secondary Structure

Generated by RNAfold
Minimum free energy (MFE) structure:
Secondary structure that contributes a minimum of free energy.
Ensemble properties:
Thermodynamic properties of the Boltzmann ensemble.
Minimum free energy
-47.40 kcal/mol
Thermodynamic ensemble
Free energy: -48.85 kcal/mol
Frequency: 0.0951
Diversity: 6.69
MFE Structure Visualization
Structure Prediction
MFE Structure Prediction
.((((......((((((((.((((..(.((((((((((((((......(((((((.........))))))))))))))))))))).)..)))).))))).)))...))))
Thermodynamic Ensemble Prediction
.((((......((((((((.((((..(.(((((((((((((({,....,{(((((......,..))))))))))))))))))))).}..)))).))))).)))...))))
Forensic Context

A study in humans demonstrated that hsa-miR-223 is highly overexpressed in saliva and showed high sensitivity and specificity for saliva identification with an AUC of 1.00 [Park et al. DOI:10.1002/elps.201400075]. A separate review of human skin burn and wound healing studies reported that hsa-miR-223 was upregulated 4 days post-burn in deep partial thickness burn skin versus normal skin and was also upregulated 24 hours post-injury in skin wounds versus unwounded skin [Siu et al. DOI:10.1111/wrr.13100]. A study in humans demonstrated that the mir-223 is a saliva-specific marker, showing significantly higher expression in saliva compared to peripheral blood, menstrual blood, semen, and vaginal secretions (p < 0.0001) and remaining stable in dried samples for up to 24 months [Chen et al. DOI:10.1016/j.legalmed.2023.102312]. Separately, a study in mice found the mir-223 was downregulated in myocardial tissue after acute myocardial infarction and was identified as regulating heart rate by directly targeting the Slc8a1 gene, with overexpression decreasing Slc8a1 expression [Tuerxun et al. DOI:10.1007/s12013-024-01528-x].