Basic Information

Symbol
hsa-mir-106a
RNA class
miRNA miRNA hairpin
Alias
MIR106A MicroRNA 106a Hsa-MiR-106a-5p Hsa-Mir-106a Hsa-MiR-106a-3p MIRN106A Hsa-Mir-17-P1c_pre MIMAT0000103 MIMAT0004517 MI0000113 Mir-106a Mir-106
Location (GRCh38)
Forensic tag(s)
Tissue/body fluid identification

Sequence & Structure

Transcript ID
hsa-mir-106a
Sequence length
81 nt
GC content
0.4198

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
-34.40 kcal/mol
Thermodynamic ensemble
Free energy: -36.09 kcal/mol
Frequency: 0.0649
Diversity: 6.18
MFE Structure Visualization
Structure Prediction
MFE Structure Prediction
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Thermodynamic Ensemble Prediction
((.(((..(((((((((((((((((.(((({,(((,((....})}.)))))))).))))))))))).))))))..))).))
Forensic Context

A study in humans demonstrated that the mir-106a is a highly over-expressed miRNA marker for venous blood identification, confirmed by RT-PCR validation. This marker showed no significant degradation after one year of storage under laboratory conditions, and its TaqMan assay required only subpicogram amounts of total RNA for detection, demonstrating high sensitivity and stability for forensic body fluid identification [Zubakov et al. DOI:10.1007/s00414-009-0402-3]. A separate investigation in human peripheral whole blood found the mir-106a was significantly negatively correlated with age, indicating its expression levels are a confounding variable that must be considered in analytical profiles [Meder et al. DOI:10.1373/clinchem.2014.224238]. A study in humans demonstrated that the mir-106a was significantly downregulated in peripheral blood at 0, 24, and 48 hours after ICU admission in severely injured trauma patients compared to healthy controls, with the greatest decrease at 24 hours, and its levels appeared more downregulated in patients who developed infection [Galbraith et al. DOI:10.1016/j.surg.2018.05.042]. This downregulation targets and correlates with the expression of key immune regulators TNF-α and IL-10, indicating its role in post-injury immune dysfunction.