Basic Information

Symbol
hsa-mir-210
RNA class
miRNA miRNA hairpin
Alias
MIR210 MicroRNA 210 Hsa-MiR-210-3p Hsa-Mir-210 Hsa-MiR-210-5p MIRN210 Hsa-Mir-210_pre MIMAT0000267 MIMAT0026475 MI0000286 Mir-210
Location (GRCh38)
11:568089-568198
UCSC Genome Browser Search in Marker Scope
Forensic tag(s)
Mechanical injury analysis Wound age identification
External database
HGNC NCBI Ensembl OMIM miRBase RNAcentral

Sequence & Structure

Transcript ID
hsa-mir-210
Sequence length
110 nt
GC content
0.7273

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
-59.50 kcal/mol
Thermodynamic ensemble
Free energy: -60.29 kcal/mol
Frequency: 0.2788
Diversity: 4.05
MFE Structure Visualization
Structure Prediction
MFE Structure Prediction
....((..((((.(((((((((((..(((((.(((..(((((((((.((.((((...))).).)).)))))).))).))).)))))..)))))))))))..))))..)).
Thermodynamic Ensemble Prediction
....((..((((.(((((((((((,.(((((.(((..(((((((((.((.((((...))).).)).)))))).))).))).))))).,)))))))))))..))))..)).
Forensic Context

A study in human denatured dermis from deep burn patients demonstrated that the mir-210 was down-regulated 0.0479-fold compared to paired normal skin, as validated by miRNA microarray and real-time RT-PCR [Liang et al. DOI:10.1016/j.burns.2011.10.014]. A separate review of human studies confirmed the mir-210 is down-regulated in deep partial thickness burn skin four days post-burn and is also down-regulated in burn hypertrophic scar tissue versus normal skin [Siu et al. DOI:10.1111/wrr.13100]. A study in mice demonstrated that the mir-210 expression increased at 3, 6, and 24 hours at the injury epicenter in a long spinal cord compression model, but only at 24 hours in a short compression model, with significant differences between models at 3 and 6 hours [Ziu et al. DOI:10.1016/j.spinee.2013.08.015]. In mammalian cells, the mir-210 is potently induced by hypoxia in a HIF-dependent manner and targets genes involved in mitochondrial function, DNA repair, cell cycle, and HIF stabilization [Nallamshetty et al. DOI:10.1016/j.freeradbiomed.2013.05.022].