Basic Information

Symbol
hsa-mir-23b
RNA class
miRNA miRNA hairpin
Alias
MIR23B MicroRNA 23b Hsa-MiR-23b-5p Hsa-Mir-23b MIRN23B Hsa-Mir-23-P2_pre Hsa-MiR-23b-3p MIMAT0004587 MIMAT0000418 MI0000439 MiRNA23B Mir-23b
Location (GRCh38)
9:95085208-95085304
UCSC Genome Browser Search in Marker Scope
Forensic tag(s)
Cause of death analysis Sudden death from CNS diseases
External database
HGNC NCBI Ensembl OMIM miRBase RNAcentral

Sequence & Structure

Transcript ID
hsa-mir-23b
Sequence length
97 nt
GC content
0.5052

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
-36.00 kcal/mol
Thermodynamic ensemble
Free energy: -38.14 kcal/mol
Frequency: 0.0310
Diversity: 11.10
MFE Structure Visualization
Structure Prediction
MFE Structure Prediction
.(((((.(.(((((.(((.(((((((((((((((.((((((..............)))))))).))))))))))..))).))).))).)))))))).
Thermodynamic Ensemble Prediction
.{((((,,.{{(((.(((.(((((((((((((((.((((((...........,..)))))))),})))))))))..))).))).))).}))))})}.
Forensic Context

A study in human deep partial thickness burn patients demonstrated that the mir-23b was downregulated in denatured dermis compared to paired normal skin four days post-burn, with a 0.2128-fold change [Liang et al. DOI:10.1016/j.burns.2011.10.014]. This downregulation was also observed in human skin wounds 24 hours post-injury and in heat-shocked fibroblasts 2 and 24 hours post-burn, identifying it as one of five key miRNAs altering fibroproliferative markers and cell behaviors post-burn [Siu et al. DOI:10.1111/wrr.13100]. A study in rodents demonstrated that the mir-23b is restricted to astrocytes and shows reduced expression after spinal cord injury, which may reflect oligodendrocyte loss, and it is a central actor in myelin maintenance and remyelination [Nieto-Diaz et al. DOI:10.3389/fncel.2014.00053]. In burn injury research, the mir-23b is noted to promote fibroblast proliferation and migration through Smad3 [Badanina et al. DOI:10.3390/ijms262010060].