MIR492

gene
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Also known as hsa-mir-492

Summary

MIR492 (microRNA 492, HGNC:32081) is a microRNA gene on chromosome 12q22.

microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop.

Source: NCBI Gene 574449 — RefSeq curated summary.

At a glance

  • Gene type: non-coding (miRNA) — no protein product; not a drug target. Variant/disease associations are omitted (they would be positional, from an overlapping protein-coding gene).

Identifiers

Gene identifiers

FieldValue
HGNC IDHGNC:32081
Approved symbolMIR492
NamemicroRNA 492
Location12q22
Locus typeRNA, micro
StatusApproved
Aliaseshsa-mir-492
Ensembl geneENSG00000283998
Ensembl biotypemiRNA
OMIM614384
Entrez574449
RNAcentralURS0000476A52 — miRNA, 116 nt, 3 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 1 — 1 miRNA

ENST00000638676

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000638676 — 1 exons

ExonStartEnd
ENSE000038020789483439894834513

Expression profiles

Bgee: expression breadth broad, 46 present calls, max score 75.84.

Top tissues by expression

46 total, by Bgee expression score (0-100, higher = more expressed):

TissueAnatomy IDExpression scoreQuality
esophagogastric junction muscularis propriaUBERON:003584175.84gold quality
heart left ventricleUBERON:000208475.45gold quality
body of pancreasUBERON:000115073.11gold quality
islet of LangerhansUBERON:000000672.90gold quality
gastrocnemiusUBERON:000138870.20gold quality
stomachUBERON:000094569.37gold quality
body of stomachUBERON:000116169.24gold quality
bloodUBERON:000017869.08gold quality
subcutaneous adipose tissueUBERON:000219068.97gold quality
esophagus mucosaUBERON:000246968.78gold quality
ectocervixUBERON:001224968.59gold quality
lower esophagus muscularis layerUBERON:003583368.13gold quality
anterior cingulate cortexUBERON:000983567.82gold quality
minor salivary glandUBERON:000183066.91gold quality
right ovaryUBERON:000211866.89gold quality
small intestine Peyer’s patchUBERON:000345466.66gold quality
transverse colonUBERON:000115766.14gold quality
intestineUBERON:000016066.05gold quality
skin of legUBERON:000151165.83gold quality
omental fat padUBERON:001041465.53gold quality
left uterine tubeUBERON:000130365.46gold quality
colonUBERON:000115565.44gold quality
endocervixUBERON:000045865.34gold quality
cerebellar hemisphereUBERON:000224565.33gold quality
right frontal lobeUBERON:000281064.45gold quality
myometriumUBERON:000129664.37gold quality
tibial nerveUBERON:000132364.32gold quality
right atrium auricular regionUBERON:000663164.06gold quality
urinary bladderUBERON:000125563.55gold quality
upper lobe of left lungUBERON:000895263.00gold quality

Single-cell (SCXA)

Detected in 1 experiment(s), a significant marker in 0.

ExperimentMarker?Max mean expression
E-ANND-3no0.00

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 24)

  • miR-492 can originate from the coding sequence of the HB marker gene keratin 19 (KRT19) (PMID:21319197)
  • study suggests that miR-492 may physiologically suppress BSG expression and the BSG rs8259 polymorphism is associated with decreased psoriasis susceptibility through affecting miR-492 binding. (PMID:21655935)
  • miR-492 exerts a potent anti-angiogenic activity in endothelial cells. (PMID:23802567)
  • miR-492 contributes to insulin resistance and endothelial dysfunction induced by high glucose, via directly downregulating resistin expression. (PMID:24526524)
  • Data indicate that elevated miR-492 expression in prostate tumors that resulted in diminished myeloid zinc-finger 1 (MZF-1) and ferroportin (FPN). (PMID:25284586)
  • Ectopic expression of miR-492 led to downregulation of SOX7 protein. (PMID:25407488)
  • the present study provided novel insights into the potential mechanisms involved in Clear cell renal cell carcinoma and it is hypothesized that miR-492 may become a promising therapeutic agent in the treatment of Clear cell renal cell carcinoma (PMID:25815441)
  • The miR-492/CD147 axis might play an essential role in the Oxaliplatin resistance of colon cancer cells. (PMID:25862460)
  • The potential use of miR-492 rs2289030 as a prognostic marker . (PMID:26753964)
  • p21-activated kinase (PAK7) was identified as the putative target of miR492 in osteosarcoma (OS), and we further found a significantly inverse correlation between PAK7 and miR492 in OS specimens. (PMID:28677719)
  • Data show that tissue inhibitor of metalloproteinase 2 (TIMP2) is a direct target of miR-492 that modulates cervical cancer cell invasion. (PMID:28802022)
  • miR-492 may be involved in the regulation of OK antigen expression on red blood cells with the BSG rs8259 TT genotype. (PMID:28981932)
  • miR-492 significantly enhances cell proliferation, anchorage-independent growth, migration and invasion of hepatoblastoma cells. High miR-492 expression correlates with high-risk or aggressive tumours and further bears potential for predicting reduced event-free survival. The study identified miR-492 and its target CD44 as regulators of a number of biological features important for malignancy and metastasis. (PMID:29314711)
  • Diabetic Cardiovascular Complications are associated with decreased levels of miR-492 suggesting that MIR-492 may be novel biomarkers. (PMID:29459239)
  • In conclusion, miR492 inhibition may impede the malignant behaviour of retinoblastoma (RB) by directly targeting LATS2. Therefore, targeting this miRNA may be an effective therapeutic method for treating patients with RB. (PMID:30592270)
  • study demonstrated that miR-492 was over-expressed in Prostate Cancer and exerted tumor-promoting function in PCa cells via repressing SOCS2 expression. (PMID:30779065)
  • miR-492 promotes chemoresistance to CDDP and metastasis by targeting inhibiting DNMT3B and induces stemness in gastric cancer. (PMID:32065219)
  • The overexpression of LATS2 repressed the growth and invasion of ACHN and 786-O cells. circ_0001368 upregulated the LATS2 expression and suppressed ACHN and 786-O cell growth and invasion by sponging miR-492. (PMID:32428698)
  • Effects of miR-492 on migration, invasion, EMT and prognosis in ovarian cancer by targeting SOX7. (PMID:32521870)
  • Association between miR-492 rs2289030 G>C and susceptibility to Hirschsprung disease in southern Chinese children. (PMID:33103535)
  • Association of miRNA-492 rs2289030 G>C and miRNA-938 rs2505901 T>C Gene Polymorphisms with Biliary Atresia Susceptibility. (PMID:34353423)
  • The immunogenic involvement of miRNA-492 in mycoplasma pneumoniae infection in pediatric patients. (PMID:36195304)
  • NamiRNA-enhancer network of miR-492 activates the NR2C1-TGF-beta/Smad3 pathway to promote epithelial-mesenchymal transition of pancreatic cancer. (PMID:36591938)
  • hsa_circ_0129047 Upregulates LYVE1 to Inhibit Hepatocellular Carcinoma Progression by Sponging miR-492. (PMID:37810197)

Cross-species orthologs

0 orthologs

Protein

Non-coding RNA — no protein product; not a drug target.

Function

No curated pathway, Gene-Ontology, or interaction data.

Disease & clinical

No curated disease, variant, or cancer-driver associations.

Drugs & pharmacology

No drug or pharmacology data — not an established drug target.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.