HCSGD entry for MIR183


1. General information

Official gene symbolMIR183
Entrez ID406959
Gene full namemicroRNA 183
Other gene symbolsMIRN183 miR-183 miRNA183
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

Not in the Gene ontology

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.98971427380.31316052580.99999024731.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954--
GSE13712_SHEAR--
GSE13712_STATIC--
GSE19018--
GSE19899_A1--
GSE19899_A2--
PubMed_21979375_A1--
PubMed_21979375_A2--
GSE35957--
GSE36640--
GSE54402--
GSE9593--
GSE43922Up0.0133152163
GSE24585Down-0.2555204013
GSE37065Down-0.0352233834
GSE28863_A1--
GSE28863_A2--
GSE28863_A3--
GSE28863_A4--
GSE48662--

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase
No target information from mirTarBase
  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 2 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27116545PURPOSE: The purpose of this study was to investigate the mechanisms by which miR-183 may contribute to the phenotypic alterations associated with stress-induced senescence of human trabecular meshwork (HTM) cells
27116545METHODS: Changes in gene expression induced by miR-183 in HTM cells were evaluated by gene array analysis, confirmed by quantitative-PCR (Q-PCR), and analyzed by MetaCore pathway analysis
27116545A plasmid expressing KIAA0101 without its 3'-untranslated region (3'-UTR) was cotransfected with miR-183 to evaluate the role of KIAA0101 on the effects induced by miR-183
27116545RESULTS: miR-183 affected the expression of multiple genes involved in cell cycle regulation and DNA damage response in HTM cells
27116545Forced expression of miR-183 in HTM and HDF resulted in a significant decrease in proliferation in primary HTM and HDF cells but not in HeLa cells
27116545In all cell types tested, overexpression of miR-183 resulted in increased DNA damage under UV irradiation
27116545CONCLUSIONS: Our results suggest that the observed up-regulation of miR-183 after stress-induced senescence in HTM cells may contribute to reinforce cellular senescence by inhibiting cell cycle progression through multiple gene targets and limiting the DNA repair mechanisms through inhibition of KIAA0101
19940135Targeting of integrin beta1 and kinesin 2alpha by microRNA 183
19940135MicroRNA 183 (miR-183) has been reported to inhibit tumor invasiveness and is believed to be involved in the development and function of ciliated neurosensory organs
19940135We have recently found that expression of miR-183 increased after the induction of cellular senescence by exposure to H(2)O(2)
19940135To gain insight into the biological roles of miR-183 we investigated two potential novel targets: integrin beta1 (ITGB1) and kinesin 2alpha (KIF2A)
19940135Targeting of the 3'-untranslated region (3'-UTR) of ITGB1 and KIF2A by miR-183 was confirmed by luciferase assay
19940135Transfection with miR-183 led to a significant decrease in cell invasion and migration capacities of HeLa cells that could be rescued by expression of ITGB1 lacking the 3'-UTR
19940135Although miR-183 had no effects on cell adhesion in HeLa cells, it significantly decreased adhesion to laminin, gelatin, and collagen type I in normal human diploid fibroblasts and human trabecular meshwork cells
19940135Targeting of KIF2A by miR-183 resulted in some increase in the formation of cells with monopolar spindles in HeLa cells but not in human diploid fibroblast or human trabecular meshwork cells
19940135The regulation of ITGB1 expression by miR-183 provides a new mechanism for the anti-metastatic role of miR-183 and suggests that this miRNA could influence the development and function in neurosensory organs, and contribute to functional alterations associated with cellular senescence in human diploid fibroblasts and human trabecular meshwork cells
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