| Gene name: | MIR200A |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Keratinocyte |
| Experiment: | qRT-PCR//Western blot |
| Description: | Altogether, these findings point miR-200a as key player in primary human keratinocyte aging since its overexpression reduces oxidative DNA repair activity and may induce cell cycle arrest via p16 up-regulation and fuels chronic inflammation via NLRP3 activation. |
| Target gene: | OGG1-2A//NRLP3//IL-1β//BMI-1//P16 |
| Official symbol(s): | OGG1-2A//NLRP3//IL1B//BMI-1//P16 |
| R-AG-Target gene: | Downregulation//Upregulation//Upregulation//Downregulation//Upregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Luciferase reporter assay//qRT-PCR//Western blot |
| Target gene description: | HEK 293 cells have been cotransfected with a construct containing the OGG1-2a 3′-UTR downstream of a luciferase open reading frame and either with miR-200a or a miR-scramble. Relative luciferase activity was significantly down-regulated (~29%) upon miR-200a overexpression.As expected, following miR-200a expression ,a significant decrease of OGG1-2a expression was observed in both cell types.Of note, miR-200a overexpression induced also a significant increase of NRLP3, caspase 1, and IL-1β expression mainly in fibroblasts.Following miR-200a expression, Bmi-1 expression significantly decreased at both mRNA and protein levels in HEK 293 cells and primary human fibroblasts. Simultaneously, a significant increase of the senescence mediator p16 was observed . |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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