| Gene name: | CLIC1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVECs |
| Experiment: | qRT-PCR |
| Description: | Upregulating CLIC1 in HUVECs promoted cell senescence, evidenced by the mRNA levels of p16, PAI-1, and Sirt1. However, CLIC1 silencing decreased H2O2 induced cellular senescence. |
| Target gene: | NRF2 |
| Official symbol(s): | NRF2 |
| R-AG-Target gene: | Downregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot//Immunofluorescence |
| Target gene description: | The findings revealed that even though H2O2 slightly induced nuclear translocation of Nrf2, IAA94 treatment or CLIC1 knockdown significantly increased Nrf2 translocation in H2O2-treated HUVECs. Nuclear levels of the Nrf2 protein were determined by Western blot analysis. H2O2 increased the nuclear protein expression levels of Nrf2 while IAA94 treatment increased the Nrf2 protein levels in the nuclear fraction. Nrf2 protein expression in the nuclear fraction demonstrated that overexpression of CLIC1 inhibited Nrf2 translocation. |
| Regulatory pathway: | NRF2-HO1//AMPK-AKT-GSK3β |
| R-AG-Pathway: | Downregulation |
| Pathway experiment: | Western blot |
| Pathway description: | Overexpression of CLIC1 inhibited the activation of the Nrf2/HO-1 pathway and promoted oxidative stress injury in HUVECs. IAA-94 treatment activated the AMPK/AKT/GSK3β pathway while CLIC1 knockdown enhanced the expresson of p-AMPK/total AMPK. However, CLIC1 overexpression significantly decreased the ratio of p-AMPK Thr172 to total-AMPK. |
Annotation:
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