Gene name: | STING1 |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | Chondrocytes |
Gene ID: | 340061 |
Category: | protein coding |
Phenotype: | Osteoarthritis |
Experimental category: | L |
PMID: | 33414452 |
Experiment: | SA-β-gal activity assay//Western blot |
Description: | The results showed higher p16INK4a and p21 protein mea- sures in the STING-overexpressed and IL-1β-treated chondrocytes. Although STING knockdown significantly reduced the IL-1β-simulated upregulation of p16INK4a and p21 proteins, the knockdown of STING alone did not affect these proteins expression levels. We established that si-P65 remarkably reduced the expression of STING-induced senescence-associated (p16INK4a and p21), and apoptosis-associated (BAX, Cyto-c, as well as cleaved- caspase-3) proteins and increased the expression of BCL-2. The SA-β-gal and TUNEL staining confirmed that STING regulates senescence and apopto- sis via the NF-κB-signaling axis activation. |
Regulatory pathway: | NF-κB |
R-AG-Pathway: | Activation |
Official symbol(s): | NFKB1 |
Pathway experiment: | Western blot//Immunofluorescence//SA-β-gal activity assay//TUNEL assay |
Pathway description: | The results showed that higher phosphorylation of P65 and iκb protein levels were seen in STING overexpressing and IL-1β treated chondrocytes.The analysis of the immunofluorescence of nuclear P65 confirmed that STING activates NF-κB signaling.STING mediates the degradation of the ECM degradation through the NF-κBsignaling cascade.STING regulates senescence and apoptosis via the NF-κB-signaling axis activation.Si-P65 remarkably reduced the expression of STING-induced senescence-associated (p16INK4a and p21),and apoptosis-associated (BAX,Cyto-c,as well as cleavedcaspase-3) proteins and increased the expression of BCL-2. The SA-β-gal and TUNEL staining confirmed that STING regulates senescence and apoptosis via the NF-κB-signaling axis activation. |
Annotation:
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