Gene name: | TLR2 |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | IMR-90 |
Experiment: | Crystal violet assay//SA-β-gal activity assay |
Description: | Overexpression of TLR2 induced cell cycle arrest and an increase in the number of senescence-associated β-galactosidase (SA-β-Gal)–positive cells. |
Target gene: | P21//P16//P15INK4B//P53 |
Official symbol(s): | P21//P16//P15INK4B//P53 |
R-AG-Target gene: | --//--//--//-- |
Subcategory: | Unclear |
Target gene experiment: | Western blot |
Target gene description: | ?Suppression of TLR2 and TLR10 resulted in a decrease in p21CIP1, p16INK4a, and p15INK4b?mRNA expression and a reduction of p53 protein levels. |
Regulatory pathway: | NF-κB//P38 MAPK//A-SAA |
R-AG-Pathway: | --//--//-- |
Official symbol(s): | NFKB1//MAKP14//SAA1 |
Pathway experiment: | Western blot//qRT-PCR |
Pathway description: | A significant enrichment in genes regulated by NF-κB in OIS (22) was observed in the transcriptome of control cells compared to TLR2-depleted cells ;We also observed a marked decrease in p38 MAPK phosphorylation in TLR2- and TLR10-depleted cells in OIS .Western blot of the conditioned medium from IMR90 ER:RAS cells showed an accumulation of A-SAAs, which was reduced following siRNA knockdown of SAA1 and SAA2, suggesting that A-SAAs are components of the SASP.Further mRNA analysis by quantitative reverse transcription polymerase chain reaction (qRT-PCR) of AA1, SAA2, SERPINA3, PTGS2, STAT3, and IL-6R expression con-firmed these results, indicating that the expression of A-SAAs is highly induced during OIS and is dependent on TLR2 and TLR10. |
Annotation:
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