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CYLD activates cell death. 36 / 39
                        
    
      
      
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
      
    
      
      
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                                  "The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay revealed a significant degree of protection exerted by both CYLD siRNA sequences in comparison to their respective controls (Fig. 1d; Supplementary Fig. S1b), and fluorescence-activated cell sorter (FACS) analysis of AnnexinV/propidium iodide (PI)-stained cells confirmed that CYLD depletion prevented oxidative cell death (Fig. 1e)."
          
                              
          
                               
                            
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                                  "In STAT1 KO HeLa cells, dox-induced expression of IRF1 also induced expression of CYLD and caspase-8 and caused cell death in the presence of TNF (Fig. 6 B), indicating that IRF1 is sufficient for the IFNγ-induced expression of CYLD and caspase-8.Next, we performed IRF1 chromatin immunoprecipitation (ChIP) followed by quantitative PCR (qPCR) and found that IRF1, but not the IRF1 W11R mutant variant, bound to the promoter regions of the CYLD and CASP8 loci (Fig. 6, C and D)."
          
                              
          
                               
                            
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                                  "The results showed that CYLD knockdown in DU145 cells decreased cell death and intracellular lipid peroxidation levels (Fig. 3H, I), while CYLD overexpression in PC-3 and DU145 cells increased cell death and intracellular lipid peroxidation levels (Fig. 3J, K and supplemental Fig. 3D, E)."