 
            IndraLab
Statements
CYLD inhibits apoptotic process. 38 / 39
                        
    
      
      
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
      
    
      
      
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                                  "Mechanistic investigations demonstrated that induction of apoptosis by CYLD knockdown was caused by upregulation of receptor-interacting protein kinase 1 ( RIPK1 ) that was associated with elevated K63-linked polyubiquitination of the protein , indicating that CYLD is critical for controlling RIPK1 expression in these cells ."
          
                              
          
                               
                            
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                                  "As Fas associated protein with death domain (FADD), cellular inhibitor of apoptosis 1 (cIAP1), and cIAP2 are all known to regulate RIPK1 mediated apoptosis XREF_BIBR, we compared the expression levels of FADD, cIAP1, and cIAP2 between Mel-FH and Mel-CV cells that displayed different sensitivity to apoptosis induced by silencing of CYLD."
          
                              
          
                               
                            
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                                  "Since the proapoptotic function of RIPK1 can be prevented by phosphorylation of Ser320 or Ser25 XREF_BIBR, we introduced the RIPK1 mutant with Ser320 or Ser25 constitutively phosphorylated into Mel-CV and ME1007 cells to test whether it impinges on apoptosis induced by silencing of CYLD."
          
                              
          
                               
                            
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                                  "16
 More recently, MALT1‐mediated CYLD cleavage was implicated in BcR‐signaling, NF‐κB activation, and proliferation in mantle cell lymphoma (MCL) and diffuse large B‐cell lymphoma (DLBCL)
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, while it was also reported that BTK inhibitors induce apoptosis in non‐GCB‐DLBCL by decreasing CYLD phosphorylation."