 
            IndraLab
Statements
UCHL1 activates apoptotic process. 72 / 78
                        
    
      
      
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
      
    
      
      
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                                  "Loss of UCHL1, a deubiquitating enzyme responsible for regenerating monoubiquitin from the ubiquitin protein complex, decreased the rate of apoptosis in the first round of spermatogenesis and increased the numbers of premeiotic germ cells in immature mice [XREF_BIBR], whereas asymmetric distribution of UCHL1 in spermatogonia is associated with maintenance and differentiation of spermatogonial stem cells [XREF_BIBR]."
          
                              
          
                               
                            
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                                  "These chalcone derivatives effectively inhibit the activity of DUB, such as USP5, UCH-L3, USP2, UCH-L1, and USP8, leading to irreversible cell cycle arrest in breast, ovarian, and cervical cancer cells (IC50 = 1.5-12.5 µM), as well as inhibiting their proliferation and initiating apoptosis."
          
                              
          
                               
                            
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                                  "Loss of UCH-L1 decreased the rate of apoptosis in the first round of spermatogenesis and increased the numbers of premeiotic germ cells in immature mice, but spermatogenesis was partially impaired with significant reduction of spermatogonia and primary spermatocytes which mainly go to apoptosis in adult mice."
          
                              
          
                               
                            
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                                  "This effect of UCHL1 on NF-κB signaling was abrogated by Sp1 overexpression.In conclusion, the present study suggested that UCHL1, negatively regulated by Sp1, could promote H  O  -mediated cell injury, oxidative stress, apoptosis and senescence and inhibit NF-κB signaling in an in vitro model of ARHL."
          
                              
          
                               
                            
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                                  "Further analysis of the embryonic MSCs revealed that: 1) proinflammatory cytokines and related genes  TNF ,  TNFSF13B ,  TNFRSF12A ,  TNFAIP6 , and  C1QTNF6  are significantly involved in the MSC-induced immune responses in cavernous hemangiomas; 2)  UCHL1  is up-regulated in the embryonic MSC apoptosis induced by proinflammatory cytokines; 3) the UCHL1-induced apoptosis of MSCs may play an important role in the MSC-induced immune responses in cavernous hemangiomas; and 4)  UCHL1  can be used as a marker gene to detect embryonic MSCs at different apoptosis stages."