 
            IndraLab
Statements
YOD1 activates cell population proliferation. 18 / 18
                        
    
      
      
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
      
    
      
      
        |
        
      
      
        
      
        
      
        
          
          18
          
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
        
      
      
    
  
                      
                    
                                      reach
                                
                                  
                                
                                
          
          
                                  "We provide evidence for the first time that YOD1 contributes to changing the abilities of cell proliferation and migration regulated by TGF-β3 signaling pathway, which may be involved in the pathogenesis of NSCL/P.We explored the effects of YOD1 siRNA on the proliferation and migration of HOK cells."
          
                              
          
                               
                            
                                      reach
                                
                                  
                                
                                
          
          
                                  "These results indicate that silencing YOD1 in APL cells can suppress cell proliferation, induce cell apoptosis and cell differentiation in a PML/RARα-dependent manner.Next, to confirm that YOD1 could be an effective therapeutic target in AML, we evaluated the effect of YOD1 inhibition on normal human hematopoietic stem cells (HSCs)."