FIGURE
            Fig. 4
- ID
- ZDB-FIG-100304-15
- Publication
- Wan et al., 2010 - Negative Feedback Regulation of Wnt4 Signaling by EAF1 and EAF2/U19
- Other Figures
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                        Fig. 4
                    
                    
                
                
            
        
        
    
        
            
            
| Both zebrafish eaf1 and eaf2/u19 suppress zebrafish wnt4a expression. (A) Whole-mount in situ hybridization analysis of zebrafish wnt4a expression in embryos injected with eaf1 mRNA, eaf2/u19 mRNA, Eaf1-MO and Eaf2-MO at 12-somite stage. The embryos without injection were used as control. (B) The expression of zebrafish wnt4a mRNA was suppressed by ectopic expression of zebrafish eaf1 and eaf2/u19 (a) and up-regulated by knockdown Eaf1 and Eaf2/U19 (b) as revealed by semi-quantitative RT-PCR analysis at 12-somte stage. | 
                
                    
                        Expression Data
                    
                    
                
                
            
        
        
    
        
            
            
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| Anatomical Term: | |
| Stage: | 10-13 somites | 
                
                    
                        Expression Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Antibody Labeling
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Phenotype Data
                    
                    
                
                
            
        
        
    
        
            
            
            
            
    
    
                
                    
                        Phenotype Detail
                    
                    
                
                
            
        
        
    
        
            
                
            
        
    
    
    
                
                    
                        Acknowledgments
                    
                    
                
                
            
        
        
    
        
            
            
                
                    
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      Full text @ PLoS One
                
                
            
        
        
    
    
     
        