The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

The C-terminal half-fragment of the Sendai virus C protein prevents the gamma-activated factor from binding to a gamma-activated sequence site.

Sendai virus C protein associates with the signal transducer and activator of transcription (STAT) 1 and inhibits the interferon (IFN) response. We report a molecular basis for the anti-IFN-gamma mechanism of Sendai virus. The C-terminal half-fragment of the C protein (D1) retains both the STAT1-binding and the anti-IFN-gamma abilities comparable to those of the full-size C. IFN-gamma stimulation generates phosphorylated-STAT1 even in the presence of the C or the D1. The phosphorylated-STAT1 generated in the D1-expressing cells forms an aberrant complex, which does not bind to a gamma-activated sequence (GAS) probe. Purified D1, indeed, inhibits in vitro the binding of the phosphorylated-STAT1 dimer to the GAS probe. The D1, however, binds to the STAT1 N-terminal domain, but not the DNA binding domain. These results suggest the possibility that the C protein prevents the gamma- activated factor from binding to GAS elements through its interaction with the STAT1 N-terminal domain.[1]

References

 
WikiGenes - Universities