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)
 

Editor

Share

Personal info

View

Links

About

Terms

 

 
 
 
 

Gcn4 negatively regulates expression of genes subjected to nitrogen catabolite repression.

It has been considered that three key elements participate in nitrogen catabolite repression (NCR) of Saccharomyces cerevisiae: the GLN3 and GAT1/NIL1- encoded transcriptional activators and their negative regulator Ure2. The fact that expression of various NCR-sensitive genes is not derepressed in the absence of Ure2 has led to the proposition that there must exist a protein with a similar function to that of Ure2. The results presented in this paper show that various NCR-sensitive genes are derepressed through GLN3-mediated transcriptional activation in a gcn4Delta mutant. This effect is additive to that exerted by the lack of Ure2 and to that evoked in rapamycin-treated cultures. Our results uncover the fact that NCR is not solely achieved through the action of Gln3, Gat1, and Ure2. Since Gcn4 regulates the expression of a broad spectrum of genes, the lack of this transcriptional activator could prevent the expression of a potential Gln3 antagonist. Alternatively, Gcn4 could directly hinder Gln3 functioning.[1]

References

  1. Gcn4 negatively regulates expression of genes subjected to nitrogen catabolite repression. Sosa, E., Aranda, C., Riego, L., Valenzuela, L., DeLuna, A., Cantú, J.M., González, A. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
 
WikiGenes - Universities