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

 

 
 
 
 

Negative regulation of forkhead transcription factor AFX (Foxo4) by CBP-induced acetylation.

AFX (also called Foxo4), a member of mammalian FOXO forkhead transcription factors, is the homolog of DAF-16, which contributes longevity and oxidative stress in Caenorhabditis elegans. Here, we show that CREB-binding protein (CBP) interacts with AFX via CH1 region and acetylates it at the three lysine residues (K186, K189, and K408). Trichostatin A (TSA) repressed the AFX-stimulated transcription, and substitution of the lysine residues with arginine (K186, 189, 408R) enhanced the transcriptional activity of AFX. Furthermore, TSA suppressed the expression of p27kip1 gene induced by AFX in HEK293T cells. Compared to the coexpression of CBP wild-type, a HAT activity-deficient mutant (DeltaHAT) efficiently leads the cooperative activation of AFX transcription in HepG2 cells. Taken together, these results demonstrate that CBP- induced acetylation of AFX is a novel modification mechanism by which AFX keeps the transcriptional activity mitigating in the nucleus.[1]

References

  1. Negative regulation of forkhead transcription factor AFX (Foxo4) by CBP-induced acetylation. Fukuoka, M., Daitoku, H., Hatta, M., Matsuzaki, H., Umemura, S., Fukamizu, A. Int. J. Mol. Med. (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