Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Garbuglia, M. et al.

Role of the C-terminal extension in the interaction of S100A1 with GFAP, tubulin, the S100A1- and S100B-inhibitory peptide, TRTK-12, and a peptide derived from p53, and the S100A1 inhibitory effect on GFAP polymerization.

Whereas native and recombinant S100A1 inhibited GFAP assembly, a truncated S100A1 lacking the last six C-terminal residues (Phe88-Ser93) (S100A1Delta88-93) proved unable to do so. The inhibitory effects of native and recombinant S100A1 on GFAP assembly were blocked by both TRTK-12, a synthetic peptide derived from the alpha-subunit of the actin capping protein, CapZ, and a synthetic peptide derived from the tumor-suppressor protein, p53, in a dose-dependent manner. By fluorescent spectroscopy, TRTK-12 and the p53 peptide, like GFAP and tubulin, caused a dose- and Ca2+-dependent blue-shift of the fluorescence maximum of acrylodan-S100A1. In contrast, GFAP, tubulin, TRTK-12, or the p53 peptide caused no significant changes in the fluorescence spectrum of acrylodan-S100A1Delta88-93. By chemical crosslinking, both TRTK-12 and the p53 peptide strongly reduced or blocked the formation of GFAP-S100A1 or tubulin-S100A1 complexes, respectively, and S100A1Delta88-93 was unable to complex with tubulin, whereas a remarkably reduced complexation of GFAP with the truncated protein was observed. All the above observations show that the C-terminal extension of S100A1 is an essential part of the S100A1 site implicated in the recognition of GFAP, tubulin, p53, and the alpha-subunit of CapZ.[1]

References

Role of the C-terminal extension in the interaction of S100A1 with GFAP, tubulin, the S100A1- and S100B-inhibitory peptide, TRTK-12, and a peptide derived from p53, and the S100A1 inhibitory effect on GFAP polymerization. Garbuglia, M., Verzini, M., Rustandi, R.R., Osterloh, D., Weber, D.J., Gerke, V., Donato, R. Biochem. Biophys. Res. Commun. (1999) [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 WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

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.