Linked Life Data

9920729

Source:http://linkedlifedata.com/resource/pubmed/id/9920729

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-2-25
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
254
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
36-41
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
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.
pubmed:affiliation
Department of Experimental Medicine and Biochemical Science, University of Perugia, Perugia, Italy.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't