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Biochem Biophys Res Commun ; 307(4): 810-3, 2003 Aug 08.
Article in English | MEDLINE | ID: mdl-12878182

ABSTRACT

The purpose of this report was to determine the effect of prion protein (PrP) gene disruption on T lymphocyte function. Previous studies have suggested that normal cellular prion protein (PrP(c)) binds to copper and Cu(2+) is essential for interleukin-2 (IL-2) mRNA synthesis. In this study, IL-2 mRNA levels in a copper-deficient condition were investigated using T lymphocytes from prion protein gene-deficient (PrP(0/0)) and wild-type mice. Results showed that Cu(2+) deficiency had no effect on PrP(c) expression in Con A-activated splenocytes. However, a delay in IL-2 gene expression was observed in PrP(0/0) mouse T lymphocyte cultures using Con A and Cu(2+)-chelator. These results suggest that PrP(c) expression may play an important role in rapid Cu(2+) transfer in T lymphocytes. The rapid transfer of Cu(2+) in murine T lymphocytes could be one of the normal functions of PrP(c).


Subject(s)
Copper/pharmacology , PrPC Proteins/physiology , T-Lymphocytes/immunology , Amino Acid Sequence , Animals , Cells, Cultured , Copper/metabolism , Interleukin-2/biosynthesis , Interleukin-2/genetics , Mice , Mice, Knockout , Molecular Sequence Data , PrPC Proteins/genetics , PrPC Proteins/metabolism , RNA, Messenger/biosynthesis , T-Lymphocytes/drug effects , T-Lymphocytes/metabolism
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