Reference - Detail
|Author||Hayashi K, Kamikawa Y.|
|Title||HSP90 is crucial for regulation of LAT expression in activated T cells.|
T cell response initiated by engagement of T cell receptor (TCR) is dependent on signal transduction events composed of protein kinases and adaptor proteins. However, the molecular mechanism for gene expression of these proteins is not entirely understood. Here we identified Heat Shock Protein 90 (HSP90) as an essential regulator for gene expression of Linker for activation of T cells (LAT) in primarily activated human T cells. Primarily activated T cells continuously synthesized LAT protein and treatment of cells with 17-AAG, a pharmacological inhibitor of HSP90, decreased LAT protein level following reduction of LAT mRNA. Furthermore, promoter activity of LAT gene was dramatically inhibited by 17-AAG. These results reveal a novel role of HSP90 as a positive regulator for expression of LAT gene in activated T cells.
|MeSH||Adaptor Proteins, Signal Transducing / genetics* Adaptor Proteins, Signal Transducing / metabolism Benzoquinones / pharmacology Cell Membrane / drug effects Cell Membrane / metabolism Down-Regulation / drug effects Enzyme Inhibitors / pharmacology Gene Expression Regulation* / drug effects HSP90 Heat-Shock Proteins / antagonists & inhibitors HSP90 Heat-Shock Proteins / metabolism* Humans Jurkat Cells Lactams, Macrocyclic / pharmacology Leupeptins / pharmacology Lymphocyte Activation / drug effects Lymphocyte Activation / immunology* Membrane Proteins / genetics* Membrane Proteins / metabolism Promoter Regions, Genetic / genetics Proteasome Endopeptidase Complex / metabolism Proteasome Inhibitors Protein Transport / drug effects RNA, Messenger / genetics RNA, Messenger / metabolism T-Lymphocytes / cytology T-Lymphocytes / drug effects T-Lymphocytes / immunology*|
|WOS Category||IMMUNOLOGY BIOCHEMISTRY & MOLECULAR BIOLOGY|
|Human and Animal Cells|