Regulation of calcium signalling in T lymphocytes by the second messenger cyclic ADP-ribose
Cyclic ADP-ribose (cADPR) is a natural compound that mobilizes calcium ions in several eukaryotic cells. Although it can lead to the release of calcium ions in T lymphocytes, it has not been firmly established as a second messenger in these cells. Here, using high-performance liquid chromatography a...
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| Veröffentlicht in: | Nature (London) 1999-03, Vol.398 (6722), p.70-73 |
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| creator | Guse, Andreas H da Silva, Cristina P Berg, Ingeborg Skapenko, Alla L Weber, Karin Heyer, Petra Hohenegger, Martin Ashamu, Gloria A Schulze-Koops, Hendrik Potter, Barry V. L Mayr, Georg W |
| description | Cyclic ADP-ribose (cADPR) is a natural compound that mobilizes calcium ions in several eukaryotic cells. Although it can lead to the release of calcium ions in T lymphocytes, it has not been firmly established as a second messenger in these cells. Here, using high-performance liquid chromatography analysis, we show that stimulation of the T-cell receptor/CD3 (TCR/CD3) complex results in activation of a soluble ADP-ribosyl cyclase and a sustained increase in intracellular levels of cADPR. There is a causal relation between increased cADPR concentrations, sustained calcium signalling and activation of T cells, as shown by inhibition of TCR/CD3-stimulated calcium signalling, cell proliferation and expression of the early- and late-activation markers CD25 and HLA-DR by using cADPR antagonists. The molecular target for cADPR, the type-3 ryanodine receptor/calcium channel, is expressed in T cells. Increased cADPR significantly and specifically stimulates the apparent association of [3H]ryanodine with the type-3 ryanodine receptor, indicating a direct modulatory effect of cADPR on channel opening. Thus we show the presence, causal relation and biological significance of the major constituents of the cADPR/calcium-signalling pathway in human T cells. |
| doi_str_mv | 10.1038/18024 |
| format | Article |
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There is a causal relation between increased cADPR concentrations, sustained calcium signalling and activation of T cells, as shown by inhibition of TCR/CD3-stimulated calcium signalling, cell proliferation and expression of the early- and late-activation markers CD25 and HLA-DR by using cADPR antagonists. The molecular target for cADPR, the type-3 ryanodine receptor/calcium channel, is expressed in T cells. Increased cADPR significantly and specifically stimulates the apparent association of [3H]ryanodine with the type-3 ryanodine receptor, indicating a direct modulatory effect of cADPR on channel opening. 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There is a causal relation between increased cADPR concentrations, sustained calcium signalling and activation of T cells, as shown by inhibition of TCR/CD3-stimulated calcium signalling, cell proliferation and expression of the early- and late-activation markers CD25 and HLA-DR by using cADPR antagonists. The molecular target for cADPR, the type-3 ryanodine receptor/calcium channel, is expressed in T cells. Increased cADPR significantly and specifically stimulates the apparent association of [3H]ryanodine with the type-3 ryanodine receptor, indicating a direct modulatory effect of cADPR on channel opening. 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L</au><au>Mayr, Georg W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of calcium signalling in T lymphocytes by the second messenger cyclic ADP-ribose</atitle><jtitle>Nature (London)</jtitle><addtitle>Nature</addtitle><date>1999-03-04</date><risdate>1999</risdate><volume>398</volume><issue>6722</issue><spage>70</spage><epage>73</epage><pages>70-73</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><coden>NATUAS</coden><abstract>Cyclic ADP-ribose (cADPR) is a natural compound that mobilizes calcium ions in several eukaryotic cells. Although it can lead to the release of calcium ions in T lymphocytes, it has not been firmly established as a second messenger in these cells. Here, using high-performance liquid chromatography analysis, we show that stimulation of the T-cell receptor/CD3 (TCR/CD3) complex results in activation of a soluble ADP-ribosyl cyclase and a sustained increase in intracellular levels of cADPR. There is a causal relation between increased cADPR concentrations, sustained calcium signalling and activation of T cells, as shown by inhibition of TCR/CD3-stimulated calcium signalling, cell proliferation and expression of the early- and late-activation markers CD25 and HLA-DR by using cADPR antagonists. The molecular target for cADPR, the type-3 ryanodine receptor/calcium channel, is expressed in T cells. Increased cADPR significantly and specifically stimulates the apparent association of [3H]ryanodine with the type-3 ryanodine receptor, indicating a direct modulatory effect of cADPR on channel opening. Thus we show the presence, causal relation and biological significance of the major constituents of the cADPR/calcium-signalling pathway in human T cells.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>10078531</pmid><doi>10.1038/18024</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-0836 |
| ispartof | Nature (London), 1999-03, Vol.398 (6722), p.70-73 |
| issn | 0028-0836 1476-4687 |
| language | eng |
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| source | MEDLINE; Nature; Alma/SFX Local Collection |
| subjects | Adenosine Diphosphate Ribose - analogs & derivatives Adenosine Diphosphate Ribose - antagonists & inhibitors Adenosine Diphosphate Ribose - metabolism Adenosine Diphosphate Ribose - pharmacology Calcium Calcium - metabolism Calcium channels Calcium Signaling CD3 Complex - immunology CD3 Complex - metabolism Cellular biology Chromatography, High Pressure Liquid Cyclic ADP-Ribose Enzyme Activation Enzymes Humans Inositol 1,4,5-Trisphosphate - antagonists & inhibitors Inositol 1,4,5-Trisphosphate - metabolism Ions Jurkat Cells Liquid chromatography Lymphocyte Activation Lymphocytes Ryanodine - metabolism Ryanodine Receptor Calcium Release Channel - metabolism Second Messenger Systems T-Lymphocytes - immunology T-Lymphocytes - metabolism |
| title | Regulation of calcium signalling in T lymphocytes by the second messenger cyclic ADP-ribose |
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