Early response gene signalling cascades activated by ionising radiation in primary human B cells.
dc.contributor.author | Wilson, R E | |
dc.contributor.author | Taylor, S L | |
dc.contributor.author | Atherton, Graham T | |
dc.contributor.author | Johnston, D | |
dc.contributor.author | Waters, C M | |
dc.contributor.author | Norton, John D | |
dc.date.accessioned | 2010-06-07T10:36:22Z | |
dc.date.available | 2010-06-07T10:36:22Z | |
dc.date.issued | 1993-12 | |
dc.identifier.citation | Early response gene signalling cascades activated by ionising radiation in primary human B cells. 1993, 8 (12):3229-37 Oncogene | en |
dc.identifier.issn | 0950-9232 | |
dc.identifier.pmid | 8247526 | |
dc.identifier.uri | http://hdl.handle.net/10541/100398 | |
dc.description.abstract | We have used a panel of 13 protein kinase C-responsive immediate early gene probes to dissect the cellular signalling pathways activated by ionising gamma radiation in primary human B cells. Of these 13 genes, a delayed transient induction was observed for only 8: c-fos, c-jun, jun-B, jun-D, c-myc, ergI/krox 24 and two 'anonymous' genes, 3L3 and 19A. Expression of c-myc and c-fos mRNAs was paralleled by the appearance of their encoded proteins suggesting that these oncoproteins may couple radiation signalling to cellular responses. Of three protein kinase C-coupled transcription factors examined by gel retardation assay, (AP1, NF kappa B, EgrK/Krox24) only NF kappa B and, to a lesser extent, AP1 was stimulated in response to irradiation. These observations are not obviously compatible with a simple model invoking protein kinase C in radiation signalling in primary B cells and suggest that the pleiotropic effects of ionising radiation on this cell type are mediated through a distinct cellular signalling cascade. | |
dc.language.iso | en | en |
dc.subject.mesh | B-Lymphocytes | |
dc.subject.mesh | Base Sequence | |
dc.subject.mesh | Blotting, Northern | |
dc.subject.mesh | Blotting, Western | |
dc.subject.mesh | Cells, Cultured | |
dc.subject.mesh | DNA | |
dc.subject.mesh | DNA-Binding Proteins | |
dc.subject.mesh | Early Growth Response Protein 1 | |
dc.subject.mesh | Gene Expression Regulation | |
dc.subject.mesh | Genes, Immediate-Early | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Immediate-Early Proteins | |
dc.subject.mesh | Molecular Sequence Data | |
dc.subject.mesh | NF-kappa B | |
dc.subject.mesh | Protein Kinase C | |
dc.subject.mesh | Proto-Oncogene Proteins c-fos | |
dc.subject.mesh | Proto-Oncogene Proteins c-jun | |
dc.subject.mesh | Proto-Oncogene Proteins c-myc | |
dc.subject.mesh | RNA, Messenger | |
dc.subject.mesh | Radiation, Ionizing | |
dc.subject.mesh | Retroviridae Proteins, Oncogenic | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Tetradecanoylphorbol Acetate | |
dc.subject.mesh | Transcription Factors | |
dc.subject.mesh | Transcription, Genetic | |
dc.title | Early response gene signalling cascades activated by ionising radiation in primary human B cells. | en |
dc.type | Article | en |
dc.contributor.department | CRC Department of Carcinogenesis, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester, UK. | en |
dc.identifier.journal | Oncogene | en |
html.description.abstract | We have used a panel of 13 protein kinase C-responsive immediate early gene probes to dissect the cellular signalling pathways activated by ionising gamma radiation in primary human B cells. Of these 13 genes, a delayed transient induction was observed for only 8: c-fos, c-jun, jun-B, jun-D, c-myc, ergI/krox 24 and two 'anonymous' genes, 3L3 and 19A. Expression of c-myc and c-fos mRNAs was paralleled by the appearance of their encoded proteins suggesting that these oncoproteins may couple radiation signalling to cellular responses. Of three protein kinase C-coupled transcription factors examined by gel retardation assay, (AP1, NF kappa B, EgrK/Krox24) only NF kappa B and, to a lesser extent, AP1 was stimulated in response to irradiation. These observations are not obviously compatible with a simple model invoking protein kinase C in radiation signalling in primary B cells and suggest that the pleiotropic effects of ionising radiation on this cell type are mediated through a distinct cellular signalling cascade. |