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dc.contributor.authorWilson, R E
dc.contributor.authorTaylor, S L
dc.contributor.authorAtherton, Graham T
dc.contributor.authorJohnston, D
dc.contributor.authorWaters, C M
dc.contributor.authorNorton, John D
dc.date.accessioned2010-06-07T10:36:22Z
dc.date.available2010-06-07T10:36:22Z
dc.date.issued1993-12
dc.identifier.citationEarly response gene signalling cascades activated by ionising radiation in primary human B cells. 1993, 8 (12):3229-37 Oncogeneen
dc.identifier.issn0950-9232
dc.identifier.pmid8247526
dc.identifier.urihttp://hdl.handle.net/10541/100398
dc.description.abstractWe 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.isoenen
dc.subject.meshB-Lymphocytes
dc.subject.meshBase Sequence
dc.subject.meshBlotting, Northern
dc.subject.meshBlotting, Western
dc.subject.meshCells, Cultured
dc.subject.meshDNA
dc.subject.meshDNA-Binding Proteins
dc.subject.meshEarly Growth Response Protein 1
dc.subject.meshGene Expression Regulation
dc.subject.meshGenes, Immediate-Early
dc.subject.meshHumans
dc.subject.meshImmediate-Early Proteins
dc.subject.meshMolecular Sequence Data
dc.subject.meshNF-kappa B
dc.subject.meshProtein Kinase C
dc.subject.meshProto-Oncogene Proteins c-fos
dc.subject.meshProto-Oncogene Proteins c-jun
dc.subject.meshProto-Oncogene Proteins c-myc
dc.subject.meshRNA, Messenger
dc.subject.meshRadiation, Ionizing
dc.subject.meshRetroviridae Proteins, Oncogenic
dc.subject.meshSignal Transduction
dc.subject.meshTetradecanoylphorbol Acetate
dc.subject.meshTranscription Factors
dc.subject.meshTranscription, Genetic
dc.titleEarly response gene signalling cascades activated by ionising radiation in primary human B cells.en
dc.typeArticleen
dc.contributor.departmentCRC Department of Carcinogenesis, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester, UK.en
dc.identifier.journalOncogeneen
html.description.abstractWe 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.


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