Sensitisation of c-MYC-induced B-lymphoma cells to apoptosis by ATF2.
dc.contributor.author | Walczynski, J | |
dc.contributor.author | Lyons, Steve | |
dc.contributor.author | Jones, Nic | |
dc.contributor.author | Breitwieser, Wolfgang | |
dc.date.accessioned | 2013-03-15T16:28:41Z | |
dc.date.available | 2013-03-15T16:28:41Z | |
dc.date.issued | 2013-02-18 | |
dc.identifier.citation | Sensitisation of c-MYC-induced B-lymphoma cells to apoptosis by ATF2. 2013: Oncogene | en_GB |
dc.identifier.issn | 1476-5594 | |
dc.identifier.pmid | 23416976 | |
dc.identifier.doi | 10.1038/onc.2013.28 | |
dc.identifier.uri | http://hdl.handle.net/10541/273000 | |
dc.description.abstract | Transcription factors ATF2 (activating transcription factor 2) and ATF7 (activating transcription factor 7) are highly homologous members of the activator protein 1 (AP-1) family. Their activities are growth factor and stress stimulated and they strictly require phosphorylation by mitogen-activated protein (MAP) kinases for their transcriptional functions. In samples of human B-cell lymphomas as well as Eμ-Myc-driven mouse B-cell lymphomas, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK) are significantly up-regulated compared with normal human B-cell lines and mouse B cells, respectively. The B cell-specific deletion of ATF2 and ATF7 in mice results in significantly accelerated onset of Eμ-Myc-induced lymphoma. In addition, loss of ATF2/7 desensitises Eμ-Myc lymphoma cells to spontaneous as well as stress-induced apoptosis. Our results therefore suggest that c-MYC induces stress-mediated activation of ATF2 and ATF7 and that these transcription factors regulate apoptosis in response to oncogenic transformation of B cells.Oncogene advance online publication, 18 February 2013; doi:10.1038/onc.2013.28. | |
dc.language | ENG | |
dc.language.iso | en | en |
dc.rights | Archived with thanks to Oncogene | en_GB |
dc.title | Sensitisation of c-MYC-induced B-lymphoma cells to apoptosis by ATF2. | en |
dc.type | Article | en |
dc.contributor.department | Department of Cell Regulation, Paterson Institute for Cancer Research, University of Manchester, Manchester, UK. | en_GB |
dc.identifier.journal | Oncogene | en_GB |
html.description.abstract | Transcription factors ATF2 (activating transcription factor 2) and ATF7 (activating transcription factor 7) are highly homologous members of the activator protein 1 (AP-1) family. Their activities are growth factor and stress stimulated and they strictly require phosphorylation by mitogen-activated protein (MAP) kinases for their transcriptional functions. In samples of human B-cell lymphomas as well as Eμ-Myc-driven mouse B-cell lymphomas, we find that ATF2 as well as MAP kinase c-Jun N-terminal kinase (JNK) are significantly up-regulated compared with normal human B-cell lines and mouse B cells, respectively. The B cell-specific deletion of ATF2 and ATF7 in mice results in significantly accelerated onset of Eμ-Myc-induced lymphoma. In addition, loss of ATF2/7 desensitises Eμ-Myc lymphoma cells to spontaneous as well as stress-induced apoptosis. Our results therefore suggest that c-MYC induces stress-mediated activation of ATF2 and ATF7 and that these transcription factors regulate apoptosis in response to oncogenic transformation of B cells.Oncogene advance online publication, 18 February 2013; doi:10.1038/onc.2013.28. |