| First Author | Keller U | Year | 2005 |
| Journal | Oncogene | Volume | 24 |
| Issue | 41 | Pages | 6231-40 |
| PubMed ID | 15940251 | Mgi Jnum | J:101764 |
| Mgi Id | MGI:3604950 | Doi | 10.1038/sj.onc.1208779 |
| Citation | Keller U, et al. (2005) Nfkb 1 is dispensable for Myc-induced lymphomagenesis. Oncogene 24(41):6231-40 |
| abstractText | Rel/NF-kappaB transcription factors are critical arbiters of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The p50 NF-kappaB 1 component of Rel/NF-kappaB DNA-binding dimers regulates genes involved in both cell cycle traverse and apoptosis. Nfkb 1 loss accelerates B cell growth and leads to increased B cell turnover in vivo, phenotypes akin to those manifested in B cells of Emu-Myc transgenic mice, a model of human Burkitt lymphoma. Interestingly, Emu-Myc B cells express reduced levels of cytoplasmic and nuclear NF-kappaB 1 and have reduced Rel/NF-kappaB DNA-binding activity, suggesting that Myc-mediated repression of NF-kappaB 1 might mediate its proliferative and apoptotic effects on B cells. Furthermore, Nfkb 1 expression was reduced in the majority of Emu-Myc lymphomas and was also suppressed in human Burkitt lymphoma. Nonetheless, loss of Nfkb 1 did not appreciably affect Myc's proliferative or apoptotic responses in B cells and had no effect on lymphoma development in Emu-Myc mice. Therefore, Nfkb 1 is dispensable for Myc-induced lymphomagenesis.. |
