ArticleOncogene2003
Deletion of either C-terminal transactivation subdomain enhances the in vitro transforming activity of human transcription factor REL in chicken spleen cells.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- The Unsolved Puzzle of c-Rel in B Cell Lymphoma.Cancers · 2019Review
- The Direct and Indirect Roles of NF-κB in Cancer: Lessons from Oncogenic Fusion Proteins and Knock-in Mice.Biomedicines · 2018Review
- Evidence for an oncogenic modifier role for mutant histone acetyltransferases in diffuse large B-cell lymphoma.Leukemia & lymphoma · 2016Article
- The NF-κB subunit c-Rel regulates Bach2 tumour suppressor expression in B-cell lymphoma.Oncogene · 2016Article
- The c-Rel Transcription Factor in Development and Disease.Genes & cancer · 2011Article
- Characterization of the core elements of the NF-κB signaling pathway of the sea anemone Nematostella vectensis.Molecular and cellular biology · 2011Article
- A rearranged EP300 gene in the human B-cell lymphoma cell line RC-K8 encodes a disabled transcriptional co-activator that contributes to cell growth and oncogenicity.Cancer letters · 2011Article
- c-Rel deficiency increases caspase-4 expression and leads to ER stress and necrosis in EBV-transformed cells.PloS one · 2011Article
- Histone acetyltransferase p300 is a coactivator for transcription factor REL and is C-terminally truncated in the human diffuse large B-cell lymphoma cell line RC-K8.Cancer letters · 2010Article
- Peptidyl-prolyl isomerase Pin1 markedly enhances the oncogenic activity of the rel proteins in the nuclear factor-kappaB family.Cancer research · 2009Article
- Article
- RNAi-mediated c-Rel silencing leads to apoptosis of B cell tumor cells and suppresses antigenic immune response in vivo.PloS one · 2009Article
- Deletion analysis and alternative splicing define a transactivation inhibitory domain in human oncoprotein REL.Oncogene · 2008Article
- CAPERalpha is a novel Rel-TAD-interacting factor that inhibits lymphocyte transformation by the potent Rel/NF-kappaB oncoprotein v-Rel.Journal of virology · 2008Article
- Review
- The p53 homologue DeltaNp63alpha interacts with the nuclear factor-kappaB pathway to modulate epithelial cell growth.Cancer research · 2008Article
- Ser484 and Ser494 in REL are the major sites of IKK phosphorylation in vitro: evidence that IKK does not directly enhance GAL4-REL transactivation.Gene expression · 2008Article
- Article
- Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The REL gene is amplified in many human B-cell lymphomas and we have previously shown that expression of REL from a retroviral vector can malignantly transform chicken spleen cells in vitro. To identify REL protein functions necessary for malignant transformation, we have performed deletion analysis on REL sequences encoding residues of two C-terminal subdomains that are involved in transcriptional activation. We find that deletion of both C-terminal transactivation subdomains abolishes the ability of REL to transform chicken spleen cells in vitro. In contrast, deletion of either transactivation subdomain alone, which reduces the transactivation ability of REL, enhances the transforming activity of REL. Transforming REL mutants missing C-terminal sequences can also be selected at a low frequency in vitro. The REL transactivation domain can be functionally replaced in transformation assays by a portion of the VP16 transactivation domain that activates at a level similar to REL-transforming mutants. We also find that deletion of 29 C-terminal amino acids causes the subcellular localization of REL to change from cytoplasmic to nuclear in chicken embryo fibroblasts. In contrast, wild-type REL and all transforming REL mutants are located primarily in the cytoplasm of transformed spleen cells. Nevertheless, treatment of transformed spleen cells with leptomycin B causes wild-type REL and two REL mutants to relocalize to the nucleus, and nuclear extracts from these transformed cells contain REL DNA-binding activity. Taken together, these results suggest the following: (1) that REL must activate transcription to transform cells in vitro; (2) that a reduced level of transactivation enhances the oncogenicity of REL; (3) that REL shuttles from the cytoplasm to the nucleus in transformed chicken spleen cells; and (4) that mutations in REL, in addition to amplifications, could activate its oncogenicity in human lymphomas.
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Registered trials
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