ArticleOncogene2008
Deletion analysis and alternative splicing define a transactivation inhibitory domain in human oncoprotein REL.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- SARS-CoV-2 NSP14 MTase activity is critical for inducing canonical NF-κB activation.Bioscience reports · 2024Article
- Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024Review
- The implications of alternative pre-mRNA splicing in cell signal transduction.Experimental & molecular medicine · 2023Review
- Article
- Dynamic Variations of 3'UTR Length Reprogram the mRNA Regulatory Landscape.Biomedicines · 2021Review
- Article
- Regulation of B-cell function by NF-kappaB c-Rel in health and disease.Cellular and molecular life sciences : CMLS · 2020Review
- Myeloid-Derived Suppressor Cell Differentiation in Cancer: Transcriptional Regulators and Enhanceosome-Mediated Mechanisms.Frontiers in immunology · 2020Review
- The Unsolved Puzzle of c-Rel in B Cell Lymphoma.Cancers · 2019Review
- A haplotype variant of the human chromogranin A gene (The Journal of biological chemistry · 2017Article
- c-Rel and its many roles in cancer: an old story with new twists.British journal of cancer · 2016Review
- Identification of an NF-κB p50/p65-responsive site in the human MIR155HG promoter.BMC molecular biology · 2013Article
- Function of alternative splicing.Gene · 2013Review
- 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
- NF-kappaB down-regulates expression of the B-lymphoma marker CD10 through a miR-155/PU.1 pathway.The Journal of biological chemistry · 2011Article
- Article
- Article
- Review
- 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
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Misregulation of REL, a nuclear factor-kappaB family transcription factor, has been implicated in several human lymphoid malignancies. REL has a conserved N-terminal DNA-binding/dimerization domain called the Rel homology domain (RHD) and a C-terminal transactivation domain (TAD). Here, we define the sequences (amino acids (aa) 323-422) between the RHD and TAD as a REL inhibitory domain (RID) because deletion of these sequences increases both REL transactivation and DNA binding. Furthermore, we have characterized two REL mRNA splice variants that encode proteins with alterations near RID: one lacking exon 9 sequences (aa 308-330; RELDelta9) and one with an exonized Alu fragment insertion of 32 aa after aa 307 (REL+Alu). Deletion of RID or exon 9-encoded sequences increases transactivation by GAL4-REL by approximately threefold. Moreover, deletion of RID or exon 9 sequences increases transactivation by full-length REL from certain kappaB site-containing promoters and increases DNA binding by REL. Deletion of RID does not affect REL's ability to transform chicken spleen cells. Reverse transcriptase-polymerase chain reaction analysis of mRNA from both primary lymphoma samples and several transformed tissue culture cell lines indicates that the RELDelta9 splice variant is preferentially expressed in lymphoma, suggesting that the REL transcript lacking exon 9 could serve as a marker for certain types of lymphoid tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.