ArticleOncogene2003
Cyclin E and Bcl-xL cooperatively induce cell cycle progression in c-Rel-/- B 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 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 55 citations in OpenAlex.
- c-Rel plays a key role in deficient activation of B cells from a non-X-linked hyper-IgM patient.Blood · 2006Trial
- Nicotiana glauca leaf extract exhibits synergistic antioxidant and anticancer activities revealed by phytochemical profiling and molecular docking.Scientific reports · 2026Article
- NF-κB subunits direct kinetically distinct transcriptional cascades in antigen receptor-activated B cells.Nature immunology · 2023Article
- SHCBP1 contributes to the proliferation and self‑renewal of cervical cancer cells and activation of the NF‑κB signaling pathway through EIF5A.Oncology letters · 2023Article
- The NFκB signaling system in the generation of B-cell subsets: from germinal center B cells to memory B cells and plasma cells.Frontiers in immunology · 2023Review
- microRNA-106b-5p Promotes Cell Growth and Sensitizes Chemosensitivity to Sorafenib by Targeting the BTG3/Bcl-xL/p27 Signaling Pathway in Hepatocellular Carcinoma.Journal of oncology · 2022Article
- Regulation of B-cell function by NF-kappaB c-Rel in health and disease.Cellular and molecular life sciences : CMLS · 2020Review
- c-Rel gain in B cells drives germinal center reactions and autoantibody production.The Journal of clinical investigation · 2020Article
- BCR-Induced CaCell reports · 2020Article
- Collateral Sensitivity of Parthenolide via NF-κB and HIF-α Inhibition and Epigenetic Changes in Drug-Resistant Cancer Cell Lines.Frontiers in pharmacology · 2019Article
- NFκB1 is essential to prevent the development of multiorgan autoimmunity by limiting IL-6 production in follicular B cells.The Journal of experimental medicine · 2016Article
- MicroRNA-302/367 cluster governs hESC self-renewal by dually regulating cell cycle and apoptosis pathways.Stem cell reports · 2015Article
- A pathway switch directs BAFF signaling to distinct NFκB transcription factors in maturing and proliferating B cells.Cell reports · 2014Article
- c-Rel regulates Ezh2 expression in activated lymphocytes and malignant lymphoid cells.The Journal of biological chemistry · 2014Article
- Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferation, and survival of B cells.Genes & development · 2012Article
- The c-Rel Transcription Factor in Development and Disease.Genes & cancer · 2011Article
- c-Rel deficiency increases caspase-4 expression and leads to ER stress and necrosis in EBV-transformed cells.PloS one · 2011Article
- Roles of the NF-kappaB pathway in lymphocyte development and function.Cold Spring Harbor perspectives in biology · 2010Review
- RNAi-mediated c-Rel silencing leads to apoptosis of B cell tumor cells and suppresses antigenic immune response in vivo.PloS one · 2009Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Aberrant overexpression of the c-rel protooncogene is associated with lymphoid malignancy, while c-rel deletion produces severe lymphoproliferative defects and immunodeficiency. To investigate the mechanism of c-rel-induced proliferation and cell cycle progression in B lymphocytes, we have compared signaling events elicited through the BCR in c-rel-/- and wild-type B cells. BCR stimulation of c-rel-/- B cells fails to induce proper cyclin expression, resulting in G1 phase arrest, but it is unclear whether these defects are in fact secondary events of decreased B-cell survival, since c-rel deletion also affects the expression of antiapoptotic genes such as bcl-xL. Here, we use the bcl-xL transgene to correct the viability of c-rel-deficient B cells, and show that the inhibition of apoptosis does not necessarily confer hyperproliferation of B cells activated through the BCR. c-rel-/- B cells still fail to enter the S phase despite improved survival by bcl-xL overexpression, suggesting that c-Rel-associated cell cycle progression is dependent on more than just enhanced cell viability. Overexpression of cyclin E protein, however, can cooperate with Bcl-xL to restore cell cycle progression to c-rel-/- B cells via induction of the cyclin-CDK/Rb-E2F pathway. Furthermore, we show that c-Rel can directly regulate transcription of the e2f3a promoter/enhancer, which is then likely to lead to transcriptional activation of the cyclin E promoter by E2F3a. Hence, these studies provide clear evidence that control of lymphocyte proliferation via c-Rel is linked to a cyclin-dependent process, and suggest that c-Rel not only activates antiapoptotic signaling but also the induction of cell cycle progression.
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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.