ArticleMolecular and cellular biology2000
The Rel/NF-kappaB family directly activates expression of the apoptosis inhibitor Bcl-x(L).
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 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.
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Who cites it
297 citing papers in PubMed, 749 citations in OpenAlex.
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- Sensitising PDAC to Gemcitabine by Suppressing NF-κB Pathway and Enhancing Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- CAR Intrinsic Design Pre-Shapes Transcriptional and Metabolic Networks in CAR T Cells.Metabolites · 2026Article
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- Correlation between metabolic unhealth and prostate cancer -an inverse probability weighting study.BMC urology · 2025Article
- Reactive Oxygen Species Across Death Pathways: Gatekeepers of Apoptosis, Ferroptosis, Pyroptosis, Paraptosis, and Beyond.International journal of molecular sciences · 2025Review
- Synergy and antagonism in the integration of BCR and CD40 signals that control B-cell population expansion.Molecular systems biology · 2025Article
- Interaction between NF-κB and PLAC8 impairs autophagy providing a survival advantage to prostate cells transformed by cadmium.Science advances · 2025Article
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- The effect of AKT inhibition in α-synuclein-dependent neurodegeneration.Frontiers in molecular neuroscience · 2025Article
- Aloperin improves liver non-alcoholic steatohepatitisArchives of medical science : AMS · 2025Article
- Nuclear Factor Kappa B p65: A Possible Biomarker for Persistent Inflammation in HIV-1 Infection?Cureus · 2024Review
- Venetoclax acts as an immunometabolic modulator to potentiate adoptive NK cell immunotherapy against leukemia.Cell reports. Medicine · 2024Article
237 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factors of the Rel/NF-kappaB family are key regulators of immune and inflammatory responses and contribute to lymphocyte proliferation, survival, and oncogenesis. The absolute correlation between the antiapoptotic and oncogenic activities of the Rel/NF-kappaB oncoprotein v-Rel emphasizes the importance of characterizing the death antagonists under NF-kappaB control. Our recent finding that the prosurvival Bcl-2 homolog Bfl-1 (also called A1) is a direct transcriptional target of NF-kappaB raised the issue of whether NF-kappaB is a specific or global regulator of death antagonists in the Bcl-2 family. Here, we demonstrate that NF-kappaB differentially regulates the expression of particular Bcl-2-related death inhibitors and that it directly activates the expression of Bcl-x(L). While Bcl-x(L) was significantly upregulated by c-Rel and RelA, Bcl-2 was not. Importantly, stimuli that activate endogenous NF-kappaB factors also upregulated bcl-x gene expression and this effect was antagonized by an inhibitor of NF-kappaB activity. The expression of bcl-x suppressed apoptosis in the presence or absence of NF-kappaB activity. Functional analysis of the bcl-x promoter demonstrated that it is directly controlled by c-Rel. These results establish that NF-kappaB directly regulates the expression of distinct prosurvival factors in the Bcl-2 family, such as Bcl-x(L) and Bfl-1/A1. These findings raise the possibility that some of these factors may contribute to oncogenesis associated with aberrant Rel/NF-kappaB activity.
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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.