ArticleOncogene2006
NF-kappaB regulates the stability and activity of p73 by inducing its proteolytic degradation through a ubiquitin-dependent proteasome pathway.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 22 citations in OpenAlex.
- Loss of p73 Expression Contributes to Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024Article
- The Emerging Role of the Major Histocompatibility Complex Class I in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2017Review
- TAp73 upregulates IL-1β in cancer cells: Potential biomarker in lung and breast cancer?Biochemical and biophysical research communications · 2017Article
- TAp73 protein stability is controlled by histone deacetylase 1 via regulation of Hsp90 chaperone function.The Journal of biological chemistry · 2013Article
- Article
- Regulation of p73 activity by post-translational modifications.Cell death & disease · 2012Review
- The role of RelA (p65) threonine 505 phosphorylation in the regulation of cell growth, survival, and migration.Molecular biology of the cell · 2011Article
- p73 as a pharmaceutical target for cancer therapy.Current pharmaceutical design · 2011Review
- Regulation of ΔNp63α by NFκΒ.Cell cycle (Georgetown, Tex.) · 2010Article
- Arsenic trioxide induces apoptosis in NB-4, an acute promyelocytic leukemia cell line, through up-regulation of p73 via suppression of nuclear factor kappa B-mediated inhibition of p73 transcription and prevention of NF-kappaB-mediated induction of XIAP, cIAP2, BCL-XL and survivin.Medical oncology (Northwood, London, England) · 2010Article
- IKKbeta-mediated nuclear factor-kappaB activation attenuates smac mimetic-induced apoptosis in cancer cells.Molecular cancer therapeutics · 2009Article
- Blockage of NF-kappaB by IKKbeta- or RelA-siRNA rather than the NF-kappaB super-suppressor IkappaBalpha mutant potentiates adriamycin-induced cytotoxicity in lung cancer cells.Journal of cellular biochemistry · 2008Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor kappa B (NF-kappaB), which exists as heterodimeric complexes composed of p50 and p65, has been shown to play an important role in cell survival processes. In the present study, we found for the first time that NF-kappaB has an ability to induce the ubiquitin-dependent proteasomal degradation of proapoptotic p73alpha. The activation of NF-kappaB in tumor necrosis factor alpha (TNF-alpha)-stimulated H1299 cells resulted in a significant reduction in the amounts of the endogenous p73alpha. Consistent with these results, TNF-alpha-mediated downregulation of p73alpha was observed in wild-type (WT) mouse embryonic fibroblasts (MEFs) but not in p65-deficient MEFs. Ectopic expression of NF-kappaB decreased a half-life of p73alpha by increasing its ubiquitination levels, and thereby inhibiting the transcriptional activity as well as proapoptotic function of p73alpha, whereas NF-kappaB had undetectable effects on p53. Immunoprecipitation experiments demonstrated that, under our experimental conditions, NF-kappaB does not bind to p73alpha in mammalian cultured cells. In contrast to WT p65, the COOH-terminal deletion mutant of p65 (p65DeltaC) failed to reduce the expression levels of p73alpha, suggesting that NF-kappaB-mediated proteolytic degradation of p73alpha requires the transcriptional activity of NF-kappaB. Taken together, our present results imply that NF-kappaB-mediated degradation of proapoptotic p73 is a novel inhibitory mechanism of p73 that regulates cell survival and death.
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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.