ArticleProceedings of the National Academy of Sciences of the United States of America2010
The antiapoptotic DeltaNp73 is degraded in a c-Jun-dependent manner upon genotoxic stress through the antizyme-mediated pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- High ΔNp73/TAp73 ratio is associated with poor prognosis in acute promyelocytic leukemia.Blood · 2015Trial
- Antizyme inhibitor family: biological and translational research implications.Cell communication and signaling : CCS · 2024Review
- EPLIN-β is a novel substrate of ornithine decarboxylase antizyme 1 and mediates cellular migration.Journal of cell science · 2023Article
- Deciphering the Nature ofCancers · 2021Article
- Review
- Role of Antizyme Inhibitor Proteins in Cancers and Beyond.OncoTargets and therapy · 2021Review
- Inhibition of tumor suppressor p73 by nerve growth factor receptor via chaperone-mediated autophagy.Journal of molecular cell biology · 2020Article
- Inhibition of the polyamine synthesis enzyme ornithine decarboxylase sensitizes triple-negative breast cancer cells to cytotoxic chemotherapy.The Journal of biological chemistry · 2020Article
- Image-Based Network Analysis of DNp73 Expression by Immunohistochemistry in Rectal Cancer Patients.Frontiers in physiology · 2019Article
- The antizyme family for regulating polyamines.The Journal of biological chemistry · 2018Review
- Antizyme Inhibitors in Polyamine Metabolism and Beyond: Physiopathological Implications.Medical sciences (Basel, Switzerland) · 2018Review
- Novel ubiquitin-independent nucleolar c-Myc degradation pathway mediated by antizyme 2.Scientific reports · 2018Article
- TAp73 is a marker of glutamine addiction in medulloblastoma.Genes & development · 2017Article
- p73 gene in dopaminergic neurons is highly susceptible to manganese neurotoxicity.Neurotoxicology · 2017Article
- Antizyme inhibitor 1: a potential carcinogenic molecule.Cancer science · 2017Review
- p73 regulates basal and starvation-induced liver metabolism in vivo.Oncotarget · 2015Article
- Interaction of polyamines and mTOR signaling in the synthesis of antizyme (AZ).Cellular signalling · 2015Article
- A balancing act: orchestrating amino-truncated and full-length p73 variants as decisive factors in cancer progression.Oncogene · 2015Review
- A role for antizyme inhibitor in cell proliferation.Amino acids · 2015Article
- Structure and apoptotic function of p73.BMB reports · 2015Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 4 countries.
Funding
Abstract
p73, the structural and functional homologue of p53, exists as two major forms: the transactivation-proficient, proapoptotic TAp73 or the transactivation-deficient, antiapoptotic DNp73. Expectedly, expression of both these major forms has to be coordinated precisely to achieve the desired cellular outcome. Genotoxic insults resulting in cell death lead to the stabilization of TAp73, mainly through posttranslational modifications, and the concomitant degradation of DNp73, through poorly understood mechanisms. We have therefore investigated the possible mechanisms of stress-induced DNp73 degradation and show here that c-Jun, the AP-1 family member activated by stress signals and involved in stabilizing TAp73, promotes DNp73 degradation. Genotoxic stress-mediated DNp73 degradation was found to occur in a c-Jun-dependent manner through a ubiquitin-independent but proteasome-dependent mechanism. Absence or down-regulation of c-Jun expression abrogated the reduction of DNp73 levels upon stress insults, whereas overexpression of c-Jun led to its degradation. c-Jun controlled DNp73 degradation through the nonclassical, polyamine-induced antizyme (Az) pathway by regulating the latter's processing during stress response. Consistently, expression of c-Jun or Az, or addition of polyamines, promoted DNp73 degradation, whereas silencing Az expression or inhibiting Az activity in cells exposed to stress reduced c-Jun-dependent DNp73 degradation. Moreover, Az was able to bind to DNp73. These data together demonstrate the existence of a c-Jun-dependent mechanism regulating the abundance of the antiapoptotic DNp73 in response to genotoxic stress.
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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.