ArticleProceedings of the National Academy of Sciences of the United States of America2010
Differential control of TAp73 and DeltaNp73 protein stability by the ring finger ubiquitin ligase PIR2.
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 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
- High ΔNp73/TAp73 ratio is associated with poor prognosis in acute promyelocytic leukemia.Blood · 2015Trial
- Mitophagy alleviates neuronal damage after subarachnoid hemorrhage: Role of autophagy-targeting chimera 4.Neural regeneration research · 2026Article
- Construction of diagnostic model and subtype analysis of major depressive disorder based on PANoptosis key genes.BMC psychiatry · 2025Article
- RNF144A and RNF144B: Important molecules for health.Open life sciences · 2025Review
- RNF144B negatively regulates antiviral immunity by targeting MDA5 for autophagic degradation.EMBO reports · 2024Article
- Automated assembly of molecular mechanisms at scale from text mining and curated databases.Molecular systems biology · 2023Article
- Article
- Deciphering the Role of p53 and TAp73 in Neuroblastoma: From Pathogenesis to Treatment.Cancers · 2022Review
- Mechanisms of Survival of Cytomegalovirus-Infected Tumor Cells.Molecular biology · 2022Article
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Review
- Targeting Post-Translational Modifications of the p73 Protein: A Promising Therapeutic Strategy for Tumors.Cancers · 2021Review
- New immunological potential markers for triple negative breast cancer: IL18R1, CD53, TRIM, Jaw1, LTB, PTPRCAP.Discover oncology · 2021Article
- Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021Review
- Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020Review
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.International journal of molecular sciences · 2019Review
- RNF144B inhibits LPS-induced inflammatory responses via binding TBK1.Journal of leukocyte biology · 2019Article
- Pir2/Rnf144b is a potential endometrial cancer biomarker that promotes cell proliferation.Cell death & disease · 2018Article
- p53 and p73 Regulate Apoptosis but Not Cell-Cycle Progression in Mouse Embryonic Stem Cells upon DNA Damage and Differentiation.Stem cell reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
p73 is a p53-related transcription factor with fundamental roles in development and tumor suppression. Transcription from two different promoters on the p73 gene results in generation of transcriptionally active TAp73 isoforms and dominant negative DeltaNp73 isoforms with opposing pro- and anti-apoptotic functions. Therefore, the relative ratio of each isoform is an important determinant of the cell fate. Proteasomal degradation of p73 is mediated by polyubiquitination-dependent and -independent processes both of which appear, thus far, to lack selectivity for the TAp73 and DeltaNp73 isoforms. Here, we describe the characterization of another transcriptional target of TAp73; a ring finger domain ubiquitin ligase p73 Induced RING 2 protein (PIR2). Although PIR2 was initially identified a p53-induced gene (p53RFP), low abundance of PIR2 transcript in mouse embryonic fibroblasts of TAp73 KO mice compared with WT mice and comparison of PIR2 mRNA and protein levels following TAp73 or p53 overexpression substantiate TAp73 isoforms as strong inducers of PIR2. Although PIR2 expression was induced by DNA damage, its expression did not alter apoptotic response or cell cycle profile per se. However, coexpression of PIR2 with TAp73 or DeltaNp73 resulted in an increase of the TA/DeltaNp73 ratio, due to preferential degradation of DeltaNp73. Finally, PIR2 was able to relieve the inhibitory effect of DeltaNp73 on TAp73 induced apoptosis following DNA damage. These results suggest that PIR2, by being induced by TAp73 and degrading DeltaNp73, differentially regulates TAp73/DeltaNp73 stability, and, hence, it may offer a therapeutic approach to enhance the chemosensitivity of tumor cells.
Indexed as
Identifiers
What OpenQuestion holds
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.