ArticleCell death and differentiation2016
Mechanism of TAp73 inhibition by ΔNp63 and structural basis of p63/p73 hetero-tetramerization.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 41 citations in OpenAlex.
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
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- Alternative splicing in the DBD linker region of p63 modulates binding to DNA and iASPP in vitro.Cell death & disease · 2025Article
- p63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.Cells · 2025Review
- DARPins as a novel tool to detect and degrade p73.Cell death & disease · 2024Article
- p63: a crucial player in epithelial stemness regulation.Oncogene · 2023Review
- DARPins detect the formation of hetero-tetramers of p63 and p73 in epithelial tissues and in squamous cell carcinoma.Cell death & disease · 2023Article
- Article
- Disease-related p63 DBD mutations impair DNA binding by distinct mechanisms and varying degree.Cell death & disease · 2023Article
- The Splicing Factor PTBP1 RepressesCancer research communications · 2022Article
- Designed Ankyrin Repeat Proteins as a tool box for analyzing p63.Cell death and differentiation · 2022Article
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Isoform-Specific Roles of Mutant p63 in Human Diseases.Cancers · 2021Review
- Review
- Article
- Article
- Article
- Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine.Cell death and differentiation · 2018Review
- Mutant and wild-type p53 form complexes with p73 upon phosphorylation by the kinase JNK.Science signaling · 2018Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Members of the p53 tumor-suppressor family are expressed as multiple isoforms. Isoforms with an N-terminal transactivation domain are transcriptionally active, while those ones lacking this domain often inhibit the transcriptional activity of other family members. In squamous cell carcinomas, the high expression level of ΔNp63α inhibits the tumor-suppressor function of TAp73β. This can in principle be due to blocking of the promoter or by direct interaction between both proteins. p63 and p73 can hetero-oligomerize through their tetramerization domains and a hetero-tetramer consisting of two p63 and two p73 molecules is thermodynamically more stable than both homo-tetramers. Here we show that cells expressing both p63 and p73 exist in mouse epidermis and hair follicle and that hetero-tetramer complexes can be detected by immunoprecipitation in differentiating keratinocytes. Through structure determination of the hetero-tetramer, we reveal why this hetero-tetramer is the thermodynamically preferred species. We have created mutants that exclusively form either hetero-tetramers or homo-tetramers, allowing to investigate the function of these p63/p73 hetero-tetramers. Using these tools, we show that inhibition of TAp73β in squamous cell carcinomas is due to promoter squelching and not direct interaction.
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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.