ReviewJournal of molecular biology2018
p73 Alternative Splicing: Exploring a Biological Role for the C-Terminal Isoforms.
Review in Journal of molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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.
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
46 citing papers in PubMed, 65 citations in OpenAlex.
- A p53-ΔNp73 signaling axis drives selective motor neuron degeneration in spinal muscular atrophy.bioRxiv : the preprint server for biology · 2026Article
- Integrative Multimodal Profiling of TAp73 and DNp73 Reveals Isoform-Specific Transcriptomic Coregulator Landscapes in Cancer Programs.Biomolecules · 2025Article
- The Hippo signaling pathway as a therapeutic target in Alzheimer's disease.Molecular neurodegeneration · 2025Review
- A novel TAp73-inhibitory compound counteracts stemness features of glioblastoma stem cells.Molecular oncology · 2025Article
- TAp73 and ΔTAp73 isoforms show cell-type specific distributions and alterations in cancer.Scientific reports · 2024Article
- TAp73 regulates mitochondrial dynamics and multiciliated cell homeostasis through an OPA1 axis.Cell death & disease · 2024Article
- Hyperactivation of SREBP induces pannexin-1-dependent lytic cell death.Journal of lipid research · 2024Article
- Alternative splicing and related RNA binding proteins in human health and disease.Signal transduction and targeted therapy · 2024Review
- RAC1b Collaborates with TAp73α-SMAD4 Signaling to Induce Biglycan Expression and Inhibit Basal and TGF-β-Driven Cell Motility in Human Pancreatic Cancer.Biomedicines · 2024Article
- Isoform-specific disruption of theeLife · 2023Article
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- Indisulam exerts anticancer effects via modulation of transcription, translation and alternative splicing on human cervical cancer cells.American journal of cancer research · 2023Article
- p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022Review
- DNA damage response revisited: the p53 family and its regulators provide endless cancer therapy opportunities.Experimental & molecular medicine · 2022Review
- p73 is required for vessel integrity controlling endothelial junctional dynamics through Angiomotin.Cellular and molecular life sciences : CMLS · 2022Article
- p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Recent advances in cancer immunotherapy.Discover oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
p73 (encoded by TP73 gene) is a p53 related protein that functions as a transcriptional factor. Similarly to p53, following DNA damage, p73 is stabilized and activated and controls expression of target genes that are involved in the regulation of cycle arrest and apoptosis. However, great complexity to the function of this gene is given by the wide range of its non-tumor-related roles, which include neurological development, ciliogenesis and fertility. From the structural point of view, p73 displays an intricate range of regulations because it can be expressed both as an N-terminally deleted dominant-negative isoforms and as multiple alternatively spliced C-terminal isoforms, which can include or not a sterile alpha motif domain. More is known about the functions of the N-terminal isoforms of p73 (TAp73 and ΔNp73) and their opposing pro- and anti-apoptotic roles, whereas the functional differences of the distinct C-terminal splice forms of p73 are very far away from been defined. Here we summarize the current available literature regarding p73 C-terminal isoforms and the contribution of the sterile alpha motif domain to p73 function, trying to provide an unified view in this complex and sometime controversial field. Current data indicate that the full-length, TAp73α, is the major, if not the exclusive, isoform detected in physiological systems, indicating that detailed spatio-temporal expression analysis and functional studies are highly demanded to support a physiological role for the p73 alternative splicing. With this article, we also aim to emphasize the need to further investigation on the topic, refocusing the attention on what we believe are the most relevant unanswered questions.
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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.