ArticleProceedings of the National Academy of Sciences of the United States of America2009
TAp73 regulates the spindle assembly checkpoint by modulating BubR1 activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 78 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.
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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.
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Who cites it
78 citing papers in PubMed, 126 citations in OpenAlex.
- Regulatory Interplay of p53, AMPK, and mTOR in Decidualization: Implications for Reproductive Competence and Cancer Biology.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer.Seminars in cancer biology · 2024Review
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- ZNF750: A Novel Prognostic Biomarker in Metastatic Prostate Cancer.International journal of molecular sciences · 2023Article
- Deciphering the Role of p53 and TAp73 in Neuroblastoma: From Pathogenesis to Treatment.Cancers · 2022Review
- Long non-coding RNAs affecting cell metabolism in cancer.Biology direct · 2022Review
- Distinct interactors define the p63 transcriptional signature in epithelial development or cancer.The Biochemical journal · 2022Article
- Total neoadjuvant therapy for the treatment of locally advanced rectal cancer: a systematic minireview.Biology direct · 2022Review
- Targeting lipid metabolism in cancer: neuroblastoma.Cancer metastasis reviews · 2022Review
- No Time to Die: How Kidney Cancer Evades Cell Death.International journal of molecular sciences · 2022Review
- Maternal effect factors that contribute to oocytes developmental competence: an update.Journal of assisted reproduction and genetics · 2022Review
- p53-driven lipidome influences non-cell-autonomous lysophospholipids in pancreatic cancer.Biology direct · 2022Article
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- PIGN spatiotemporally regulates the spindle assembly checkpoint proteins in leukemia transformation and progression.Scientific reports · 2021Article
- Tissue-specific expression of p73 and p63 isoforms in human tissues.Cell death & disease · 2021Article
- New immunological potential markers for triple negative breast cancer: IL18R1, CD53, TRIM, Jaw1, LTB, PTPRCAP.Discover oncology · 2021Article
- Longevity pathways are associated with human ovarian ageing.Human reproduction open · 2021Article
- Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021Review
- Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedCorrection for Tomasini et al., TAp73 regulates the spindle assembly checkpoint by modulating BubR1 activity.2018 · Ruffini, Alessandro [corrected to Rufini, Alessandro]
Authors and funding
11 authors at 7 institutions in 6 countries.
Funding
Abstract
The role of various p73 isoforms in tumorigenesis has been controversial. However, as we have recently shown, the generation of TAp73-deficient (TAp73(-/-)) mice reveals that TAp73 isoforms exert tumor-suppressive functions, indicating an emerging role for Trp-73 in the maintenance of genomic stability. Unlike mice lacking all p73 isoforms, TAp73(-/-) mice show a high incidence of spontaneous tumors. Moreover, TAp73(-/-) mice are infertile and produce oocytes exhibiting spindle abnormalities. These data suggest a link between TAp73 activities and the common molecular machinery underlying meiosis and mitosis. Previous studies have indicated that the spindle assembly checkpoint (SAC) complex, whose activation leads to mitotic arrest, also regulates meiosis. In this study, we demonstrate in murine and human cells that TAp73 is able to interact directly with several partners of the SAC complex (Bub1, Bub3, and BubR1). We also show that TAp73 is involved in SAC protein localization and activities. Moreover, we show that decreased TAp73 expression correlates with increases of SAC protein expression in patients with lung cancer. Our results establish TAp73 as a regulator of SAC responses and indicate that TAp73 loss can lead to mitotic arrest defects. Our data suggest that SAC impairment in the absence of functional TAp73 could explain the genomic instability and increased aneuploidy observed in TAp73-deficient cells.
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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.