ArticleOncogene2010
An HDAC1-binding domain within FATS bridges p21 turnover to radiation-induced tumorigenesis.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Diagnostic and prognostic potential of cell-free RNAs in cerebrospinal fluid and plasma for brain tumors.NPJ precision oncology · 2025Article
- Novel Oncogenic Value of C10orf90 in Colon Cancer Identified as a Clinical Diagnostic and Prognostic Marker.International journal of molecular sciences · 2024Article
- CDKN1A/p21 in Breast Cancer: Part of the Problem, or Part of the Solution?International journal of molecular sciences · 2023Review
- Gene losses may contribute to subterranean adaptations in naked mole-rat and blind mole-rat.BMC biology · 2022Article
- Loss of fragile site-associated tumor suppressor promotes antitumor immunity via macrophage polarization.Nature communications · 2021Article
- Article
- Depletion of Gram-Positive Bacteria Impacts Hepatic Biological Functions During the Light Phase.International journal of molecular sciences · 2019Article
- From Human Cytogenetics to Human Chromosomics.International journal of molecular sciences · 2019Review
- The value of FATS expression in predicting sensitivity to radiotherapy in breast cancer.Oncotarget · 2017Article
- A functional genetic variant in fragile-site gene FATS modulates the risk of breast cancer in triparous women.BMC cancer · 2015Article
- FATS is an E2-independent ubiquitin ligase that stabilizes p53 and promotes its activation in response to DNA damage.Oncogene · 2014Article
- Stabilization of p21 (Cip1/WAF1) following Tip60-dependent acetylation is required for p21-mediated DNA damage response.Cell death and differentiation · 2013Article
- Common fragile sites: genomic hotspots of DNA damage and carcinogenesis.International journal of molecular sciences · 2012Review
- FATS is a transcriptional target of p53 and associated with antitumor activity.Molecular cancer · 2010Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a gap between the initial formation of cells carrying radiation-induced genetic damage and their contribution to cancer development. Herein, we reveal a previously uncharacterized gene FATS through a genome-wide approach and demonstrate its essential role in regulating the abundance of p21 in surveillance of genome integrity. A large exon coding the NH2-terminal domain of FATS, deleted in spontaneous mouse lymphomas, is much more frequently deleted in radiation-induced mouse lymphomas. Its human counterpart is a fragile site gene at a previously identified loss of heterozygosity site. FATS is essential for maintaining steady-state level of p21 protein and sustaining DNA damage checkpoint. Furthermore, the NH2-terminal FATS physically interacts with histone deacetylase 1 (HDAC1) to enhance the acetylation of endogenous p21, leading to the stabilization of p21. Our results reveal a molecular linkage between p21 abundance and radiation-induced carcinogenesis.
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