ArticleMolecular cancer research : MCR2015
Identification of TRIML2, a novel p53 target, that enhances p53 SUMOylation and regulates the transactivation of proapoptotic genes.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 55 citations in OpenAlex.
- Identification of Ageing-related Hub Genes in Humans, Mouse and Rat Based on Bioinformatics Analysis.Annals of neurosciences · 2025Article
- Expression of tripartite motif family-like protein 1 and 2 in early conceptus development and placentation in the pig.Reproduction & fertility · 2025Article
- The function of TRIML2 on the temozolomide resistance in glioblastoma.Annals of medicine and surgery (2012) · 2025Article
- Establishment of an anaplastic stratification signature for gastric cancer based on diverse regulated cell-death.Frontiers in immunology · 2025Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- Tripartite Motif Protein Family in Central Nervous System Diseases.Cellular and molecular neurobiology · 2023Review
- Review
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- Association of TP53 gene polymorphisms with the risk of acute lymphoblastic leukemia in Moroccan children.Molecular biology reports · 2022Article
- Reading oscillatory instructions: How cells achieve time-dependent responses to oscillating transcription factors.Current opinion in cell biology · 2022Review
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- RNA Microarray-Based Comparison of Innate Immune Phenotypes between Human THP-1 Macrophages Stimulated with Two BCG Strains.International journal of molecular sciences · 2022Article
- The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022Review
- PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation.Nature communications · 2022Article
- It's Getting Complicated-A Fresh Look at p53-MDM2-ARF Triangle in Tumorigenesis and Cancer Therapy.Frontiers in cell and developmental biology · 2022Review
- p53 signaling in cancer progression and therapy.Cancer cell international · 2021Review
- Article
- Differential Transcriptional Regulation of Polymorphic p53 Codon 72 in Metabolic Pathways.International journal of molecular sciences · 2021Article
- Tumor suppressor p53 cross-talks with TRIM family proteins.Genes & diseases · 2021Review
- Multifunctional barcoding with ClonMapper enables high-resolution study of clonal dynamics during tumor evolution and treatment.Nature cancer · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
unlabelledThe tumor-suppressor protein p53, encoded by TP53, inhibits tumorigenesis by inducing cell-cycle arrest, senescence, and apoptosis. Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino acid 72 (P72 and R72, respectively); this polymorphism alters p53 function. In general, the P72 variant shows increased ability to induce cell-cycle arrest, whereas the R72 variant possesses increased ability to induce apoptosis, relative to P72. At present, the underlying mechanisms for these functional differences are not fully understood. Toward elucidating the molecular basis for these differences, a gene-expression microarray analysis was conducted on normal human fibroblast cells that are homozygous for P72 and R72 variants, along with subclones of these lines that express a p53 short hairpin (shp53). Approximately three dozen genes were identified whose transactivation is affected by the codon 72 polymorphism. One of these is the tripartite-motif family-like 2 (TRIML2) gene, which is preferentially induced by the R72 variant. Importantly, the accumulated data indicate that TRIML2 interacts with p53, and facilitates the modification of p53 with SUMO2. TRIML2 also enhances the ability of p53 to transactivate a subset of proapoptotic target genes associated with prolonged oxidative stress, including PIDD, PIG3 (TP53I3), and PIG6 (PRODH). These data indicate that TRIML2 is part of a feed-forward loop that activates p53 in cells expressing the R72 variant, particularly after prolonged stress. IMPLICATIONS: The defined actions of TRIML2, in part, explain the underlying molecular basis for increased apoptotic potential of the R72 variant of p53.
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