ArticleNature communications2018
Structural basis for reactivating the mutant TERT promoter by cooperative binding of p52 and ETS1.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 69 citations in OpenAlex.
- The Roles of Transcription Factor Ets-1 in Neurological Disorders.Molecular neurobiology · 2026Review
- Teamwork of clustered low-affinity κB sites and accessory factors regulates transcriptional strength of NF-κB RelA dimers.Nucleic acids research · 2025Article
- A unique p52 NF-κB-ETS1 interaction ushers in a new paradigm of germinal center responses.Nature immunology · 2025Article
- The transcription complex p52-ETS1 is essential for germinal center formation.Nature immunology · 2025Article
- Evolutionarily conserved role of telomerase reverse transcriptase in programming the microenvironment via regulation of the cGAS-STING pathway.Nature cell biology · 2025Article
- The immortality mechanism of TERT promoter mutant cancers is self-reinforcing and reversible.Molecular cell · 2025Article
- Norrin in cancer: from a promising prognostic biomarker to a novel therapeutic target.Frontiers in oncology · 2025Review
- TWEAK/Fn14 signalling driven super-enhancer reprogramming promotes pro-metastatic metabolic rewiring in triple-negative breast cancer.Nature communications · 2024Article
- Aberrant non-canonical NF-κB signalling reprograms the epigenome landscape to drive oncogenic transcriptomes in multiple myeloma.Nature communications · 2024Article
- Extracellular vesicles derived from mesenchymal stem cells: the wine in Hebe's hands to treat skin aging.Precision clinical medicine · 2024Review
- NF-κB/p52 augments ETS1 binding genome-wide to promote glioma progression.Communications biology · 2023Article
- The Role of Natural Flavonoids as Telomerase Inhibitors in Suppressing Cancer Growth.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Review
- Transcriptional analysis links B cells and TERT expression to favorable prognosis in head and neck cancer.PNAS nexus · 2023Article
- AgeAnno: a knowledgebase of single-cell annotation of aging in human.Nucleic acids research · 2023Article
- Reactivation of telomerase reverse transcriptase expression in cancer: the role of TERT promoter mutations.Frontiers in cell and developmental biology · 2023Review
- Emerging mechanisms of telomerase reactivation in cancer.Trends in cancer · 2022Review
- Differential ETS1 binding to T:G mismatches within a CpG dinucleotide contributes to C-to-T somatic mutation rate of the IDH2 hotspot at codon Arg140.DNA repair · 2022Article
- Detection ofBiomedicines · 2022Review
- Genome-wide screens identify specific drivers of mutantProceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional factors ETS1/2 and p52 synergize downstream of non-canonical NF-κB signaling to drive reactivation of the -146C>T mutant TERT promoter in multiple cancer types, but the mechanism underlying this cooperativity remains unknown. Here we report the crystal structure of a ternary p52/ETS1/-146C>T TERT promoter complex. While p52 needs to associate with consensus κB sites on the DNA to function during non-canonical NF-κB signaling, we show that p52 can activate the -146C>T TERT promoter without binding DNA. Instead, p52 interacts with ETS1 to form a heterotetramer, counteracting autoinhibition of ETS1. Analogous to observations with the GABPA/GABPB heterotetramer, the native flanking ETS motifs are required for sustained activation of the -146C>T TERT promoter by the p52/ETS1 heterotetramer. These observations provide a unifying mechanism for transcriptional activation by GABP and ETS1, and suggest that genome-wide targets of non-canonical NF-κB signaling are not limited to those driven by consensus κB sequences.
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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.