ArticleMolecular and cellular biology2002
TRRAP-dependent and TRRAP-independent transcriptional activation by Myc family oncoproteins.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 135 citations in OpenAlex.
- Domain architecture and protein-protein interactions regulate KDM5A recruitment to the chromatin.Epigenetics · 2023Review
- Review
- Article
- The TRRAP transcription cofactor represses interferon-stimulated genes in colorectal cancer cells.eLife · 2022Article
- Targeting bromodomain and extra-terminal proteins to inhibit neuroblastoma tumorigenesis through regulating MYCN.Frontiers in cell and developmental biology · 2022Review
- Luminescence complementation technology for the identification of MYC:TRRAP inhibitors.Oncotarget · 2021Article
- The Diarylheptanoid Curcumin Induces MYC Inhibition and Cross-Links This Oncoprotein to the Coactivator TRRAP.Frontiers in oncology · 2021Article
- Targeting Myc Interacting Proteins as a Winding Path in Cancer Therapy.Frontiers in pharmacology · 2021Review
- Telomere Maintenance in Pediatric Cancer.International journal of molecular sciences · 2019Review
- Chromatin Bottlenecks in Cancer.Trends in cancer · 2019Review
- Formation of a structurally-stable conformation by the intrinsically disordered MYC:TRRAP complex.PloS one · 2019Article
- TRRAP stimulates the tumorigenic potential of ovarian cancer stem cells.BMB reports · 2018Article
- Identification of a panel of MYC and Tip60 co-regulated genes functioning primarily in cell cycle and DNA replication.Genes & cancer · 2018Article
- Merkel cell polyomavirus recruits MYCL to the EP400 complex to promote oncogenesis.PLoS pathogens · 2017Article
- Regulation of Telomere Homeostasis during Epstein-Barr virus Infection and Immortalization.Viruses · 2017Review
- A Syndromic Intellectual Disability Disorder Caused by Variants in TELO2, a Gene Encoding a Component of the TTT Complex.American journal of human genetics · 2016Article
- An in vivo molecular response analysis of colorectal cancer treated with Astragalus membranaceus extract.Oncology reports · 2016Article
- The Cellular Protein Complex Associated with a Transforming Region of E1A Contains c-MYC.Journal of virology · 2016Article
- Taming of the beast: shaping Myc-dependent amplification.Trends in cell biology · 2015Review
- MYC cofactors: molecular switches controlling diverse biological outcomes.Cold Spring Harbor perspectives in medicine · 2014Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
We demonstrate that transformation-transactivation domain-associated protein (TRRAP) binding and the recruitment of histone H3 and H4 acetyltransferase activities are required for the transactivation of a silent telomerase reverse transcriptase (TERT) gene in exponentially growing human fibroblasts by c-Myc or N-Myc protein. However, recruitment of TRRAP by c- or N-Myc is dispensable for the partial induction of several basally expressed genes in exponentially growing primary and immortalized fibroblasts. Furthermore, recruitment of TRRAP is required for c-Myc- or N-Myc-mediated oncogenic transformation but not for the partial restoration of the growth defect in myc-null fibroblasts. A segment of the adenovirus E1A protein fused to a transformation-defective N-Myc protein carrying a small deletion in the transactivation domain specifically restores interaction with TRRAP, activates the silent TERT gene, induces acetylation of histones H3 and H4 at the TERT promoter, and transforms primary cells. Accordingly, wild-type L-Myc is much less efficient in TRRAP binding, activation of the silent TERT gene, and transformation of primary fibroblasts. Nevertheless, L-Myc is a potent activator of several basally expressed genes and can fully restore the growth defect of myc-null cells. These results suggest a differential requirement for TRRAP for several Myc-mediated activities.
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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.