ArticleBiochimica et biophysica acta2014
MYC interacts with the human STAGA coactivator complex via multivalent contacts with the GCN5 and TRRAP subunits.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 52 citations in OpenAlex.
- Step-brothers in arms, SAGA and ATAC co-activator complexes, use different strategies.The EMBO journal · 2026Review
- Spatially-resolved Photoproximity Profiling of MYC Identifies a MYC-BAF Liability in Cancer Cells.bioRxiv : the preprint server for biology · 2025Article
- MYC: The Guardian of Its Own Chaos.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- MYCN and KAT2A form a feedforward loop to drive an oncogenic transcriptional program in neuroblastoma.Oncogenesis · 2025Article
- Beyond small molecules: advancing MYC-targeted cancer therapies through protein engineering.Transcription · 2025Review
- ATAC and SAGA histone acetyltransferase modules facilitate transcription factor binding to nucleosomes independent of their acetylation activity.Nucleic acids research · 2025Article
- Exploring the dynamics and interactions of the N-myc transactivation domain through solution nuclear magnetic resonance spectroscopy.The Biochemical journal · 2024Article
- Loss-of-function variants affecting the STAGA complex component SUPT7L cause a developmental disorder with generalized lipodystrophy.Human genetics · 2024Article
- Polyploidy Promotes Hypertranscription, Apoptosis Resistance, and Ciliogenesis in Cancer Cells and Mesenchymal Stem Cells of Various Origins: Comparative Transcriptome In Silico Study.International journal of molecular sciences · 2024Article
- MYC activity at enhancers drives prognostic transcriptional programs through an epigenetic switch.Nature genetics · 2024Article
- MYC acetylated lysine residues drive oncogenic cell transformation and regulate select genetic programs for cell adhesion-independent growth and survival.Genes & development · 2023Article
- SCARB2 drives hepatocellular carcinoma tumor initiating cells via enhanced MYC transcriptional activity.Nature communications · 2023Article
- MYC promotes global transcription in part by controlling P-TEFb complex formation via DNA-binding independent inhibition of CDK9 SUMOylation.Science China. Life sciences · 2023Article
- Heat shock factor 1 (HSF1) specifically potentiates c-MYC-mediated transcription independently of the canonical heat shock response.Cell reports · 2023Article
- MYC: a complex problem.Trends in cell biology · 2023Review
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- Genetic and Histopathological Heterogeneity of Neuroblastoma and Precision Therapeutic Approaches for Extremely Unfavorable Histology Subgroups.Biomolecules · 2022Review
- MYC protein interactors in gene transcription and cancer.Nature reviews. Cancer · 2021Review
- What do Transcription Factors Interact With?Journal of molecular biology · 2021Review
- Mechanisms of stimulation of SAGA-mediated nucleosome acetylation by a transcriptional activator.Biochemistry and biophysics reports · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
MYC is an oncogenic DNA-binding transcription activator of many genes and is often upregulated in human cancers. MYC has an N-terminal transcription activation domain (TAD) that is also required for cell transformation. Various MYC TAD-interacting coactivators have been identified, including the transcription/transformation-associated protein (TRRAP), a subunit of different histone acetyltransferase (HAT) complexes such as the human "SPT3-TAF9-GCN5 Acetyltransferase" (STAGA) complex involved in MYC transactivation of the TERT gene. However, it remains unclear whether TRRAP and/or other subunits are directly contacted by MYC within these macromolecular complexes. Here, we characterize the interactions of MYC TAD with the STAGA complex. By protein crosslinking we identify both TRRAP and the GCN5 acetyltransferase as MYC TAD-interacting subunits within native STAGA. We show that purified GCN5 binds to an N-terminal sub-domain of MYC TAD (residues 21-108) and that the interaction of GCN5 and STAGA with this sub-domain is dependent on two related sequence motifs: M2 within the conserved MYC homology box I (MBI), and M3 located between residues 100-106. Interestingly, specific substitutions within the M2/3 motifs that only moderately reduce the intracellular MYC-STAGA interaction and do not influence dimerization of MYC with its DNA-binding partner MAX, strongly inhibit MYC acetylation by GCN5 and reduce MYC binding and transactivation of the GCN5-dependent TERT promoter in vivo. Hence, we propose that MYC associates with STAGA through extended interactions of the TAD with both TRRAP and GCN5 and that the TAD-GCN5 interaction is important for MYC acetylation and MYC binding to certain chromatin loci.
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