ArticleOncogene2016
Interaction of MYC with host cell factor-1 is mediated by the evolutionarily conserved Myc box IV motif.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 49 citations in OpenAlex.
- Targeting the MYCN interaction network in neuroblastoma.Bioscience reports · 2026Review
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- Uncovering cancer dependencies in peptide-interacting protein pockets.bioRxiv : the preprint server for biology · 2026Article
- The chordoid gliomaScience signaling · 2025Article
- Integrative characterization of MYC RNA-binding function.Cell genomics · 2025Article
- Targeting MYC: Multidimensional regulation and therapeutic strategies in oncology.Genes & diseases · 2025Review
- Transcription factor 4 is a key mediator of oncogenesis in neuroblastoma by promoting MYC activity.Molecular oncology · 2025Article
- Mycb and Mych stimulate Müller glial cell reprogramming and proliferation in the uninjured and injured zebrafish retina.Development (Cambridge, England) · 2024Article
- An essential gene signature of breast cancer metastasis reveals targetable pathways.Breast cancer research : BCR · 2024Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- 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
- WDR5 facilitates recruitment of N-MYC to conserved WDR5 gene targets in neuroblastoma cell lines.Oncogenesis · 2023Article
- Article
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- Mutations in Hcfc1 and Ronin result in an inborn error of cobalamin metabolism and ribosomopathy.Nature communications · 2022Article
- MYC protein interactors in gene transcription and cancer.Nature reviews. Cancer · 2021Review
- Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler.Oncogene · 2021Article
- Article
- Target gene-independent functions of MYC oncoproteins.Nature reviews. Molecular cell biology · 2020Review
- Structural and Biophysical Insights into the Function of the Intrinsically Disordered Myc Oncoprotein.Cells · 2020Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The MYC family of oncogenes encodes a set of three related transcription factors that are overexpressed in many human tumors and contribute to the cancer-related deaths of more than 70,000 Americans every year. MYC proteins drive tumorigenesis by interacting with co-factors that enable them to regulate the expression of thousands of genes linked to cell growth, proliferation, metabolism and genome stability. One effective way to identify critical co-factors required for MYC function has been to focus on sequence motifs within MYC that are conserved throughout evolution, on the assumption that their conservation is driven by protein-protein interactions that are vital for MYC activity. In addition to their DNA-binding domains, MYC proteins carry five regions of high sequence conservation known as Myc boxes (Mb). To date, four of the Mb motifs (MbI, MbII, MbIIIa and MbIIIb) have had a molecular function assigned to them, but the precise role of the remaining Mb, MbIV, and the reason for its preservation in vertebrate Myc proteins, is unknown. Here, we show that MbIV is required for the association of MYC with the abundant transcriptional coregulator host cell factor-1 (HCF-1). We show that the invariant core of MbIV resembles the tetrapeptide HCF-binding motif (HBM) found in many HCF-interaction partners, and demonstrate that MYC interacts with HCF-1 in a manner indistinguishable from the prototypical HBM-containing protein VP16. Finally, we show that rationalized point mutations in MYC that disrupt interaction with HCF-1 attenuate the ability of MYC to drive tumorigenesis in mice. Together, these data expose a molecular function for MbIV and indicate that HCF-1 is an important co-factor for MYC.
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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.