ArticleThe EMBO journal1996
Myc-Max heterodimers activate a DEAD box gene and interact with multiple E box-related sites in vivo.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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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Who cites it
90 citing papers in PubMed, 211 citations in OpenAlex.
- Amplification of MED30 at chromosome 8q24 reprograms MYC binding to low-affinity oncogenic enhancers in cancer cells.Cell reports · 2026Article
- The Nucleolus: A Central Hub for Ribosome Biogenesis and Cellular Regulatory Signals.International journal of molecular sciences · 2025Review
- A microdeletion event at 19q13.43 in IDH-mutant astrocytomas is strongly correlated with MYC overexpression.Acta neuropathologica communications · 2024Article
- Gene Amplification of Mediator Subunit 30 Redirects the MYC Transcriptional Program and Oncogenesis.Research square · 2024Article
- Article
- Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest.International journal of molecular sciences · 2023Review
- NOC1 is a direct MYC target, and its protein interactome dissects its activity in controlling nucleolar function.Frontiers in cell and developmental biology · 2023Article
- DEAD-ly Affairs: The Roles of DEAD-Box Proteins on HIV-1 Viral RNA Metabolism.Frontiers in cell and developmental biology · 2022Review
- Integrated requirement of non-specific and sequence-specific DNA binding in Myc-driven transcription.The EMBO journal · 2021Article
- Article
- An early Myc-dependent transcriptional program orchestrates cell growth during B-cell activation.EMBO reports · 2019Article
- Genome-wide analysis of endogenously expressed ZEB2 binding sites reveals inverse correlations between ZEB2 and GalNAc-transferase GALNT3 in human tumors.Cellular oncology (Dordrecht, Netherlands) · 2018Article
- Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas.Cell systems · 2018Article
- Direct HPV E6/Myc interactions induce histone modifications, Pol II phosphorylation, and hTERT promoter activation.Oncotarget · 2017Article
- Article
- Genomic interaction between ER and HMGB2 identifies DDX18 as a novel driver of endocrine resistance in breast cancer cells.Oncogene · 2015Article
- Myc-induced anchorage of the rDNA IGS region to nucleolar matrix modulates growth-stimulated changes in higher-order rDNA architecture.Nucleic acids research · 2014Article
- Isolation and functional characterization of the promoter of a DEAD-box helicase Psp68 using Agrobacterium-mediated transient assay.Plant signaling & behavior · 2014Article
- Synthetic lethal screens as a means to understand and treat MYC-driven cancers.Cold Spring Harbor perspectives in medicine · 2014Review
- Transcriptional networks controlling the cell cycle.G3 (Bethesda, Md.) · 2013Article
30 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
5 authors at 1 institution in 1 country.
Funding
Abstract
The c-Myc protein is involved in cell proliferation, differentiation and apoptosis though heterodimerization with Max to form a transcriptionally active sequence-specific DNA binding complex. By means of sequential immunoprecipitation of chromatin using anti-Max and anti-Myc antibodies, we have identified a Myc-regulated gene and genomic sites occupied by Myc-Max in vivo. Four of 27 sites recovered by this procedure corresponded to the highest affinity 'canonical' CACGTG sequence. However, the most common in vivo binding sites belonged to the group of 'non-canonical' E box-related binding sites previously identified by in vitro selection. Several of the genomic fragments isolated contained transcribed sequences, including one, MrDb, encoding an evolutionarily conserved RNA helicase of the DEAD box family. The corresponding mRNA was induced following activation of a Myc-estrogen receptor fusion protein (Myc-ER) in the presence of a protein synthesis inhibitor, consistent with this helicase gene being a direct target of Myc-Max. In addition, as for c-Myc, the expression of MrDb is induced upon proliferative stimulation of primary human fibroblasts as well as B cells and down-regulated during terminal differentiation of HL60 leukemia cells. Our results indicate that Myc-Max heterodimers interact in vivo with a specific set of E box-related DNA sequences and that Myc is likely to activate multiple target genes including a highly conserved DEAD box protein. Therefore, Myc may exert its effects on cell behavior through proteins that affect RNA structure and metabolism.
Indexed as
Identifiers
8861962PMC452159W1902193863What OpenQuestion holds
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.