ReviewCold Spring Harbor perspectives in medicine2014
Genome recognition by MYC.
Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 111 citations in OpenAlex.
- Dual targeting of AMRC12 andTheranostics · 2026Article
- The evolutionary foundations of transcriptional regulation in animals.Nature reviews. Genetics · 2025Review
- The deubiquitinase USP36 funtions through catalytic-dependent and catalytic-independent mechanisms in Drosophila.Genetics · 2025Article
- Defining transcription factor nucleosome binding with Pioneer-seq.PLoS genetics · 2025Article
- Myc family proteins: Molecular drivers of tumorigenesis and resistance in neuroendocrine tumors.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- p53 protein degradation redefines the initiation mechanisms and drives transitional mutations in colorectal cancer.Nature communications · 2025Article
- Targeting the undruggable MYC in cancer: the rationale of using XPO1 inhibitors.Molecular biology reports · 2025Review
- Transcriptional regulation by MYC: an emerging new model.Oncogene · 2025Review
- MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer.Cancer discovery · 2024Article
- A microdeletion event at 19q13.43 in IDH-mutant astrocytomas is strongly correlated with MYC overexpression.Acta neuropathologica communications · 2024Article
- Expanding the horizons of targeted protein degradation: A non-small molecule perspective.Acta pharmaceutica Sinica. B · 2024Review
- The dimeric deubiquitinase USP28 integrates 53BP1 and MYC functions to limit DNA damage.Nucleic acids research · 2024Article
- Bromodomain Protein-directed Agents and MYC in Small Cell Lung Cancer.Current cancer drug targets · 2024Review
- BRD4 and MYC: power couple in transcription and disease.The FEBS journal · 2023Review
- MYC acetylated lysine residues drive oncogenic cell transformation and regulate select genetic programs for cell adhesion-independent growth and survival.Genes & development · 2023Article
- iTAG an optimized IMiD-induced degron for targeted protein degradation in human and murine cells.iScience · 2023Article
- Article
- Polyploidy and Myc Proto-Oncogenes Promote Stress Adaptation via Epigenetic Plasticity and Gene Regulatory Network Rewiring.International journal of molecular sciences · 2022Review
- Polycomb group ring finger protein 6 suppresses Myc-induced lymphomagenesis.Life science alliance · 2022Article
- EZH2 noncanonically binds cMyc and p300 through a cryptic transactivation domain to mediate gene activation and promote oncogenesis.Nature cell biology · 2022Article
9 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYC dimerizes with MAX to bind DNA, with a preference for the E-box consensus CACGTG and several variant motifs. In cells, MYC binds DNA preferentially within transcriptionally active promoter regions. Although several thousand promoters are bound under physiological (low MYC) conditions, these represent only a fraction of all accessible, active promoters. MYC overexpression-as commonly observed in cancer cells-leads to invasion of virtually all active promoters, as well as of distal enhancer elements. We summarize here what is currently known about the mechanisms that may guide this process. We propose that binding site recognition is determined by low-affinity protein-protein interactions between MYC/MAX dimers and components of the basal transcriptional machinery, other chromatin-associated protein complexes, and/or DNA-bound transcription factors. DNA binding occurs subsequently, without an obligate requirement for sequence recognition. Local DNA scanning then leads to preferential stabilization of the MYC/MAX dimer on high-affinity DNA elements. This model is consistent with the invasion of all active promoters that occurs at elevated MYC levels, but posits that important differences in affinity persist between physiological target sites and the newly invaded elements, which may not all be bound in a productive regulatory mode. The implications of this model for transcriptional control by MYC in normal and cancer cells are discussed in the light of the latest literature.
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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.