ArticleMolecular cell2020
Tuning Transcription Factor Availability through Acetylation-Mediated Genomic Redistribution.
Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 69 citations in OpenAlex.
- Metabolic buffering restricts phenotype switching in melanoma.The EMBO journal · 2026Article
- Genetically targeted mTORC1 inhibitor reveals transcriptional control by nuclear mTORC1.Nature chemical biology · 2026Article
- Loss of MITF activity leads to emergent cell states from the melanocyte stem cell lineage.bioRxiv : the preprint server for biology · 2026Article
- MITF, TFEB, and TFE3 drive distinct adaptive gene expression programs and immune infiltration in melanoma.Cell reports · 2025Article
- METTL10-Mediated PIAS3 Methylation Links Purine Metabolism to Gastric Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells.NAR cancer · 2025Article
- Dominant Negative Mitf Allele Impacts Melanophore and Xanthophore Development and Reveals Collaborative Interactions With Tfec in Zebrafish Chromatophore Lineages.Pigment cell & melanoma research · 2025Article
- Transcription dynamics and genome organization in the mammalian nucleus: Recent advances.Molecular cell · 2025Review
- The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State.Pigment cell & melanoma research · 2025Article
- Novel mechanisms of MITF regulation identified in a mouse suppressor screen.EMBO reports · 2024Article
- Melanocyte lineage dynamics in development, growth and disease.Development (Cambridge, England) · 2024Review
- p300 KAT Regulates SOX10 Stability and Function in Human Melanoma.Cancer research communications · 2024Article
- ALDH1A3-acetaldehyde metabolism potentiates transcriptional heterogeneity in melanoma.Cell reports · 2024Article
- p300 KAT regulates SOX10 stability and function in human melanoma.bioRxiv : the preprint server for biology · 2024Article
- DNA damage remodels the MITF interactome to increase melanoma genomic instability.Genes & development · 2024Article
- HDAC8-mediated inhibition of EP300 drives a transcriptional state that increases melanoma brain metastasis.Nature communications · 2023Article
- Acetylation reprograms MITF target selectivity and residence time.Nature communications · 2023Article
- Novel mechanisms of MITF regulation and melanoma predisposition identified in a mouse suppressor screen.bioRxiv : the preprint server for biology · 2023Article
- Deciphering the multi-scale, quantitative cis-regulatory code.Molecular cell · 2023Review
- Transcription factor EB as a key molecular factor in human health and its implication in diseases.SAGE open medicine · 2023Review
Corrections and comments
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Authors and funding
24 authors at 14 institutions in 7 countries.
Funding
Abstract
It is widely assumed that decreasing transcription factor DNA-binding affinity reduces transcription initiation by diminishing occupancy of sequence-specific regulatory elements. However, in vivo transcription factors find their binding sites while confronted with a large excess of low-affinity degenerate motifs. Here, using the melanoma lineage survival oncogene MITF as a model, we show that low-affinity binding sites act as a competitive reservoir in vivo from which transcription factors are released by mitogen-activated protein kinase (MAPK)-stimulated acetylation to promote increased occupancy of their regulatory elements. Consequently, a low-DNA-binding-affinity acetylation-mimetic MITF mutation supports melanocyte development and drives tumorigenesis, whereas a high-affinity non-acetylatable mutant does not. The results reveal a paradoxical acetylation-mediated molecular clutch that tunes transcription factor availability via genome-wide redistribution and couples BRAF to tumorigenesis. Our results further suggest that p300/CREB-binding protein-mediated transcription factor acetylation may represent a common mechanism to control transcription factor availability.
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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.