ArticlePloS one2012
N-Myc and GCN5 regulate significantly overlapping transcriptional programs in neural stem cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- Degron-independent recruitment of KAT2A expands the target space of CRBN molecular glues.Science (New York, N.Y.) · 2026Article
- Bromodomain-Driven Regulation of Stem Cells: A Potential Target for Cancer Therapeutic Intervention.Stem cell reviews and reports · 2026Review
- MYCN and KAT2A form a feedforward loop to drive an oncogenic transcriptional program in neuroblastoma.Oncogenesis · 2025Article
- Aberrant histone modifications in pediatric brain tumors.Frontiers in oncology · 2025Review
- The KAT module of the SAGA complex maintains the oncogenic gene expression program inScience advances · 2024Article
- Contributions of transcriptional noise to leukaemia evolution: KAT2A as a case-study.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Deciphering the potential role of post-translational modifications of histones in gastrointestinal cancers: a proteomics-based review with therapeutic challenges and opportunities.Frontiers in oncology · 2024Review
- KAT2A complexes ATAC and SAGA play unique roles in cell maintenance and identity in hematopoiesis and leukemia.Blood advances · 2022Article
- The role of altered protein acetylation in neurodegenerative disease.Frontiers in aging neuroscience · 2022Review
- Epigenetic histone acetylation modulating prenatal Poly I:C induced neuroinflammation in the prefrontal cortex of rats: a study in a maternal immune activation model.Frontiers in cellular neuroscience · 2022Article
- H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion.Science advances · 2021Article
- Conservation and diversity of the eukaryotic SAGA coactivator complex across kingdoms.Epigenetics & chromatin · 2021Review
- The Biological Significance of Targeting Acetylation-Mediated Gene Regulation for Designing New Mechanistic Tools and Potential Therapeutics.Biomolecules · 2021Review
- Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Dynamic modules of the coactivator SAGA in eukaryotic transcription.Experimental & molecular medicine · 2020Review
- Targeting the SAGA and ATAC Transcriptional Coactivator Complexes in MYC-Driven Cancers.Cancer research · 2020Review
- Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells.eLife · 2020Article
- GCN5 HAT inhibition reduces human Burkitt lymphoma cell survival through reduction of MYC target gene expression and impeding BCR signaling pathways.Oncotarget · 2019Article
- USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta.Development (Cambridge, England) · 2019Article
- Repression of GCN5 expression or activity attenuates c-MYC expression in non-small cell lung cancer.American journal of cancer research · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Here we examine the functions of the Myc cofactor and histone acetyltransferase, GCN5/KAT2A, in neural stem and precursor cells (NSC) using a conditional knockout approach driven by nestin-cre. Mice with GCN5-deficient NSC exhibit a 25% reduction in brain mass with a microcephaly phenotype similar to that observed in nestin-cre driven knockouts of c- or N-myc. In addition, the loss of GCN5 inhibits precursor cell proliferation and reduces their populations in vivo, as does loss of N-myc. Gene expression analysis indicates that about one-sixth of genes whose expression is affected by loss of GCN5 are also affected in the same manner by loss of N-myc. These findings strongly support the notion that GCN5 protein is a key N-Myc transcriptional cofactor in NSC, but are also consistent with recruitment of GCN5 by other transcription factors and the use by N-Myc of other histone acetyltransferases. Putative N-Myc/GCN5 coregulated transcriptional pathways include cell metabolism, cell cycle, chromatin, and neuron projection morphogenesis genes. GCN5 is also required for maintenance of histone acetylation both at its putative specific target genes and at Myc targets. Thus, we have defined an important role for GCN5 in NSC and provided evidence that GCN5 is an important Myc transcriptional cofactor in vivo.
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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.