ArticleCell reports2017
The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- Multifaceted regulatory mechanisms of the EGR family in tumours and prospects for therapeutic applications (Review).International journal of molecular medicine · 2025Review
- Article
- Deletion of TECRL promotes skeletal muscle repair by up-regulating EGR2.Proceedings of the National Academy of Sciences of the United States of America · 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
- KAT2A complexes ATAC and SAGA play unique roles in cell maintenance and identity in hematopoiesis and leukemia.Blood advances · 2022Article
- Review
- Conservation and diversity of the eukaryotic SAGA coactivator complex across kingdoms.Epigenetics & chromatin · 2021Review
- Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Retroviral Transduction of NKT Hybridoma Cells.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Acetylation in Tumor Immune Evasion Regulation.Frontiers in pharmacology · 2021Review
- Natural Killer T Lymphocytes Integrate Innate Sensory Information and Relay Context to Effector Immune Responses.Critical reviews in immunology · 2021Review
- Transcriptional Activation of MYC-Induced Genes by GCN5 Promotes B-cell Lymphomagenesis.Cancer research · 2020Article
- WDHD1 facilitates G1 checkpoint abrogation in HPV E7 expressing cells by modulating GCN5.BMC cancer · 2020Article
- USP22 controls iNKT immunity through MED1 suppression of histone H2A monoubiquitination.The Journal of experimental medicine · 2020Article
- Long Non-coding RNAs as Functional and Structural Chromatin Modulators in Acute Myeloid Leukemia.Frontiers in oncology · 2019Review
- The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7-induced cell proliferation via up-regulating E2F1.Journal of cellular and molecular medicine · 2018Article
- Epigenetic inhibition of Wnt pathway suppresses osteogenic differentiation of BMSCs during osteoporosis.Cell death & disease · 2018Article
- Natural Killer T Cells: An Ecological Evolutionary Developmental Biology Perspective.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
The development of CD1d-restricted invariant natural killer T (iNKT) cells, a population that is critical for both innate and adaptive immunity, is regulated by multiple transcription factors, but the molecular mechanisms underlying how the transcriptional activation of these factors are regulated during iNKT development remain largely unknown. We found that the histone acetyltransferase general control non-derepressible 5 (GCN5) is essential for iNKT cell development during the maturation stage. GCN5 deficiency blocked iNKT cell development in a cell-intrinsic manner. At the molecular level, GCN5 is a specific lysine acetyltransferase of early growth responsive gene 2 (EGR2), a transcription factor required for iNKT cell development. GCN5-mediated acetylation positively regulated EGR2 transcriptional activity, and both genetic and pharmacological GCN5 suppression specifically inhibited the transcription of EGR2 target genes in iNKT cells, including Runx1, promyelocytic leukemia zinc finger protein (PLZF), interleukin (IL)-2Rb, and T-bet. Therefore, our study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development.
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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.