| Deletion of Ulk1 inhibits neointima formation by enhancing KAT2A/GCN5-mediated acetylation of TUBA/alpha-tubulin in vivo. | Deletion of Ulk1 inhibits neointima formation by enhancing KAT2A/GCN5-mediated acetylation of TUBA/α-tubulin in vivo.
Ouyang C, Li J, Zheng X, Mu J, Torres G, Wang Q, Zou MH, Xie Z., Free PMC Article | 07/9/2022 |
| GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway. | GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway.
Li J, Yan C, Wang Y, Chen C, Yu H, Liu D, Huang K, Han Y., Free PMC Article | 05/14/2022 |
| Acetyltransferases GCN5 and PCAF Are Required for B Lymphocyte Maturation in Mice. | Acetyltransferases GCN5 and PCAF Are Required for B Lymphocyte Maturation in Mice.
Oksenych V, Su D, Daniel JA., Free PMC Article | 04/9/2022 |
| GCN5 maintains muscle integrity by acetylating YY1 to promote dystrophin expression. | GCN5 maintains muscle integrity by acetylating YY1 to promote dystrophin expression.
Addicks GC, Zhang H, Ryu D, Vasam G, Green AE, Marshall PL, Patel S, Kang BE, Kim D, Katsyuba E, Williams EG, Renaud JM, Auwerx J, Menzies KJ., Free PMC Article | 02/19/2022 |
| Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells. | Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells.
Domingues AF, Kulkarni R, Giotopoulos G, Gupta S, Vinnenberg L, Arede L, Foerner E, Khalili M, Adao RR, Johns A, Tan S, Zeka K, Huntly BJ, Prabakaran S, Pina C., Free PMC Article | 04/13/2021 |
| Transcriptional Activation of MYC-Induced Genes by GCN5 Promotes B-cell Lymphomagenesis. | Transcriptional Activation of MYC-Induced Genes by GCN5 Promotes B-cell Lymphomagenesis.
Farria AT, Plummer JB, Salinger AP, Shen J, Lin K, Lu Y, McBride KM, Koutelou E, Dent SYR., Free PMC Article | 04/3/2021 |
| Crystal structure of GCN5 PCAF N-terminal domain reveals atypical ubiquitin ligase structure. | Crystal structure of GCN5 PCAF N-terminal domain reveals atypical ubiquitin ligase structure.
Toma-Fukai S, Hibi R, Naganuma T, Sakai M, Saijo S, Shimizu N, Matsumoto M, Shimizu T., Free PMC Article | 03/13/2021 |
| GCN5 acetylation is required for craniofacial chondrocyte maturation. | GCN5 acetylation is required for craniofacial chondrocyte maturation.
Pezoa SA, Artinger KB, Niswander LA., Free PMC Article | 01/23/2021 |
| Islet-1 synergizes with Gcn5 to promote MSC differentiation into cardiomyocytes. | Islet-1 synergizes with Gcn5 to promote MSC differentiation into cardiomyocytes.
Xu H, Zhou Q, Yi Q, Tan B, Tian J, Chen X, Wang Y, Yu X, Zhu J., Free PMC Article | 11/21/2020 |
| that Gcn5-mediated histone acetylation promotes chromatin accessibility and nucleosome eviction in spermiogenesis | Gcn5-Mediated Histone Acetylation Governs Nucleosome Dynamics in Spermiogenesis.
Luense LJ, Donahue G, Lin-Shiao E, Rangel R, Weller AH, Bartolomei MS, Berger SL., Free PMC Article | 06/13/2020 |
| we investigated the impact of combined skeletal muscle-specific overexpression of SIRT1 and deletion of GCN5 on glucose homeostasis, skeletal muscle mitochondrial biogenesis and function, and metabolic adaptation to endurance exercise training in mice | Combined overexpression of SIRT1 and knockout of GCN5 in adult skeletal muscle does not affect glucose homeostasis or exercise performance in mice.
Svensson K, Tahvilian S, Martins VF, Dent JR, Lemanek A, Barooni N, Greyslak K, McCurdy CE, Schenk S., Free PMC Article | 05/9/2020 |
| GCN5 knockout does not enhance basal or exercise-induced mitochondrial adaptation in skeletal muscle. | Muscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptation.
Dent JR, Martins VF, Svensson K, LaBarge SA, Schlenk NC, Esparza MC, Buckner EH, Meyer GA, Hamilton DL, Schenk S, Philp A., Free PMC Article | 01/5/2019 |
| These findings established a link between GCN5 and the FGF signaling pathway and highlighted specific GCN5-MYC partnerships in gene regulation during early differentiation. | GCN5 Regulates FGF Signaling and Activates Selective MYC Target Genes during Early Embryoid Body Differentiation.
Wang L, Koutelou E, Hirsch C, McCarthy R, Schibler A, Lin K, Lu Y, Jeter C, Shen J, Barton MC, Dent SYR., Free PMC Article | 12/29/2018 |
| Sumoylation of RORgammaT regulates TH17 differentiation and thymocyte development via histone acetyltransferase KAT2A, which stabilizes the binding of SRC1 to enhance RORgammaT transcription factor activity. | Sumoylation of RORγt regulates T(H)17 differentiation and thymocyte development.
He Z, Zhang J, Huang Z, Du Q, Li N, Zhang Q, Chen Y, Sun Z., Free PMC Article | 12/22/2018 |
| Gcn5 regulates Hoxc11 gene expression through mediating site-specific H3K9 acetylation in Akt1-/- MEFs. | The histone acetylation mediated by Gcn5 regulates the Hoxc11 gene expression in MEFs.
Oh JH, Lee JY, Kong KA, Kim JM, Kim MH. | 05/19/2018 |
| study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development. | The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation.
Wang Y, Yun C, Gao B, Xu Y, Zhang Y, Wang Y, Kong Q, Zhao F, Wang CR, Dent SYR, Wang J, Xu X, Li HB, Fang D., Free PMC Article | 04/7/2018 |
| The results demonstrated that Islet1 upregulated expression of general control of amino acid biosynthesis protein 5 (Gcn5) and enhanced the binding of Gcn5 to the promoters of GATA binding protein 4 (GATA4) and NK2 homeobox 5 (Nkx2.5). In addition, Islet-1 downregulated DNA methyltransferase (DNMT)1 expression and reduced its binding to the GATA4 promoter. | Islet-1 induces the differentiation of mesenchymal stem cells into cardiomyocyte-like cells through the regulation of Gcn5 and DNMT-1.
Yi Q, Xu H, Yang K, Wang Y, Tan B, Tian J, Zhu J., Free PMC Article | 02/24/2018 |
| recovering GCN5 expression in vivo by lentiviral expression vector significantly attenuated the loss of angiogenesis in ovariectomized mouse femurs | Declining histone acetyltransferase GCN5 represses BMSC-mediated angiogenesis during osteoporosis.
Jing H, Liao L, Su X, Shuai Y, Zhang X, Deng Z, Jin Y. | 10/21/2017 |
| study reveals previously unknown physiological functions for Gcn5 and a molecular mechanism underlying these functions in regulating T cell immunity; Gcn5 may be an important new target for autoimmune disease therapy | The Histone Acetyltransferase Gcn5 Positively Regulates T Cell Activation.
Gao B, Kong Q, Zhang Y, Yun C, Dent SYR, Song J, Zhang DD, Wang Y, Li X, Fang D., Free PMC Article | 09/23/2017 |
| Together, our experiments identify a novel nonhistone substrate of GCN5, highlight an essential role for both GCN5 and RA signaling in early diencephalic development, and elucidate a novel molecular regulatory mechanism for RA signaling that is specific to the developing forebrain. | Diencephalic Size Is Restricted by a Novel Interplay Between GCN5 Acetyltransferase Activity and Retinoic Acid Signaling.
Wilde JJ, Siegenthaler JA, Dent SY, Niswander LA., Free PMC Article | 08/26/2017 |
| Methionine was the only essential amino acid that rapidly induced PGC-1alpha acetylation through activating the GCN5 acetyltransferase. | The Methionine Transamination Pathway Controls Hepatic Glucose Metabolism through Regulation of the GCN5 Acetyltransferase and the PGC-1α Transcriptional Coactivator.
Tavares CD, Sharabi K, Dominy JE, Lee Y, Isasa M, Orozco JM, Jedrychowski MP, Kamenecka TM, Griffin PR, Gygi SP, Puigserver P., Free PMC Article | 11/12/2016 |
| these results may point to the GCN5-NF-kappaB pathway as a novel potential molecular target for stem cell mediated regenerative medicine and the treatment of metabolic bone diseases such as osteoporosis. | Histone Acetyltransferase GCN5 Regulates Osteogenic Differentiation of Mesenchymal Stem Cells by Inhibiting NF-κB.
Zhang P, Liu Y, Jin C, Zhang M, Tang F, Zhou Y. | 11/5/2016 |
| In addition to reducing atrogene expression, surprisingly inhibiting NF-kappaB with IkappaBalpha-SR or by GCN5 knockdown in these muscles also enhanced AKT and mechanistic target of rapamycin (mTOR) activities, which also contributed to the reduction in atrophy. | Muscle Wasting in Fasting Requires Activation of NF-κB and Inhibition of AKT/Mechanistic Target of Rapamycin (mTOR) by the Protein Acetylase, GCN5.
Lee D, Goldberg AL., Free PMC Article | 04/23/2016 |
| Gcn5 and PCAF repress IFN-beta production in an enzymatic activity-independent and non-transcriptional manner: by inhibiting the innate immune signaling kinase TBK1 in the cytoplasm. | Gcn5 and PCAF negatively regulate interferon-β production through HAT-independent inhibition of TBK1.
Jin Q, Zhuang L, Lai B, Wang C, Li W, Dolan B, Lu Y, Wang Z, Zhao K, Peng W, Dent SY, Ge K., Free PMC Article | 08/18/2015 |
| GCN5 and HDAC1 are the crucial enzymes that regulating epigenetic reprogramming; we observed dynamic changes in the expression levels of GCN5 and HDAC1 during embryo development | Expression of histone acetyltransferase GCN5 and histone deacetylase 1 in the cultured mouse preimplantation embryos.
Liu X, Zhao D, Zheng Y, Wang L, Qian Y, Xu C, Huang H, Hwa YL, Jin F. | 12/20/2014 |