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Human Polyclonal KAT2A Primary Antibody for ELISA, WB - ABIN543206
Wiper-Bergeron, Salem, Tomlinson, Wu, Haché: Glucocorticoid-stimulated preadipocyte differentiation is mediated through acetylation of C/EBPbeta by GCN5. in Proceedings of the National Academy of Sciences of the United States of America 2007
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Human Monoclonal KAT2A Primary Antibody for ICC, IF - ABIN2668945
Brand, Moggs, Oulad-Abdelghani, Lejeune, Dilworth, Stevenin, Almouzni, Tora: UV-damaged DNA-binding protein in the TFTC complex links DNA damage recognition to nucleosome acetylation. in The EMBO journal 2001
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The results unveil a tight connection between TFIIH and KAT2A that controls higher-order chromatin structure and gene expression and provide new insights into transcriptional dysregulation in a cancer-prone DNA repair-deficient disorder, Xeroderma Pigmentosum B-Cockayne Syndrome.
KAT2A expression in periodontal ligament stem cells was decreased because of periodontitis. The classical Wnt pathway was activated to inhibit the osteogenic differentiation of the cells
Was greatly suppressed by the silence of KLF5, GCN5, or GDF15.
findings suggest that epigenetic control of NP via acetylation by host acetyltransferases contributes to regulation of polymerase activity in the influenza A virus
KAT2A/2B acetylation of PLK4 prevents centrosome amplification
Results found that lack of GCN5 decreased the osteogenic differentiation of periodontal ligament stem cells (PDLSCs) and overexpression of GCN5 rescued osteogenic deficiency in PDLSCs from periodontitis patients. Mechanistically, GCN5 regulated DKK1 expression by acetylation of Histone H3 lysine 9 (H3K9) and Histone H3 lysine 14 (H3K14) to regulate Wnt/beta catenin pathway of PDLSCs.
findings reveal an important mechanism of histone modification and demonstrate that local generation of succinyl-CoA by the nuclear alpha-KGDH complex coupled with the succinyltransferase activity of KAT2A is instrumental in histone succinylation, tumour cell proliferation, and tumour development
GCN5 upregulation is especially common in UCCs. GCN5 knockdown impeded growth of specific UCCs, whereas PCAF knockdown elicited minor effects.
Our results suggest that GCN5 is present at telomeres and opposes telomere recombination, in contrast to PCAF that may indirectly favour them in ALT cells.
This report documents a novel lncRNA, GClnc1, which may act as a scaffold to recruit the WDR5 and KAT2A complex and modify the transcription of target genes. This study reveals that GClnc1 is an oncogenic lncRNA in human gastric cancer.
To understand how Gcn5 discriminates between different acyl-CoA molecules, structures of the catalytic domain of human Gcn5L2 bound to propionyl-CoA and butyryl-CoA were determined.
Data suggest that expression of GCN5 (histone acetyltransferase GCN5) is induced in skeletal muscle during a 48-hour fast; in contrast, expression of SIRT1 (sirtuin 1) remains unchanged.
Orc5 associates with the H3 histone acetyl transferase GCN5 (also known as KAT2A), and this association enhances the chromatin-opening function of Orc5.
Methionine was the only essential amino acid that rapidly induced PGC-1alpha acetylation through activating the GCN5 acetyltransferase.
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.
Acetyltransferase p300 collaborates with chromodomain helicase DNA-binding protein 4 (CHD4) to facilitate DNA double-strand break repair
Suggest lysine acetyltransfer as a potential regulator of platelet actin dynamics, and potential roles for lysine acetylation in the molecular coordination of platelet activation and function.
Data uncover GCN5 as a negative regulator of C/EBPalpha and demonstrate the importance of C/EBPalpha acetylation in myeloid differentiation.
GCN5 Potentiates Glioma Proliferation and Invasion via STAT3 and AKT Signaling Pathways
results thus demonstrate that the catalytic activity of GCN5 is stimulated by subunits of the ADA2a- or ADA2b-containing HAT modules and is further increased by incorporation of the distinct HAT modules in the ATAC or SAGA holo-complexes
GCN5 knockout does not enhance basal or exercise-induced mitochondrial adaptation in skeletal muscle.
These findings established a link between GCN5 and the FGF signaling pathway and highlighted specific GCN5-MYC partnerships in gene regulation during early differentiation.
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.
Gcn5 regulates Hoxc11 gene expression through mediating site-specific H3K9 acetylation in Akt1-/- MEFs.
study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development.
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.
recovering GCN5 expression in vivo by lentiviral expression vector significantly attenuated the loss of angiogenesis in ovariectomized mouse femurs
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
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.
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.
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 HDAC1 are the crucial enzymes that regulating epigenetic reprogramming; we observed dynamic changes in the expression levels of GCN5 and HDAC1 during embryo development
In conclusion, these data establish Kat2a as a novel and essential regulator of hippocampal memory consolidation.
Study reveals that Gcn5/PCAF facilitate adipogenesis through regulation of PPARgamma expression and regulate brown adipogenesis by influencing Prdm16 expression.
Sirt6 interacts with and modifies GCN5, enhancing GCN5's activity.
Data support a model in which p23 and GCN5 regulate diverse multistep pathways by controlling the longevity of protein-DNA complexes.
Data have defined an important role for GCN5 in NSC and provided evidence that GCN5 is an important Myc transcriptional cofactor in vivo.
KAT2A, or GCN5, is a histone acetyltransferase (HAT) that functions primarily as a transcriptional activator. It also functions as a repressor of NF-kappa-B (see MIM 164011) by promoting ubiquitination of the NF-kappa-B subunit RELA (MIM 164014) in a HAT-independent manner (Mao et al., 2009
histone acetyltransferase KAT2A
, general control of amino acid synthesis 5-like 2
, GCN5 general control of amino-acid synthesis 5-like 2
, general control of amino acid synthesis protein 5-like 2
, K(lysine) acetyltransferase 2A
, GCN5 (general control of amino-acid synthesis, yeast, homolog)-like 2
, General control of amino acid synthesis, yeast, homolog-like 2
, histone acetyltransferase GCN5
, lysine acetyltransferase 2A
, GCN5 general control of amino acid synthesis-like 2
, general control of amino acid synthesis, yeast homolog-like 2
, general control of amino acid synthesis-like 2