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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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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 (显示 DKK1 抗体) expression by acetylation of Histone H3 (显示 HIST3H3 抗体) lysine 9 (H3K9) and Histone H3 (显示 HIST3H3 抗体) lysine 14 (H3K14) to regulate Wnt (显示 WNT2 抗体)/beta catenin (显示 CTNNB1 抗体) pathway of PDLSCs.
findings reveal an important mechanism of histone modification and demonstrate that local generation of succinyl-CoA (显示 OXCT1 抗体) 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 (显示 KAT2B 抗体) 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 (显示 WDR5 抗体) 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 (显示 SIRT1 抗体)) remains unchanged.
Orc5 (显示 ORC5 抗体) associates with the H3 histone (显示 HIST1H3B 抗体) acetyl transferase (显示 HAT1 抗体) GCN5 (also known as KAT2A), and this association enhances the chromatin-opening function of Orc5 (显示 ORC5 抗体).
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 (显示 NFKB1 抗体) pathway as a novel potential molecular target for stem cell mediated regenerative medicine and the treatment of metabolic bone diseases such as osteoporosis.
Gcn5 regulates Hoxc11 (显示 HOXC11 抗体) gene expression through mediating site-specific H3K9 acetylation in Akt1 (显示 AKT1 抗体)-/- MEFs.
study revealed GCN5-mediated EGR2 (显示 EGR2 抗体) acetylation as a molecular mechanism that regulates iNKT development.
The results demonstrated that Islet1 (显示 ISL1 抗体) upregulated expression of general control of amino acid biosynthesis protein 5 (显示 CAPS 抗体) (Gcn5) and enhanced the binding of Gcn5 to the promoters of GATA binding protein 4 (GATA4 (显示 GATA4 抗体)) and NK2 homeobox 5 (Nkx2.5 (显示 NKX2-5 抗体)). In addition, Islet-1 (显示 ISL1 抗体) downregulated DNA methyltransferase (显示 DNMT1 抗体) (DNMT)1 (显示 DNMT1 抗体) expression and reduced its binding to the GATA4 (显示 GATA4 抗体) 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 (显示 NFKB1 抗体) with IkappaBalpha (显示 NFKBIA 抗体)-SR or by GCN5 knockdown in these muscles also enhanced AKT (显示 AKT1 抗体) and mechanistic target of rapamycin (mTOR (显示 FRAP1 抗体)) activities, which also contributed to the reduction in atrophy.
Gcn5 and PCAF (显示 KAT2B 抗体) repress IFN-beta (显示 IFNB1 抗体) production in an enzymatic activity-independent and non-transcriptional manner: by inhibiting the innate immune signaling kinase TBK1 (显示 TBK1 抗体) in the cytoplasm.
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