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