Browse our anti-K(lysine) Acetyltransferase 2A (KAT2A) Antibodies

Human K(lysine) Acetyltransferase 2A (KAT2A) interaction partners

1. KAT2A/2B acetylation of PLK4 (show PLK4 Antibodies) prevents centrosome amplification

2. 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 (show DKK1 Antibodies) expression by acetylation of Histone H3 (show HIST3H3 Antibodies) lysine 9 (H3K9) and Histone H3 (show HIST3H3 Antibodies) lysine 14 (H3K14) to regulate Wnt (show WNT2 Antibodies)/beta catenin (show CTNNB1 Antibodies) pathway of PDLSCs.

3. findings reveal an important mechanism of histone modification and demonstrate that local generation of succinyl-CoA (show OXCT1 Antibodies) by the nuclear alpha-KGDH complex coupled with the succinyltransferase activity of KAT2A is instrumental in histone succinylation, tumour cell proliferation, and tumour development

4. GCN5 upregulation is especially common in UCCs. GCN5 knockdown impeded growth of specific UCCs, whereas PCAF (show KAT2B Antibodies) knockdown elicited minor effects.

5. 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.

6. This report documents a novel lncRNA, GClnc1, which may act as a scaffold to recruit the WDR5 (show WDR5 Antibodies) and KAT2A complex and modify the transcription of target genes. This study reveals that GClnc1 is an oncogenic lncRNA in human gastric cancer.

7. 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.

8. 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 (show SIRT1 Antibodies)) remains unchanged.

9. Orc5 (show ORC5 Antibodies) associates with the H3 histone (show HIST1H3B Antibodies) acetyl transferase (show HAT1 Antibodies) GCN5 (also known as KAT2A), and this association enhances the chromatin-opening function of Orc5 (show ORC5 Antibodies).

10. Methionine was the only essential amino acid that rapidly induced PGC-1alpha acetylation through activating the GCN5 acetyltransferase.

Mouse (Murine) K(lysine) Acetyltransferase 2A (KAT2A) interaction partners

1. Gcn5 regulates Hoxc11 (show HOXC11 Antibodies) gene expression through mediating site-specific H3K9 acetylation in Akt1 (show AKT1 Antibodies)-/- MEFs.

2. study revealed GCN5-mediated EGR2 (show EGR2 Antibodies) acetylation as a molecular mechanism that regulates iNKT development.

3. The results demonstrated that Islet1 (show ISL1 Antibodies) upregulated expression of general control of amino acid biosynthesis protein 5 (show CAPS Antibodies) (Gcn5) and enhanced the binding of Gcn5 to the promoters of GATA binding protein 4 (GATA4 (show GATA4 Antibodies)) and NK2 homeobox 5 (Nkx2.5 (show NKX2-5 Antibodies)). In addition, Islet-1 (show ISL1 Antibodies) downregulated DNA methyltransferase (show DNMT1 Antibodies) (DNMT)1 (show DNMT1 Antibodies) expression and reduced its binding to the GATA4 (show GATA4 Antibodies) promoter.

4. recovering GCN5 expression in vivo by lentiviral expression vector significantly attenuated the loss of angiogenesis in ovariectomized mouse femurs

5. 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

6. 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.

7. Methionine was the only essential amino acid that rapidly induced PGC-1alpha acetylation through activating the GCN5 acetyltransferase.

8. these results may point to the GCN5-NF-kappaB (show NFKB1 Antibodies) pathway as a novel potential molecular target for stem cell mediated regenerative medicine and the treatment of metabolic bone diseases such as osteoporosis.

9. In addition to reducing atrogene expression, surprisingly inhibiting NF-kappaB (show NFKB1 Antibodies) with IkappaBalpha (show NFKBIA Antibodies)-SR or by GCN5 knockdown in these muscles also enhanced AKT (show AKT1 Antibodies) and mechanistic target of rapamycin (mTOR (show FRAP1 Antibodies)) activities, which also contributed to the reduction in atrophy.

10. Gcn5 and PCAF (show KAT2B Antibodies) repress IFN-beta (show IFNB1 Antibodies) production in an enzymatic activity-independent and non-transcriptional manner: by inhibiting the innate immune signaling kinase TBK1 (show TBK1 Antibodies) in the cytoplasm.