anti-K(lysine) Acetyltransferase 2A (KAT2A) Antikörper

Human K(lysine) Acetyltransferase 2A (KAT2A) Interaktionspartner

1. KAT2A/2B acetylation of PLK4 (zeige PLK4 Antikörper) 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 (zeige DKK1 Antikörper) expression by acetylation of Histone H3 (zeige HIST3H3 Antikörper) lysine 9 (H3K9) and Histone H3 (zeige HIST3H3 Antikörper) lysine 14 (H3K14) to regulate Wnt (zeige WNT2 Antikörper)/beta catenin (zeige CTNNB1 Antikörper) pathway of PDLSCs.

3. findings reveal an important mechanism of histone modification and demonstrate that local generation of succinyl-CoA (zeige OXCT1 Antikörper) 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 (zeige KAT2B Antikörper) 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 (zeige WDR5 Antikörper) 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 (zeige SIRT1 Antikörper)) remains unchanged.

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

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) Interaktionspartner

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

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

3. The results demonstrated that Islet1 (zeige ISL1 Antikörper) upregulated expression of general control of amino acid biosynthesis protein 5 (zeige CAPS Antikörper) (Gcn5) and enhanced the binding of Gcn5 to the promoters of GATA binding protein 4 (GATA4 (zeige GATA4 Antikörper)) and NK2 homeobox 5 (Nkx2.5 (zeige NKX2-5 Antikörper)). In addition, Islet-1 (zeige ISL1 Antikörper) downregulated DNA methyltransferase (zeige DNMT1 Antikörper) (DNMT)1 (zeige DNMT1 Antikörper) expression and reduced its binding to the GATA4 (zeige GATA4 Antikörper) 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 (zeige NFKB1 Antikörper) 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 (zeige NFKB1 Antikörper) with IkappaBalpha (zeige NFKBIA Antikörper)-SR or by GCN5 knockdown in these muscles also enhanced AKT (zeige AKT1 Antikörper) and mechanistic target of rapamycin (mTOR (zeige FRAP1 Antikörper)) activities, which also contributed to the reduction in atrophy.

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