Loss of Gcn5 acetyltransferase activity leads to neural tube closure defects and exencephaly in mouse embryos
about
Human ATAC Is a GCN5/PCAF-containing acetylase complex with a novel NC2-like histone fold module that interacts with the TATA-binding proteinThe ATAC acetyl transferase complex controls mitotic progression by targeting non-histone substrates.Genetic, epigenetic, and environmental contributions to neural tube closureThe p23 molecular chaperone and GCN5 acetylase jointly modulate protein-DNA dynamics and open chromatin statusToxoplasma gondii lysine acetyltransferase GCN5-A functions in the cellular response to alkaline stress and expression of cyst genesGcn5 loss-of-function accelerates cerebellar and retinal degeneration in a SCA7 mouse model.GCN5 is a required cofactor for a ubiquitin ligase that targets NF-kappaB/RelAThe SAGA continues: expanding the cellular role of a transcriptional co-activator complex.Gcn5 and SAGA regulate shelterin protein turnover and telomere maintenance.Enzymatic activity is required for the in vivo functions of CARM1.Embryonic defence mechanisms against glucose-dependent oxidative stress require enhanced expression of Alx3 to prevent malformations during diabetic pregnancy.A Kinase-Independent Role for Cyclin-Dependent Kinase 19 in p53 Response.Core promoter factor TAF9B regulates neuronal gene expression.Pulling complexes out of complex diseases: Spinocerebellar Ataxia 7.Geminin loss causes neural tube defects through disrupted progenitor specification and neuronal differentiation.N-Myc and GCN5 regulate significantly overlapping transcriptional programs in neural stem cells.K-Lysine acetyltransferase 2a regulates a hippocampal gene expression network linked to memory formationChromatin modifiers and remodellers: regulators of cellular differentiationThe chromatin regulator Brpf1 regulates embryo development and cell proliferationGenetics and development of neural tube defects.Gcn5 and PCAF negatively regulate interferon-β production through HAT-independent inhibition of TBK1.Epigenetic programming of hypoxic-ischemic encephalopathy in response to fetal hypoxia.Proper expression of the Gcn5 histone acetyltransferase is required for neural tube closure in mouse embryos.High throughput screening identifies modulators of histone deacetylase inhibitorsHistone modifiers in cancer: friends or foes?Myc and SAGA rewire an alternative splicing network during early somatic cell reprogramming.Drosophila models reveal novel insights into mechanisms underlying neurodegeneration.A unique missense allele of BAF155, a core BAF chromatin remodeling complex protein, causes neural tube closure defects in mice.Essential Nonredundant Function of the Catalytic Activity of Histone Deacetylase 2 in Mouse DevelopmentDevelopment of neurodevelopmental disorders: a regulatory mechanism involving bromodomain-containing proteinsNucleosome positioning and gene regulation: advances through genomics.Acetyltransferases (HATs) as targets for neurological therapeuticsThe chromatin-targeting protein Brd2 is required for neural tube closure and embryogenesis.Analysis of epigenetic alterations to chromatin during development.KAT2A/KAT2B-targeted acetylome reveals a role for PLK4 acetylation in preventing centrosome amplification.Lysine Acetylation and Deacetylation in Brain Development and NeuropathiesCrucial roles of histone-modifying enzymes in mediating neural cell-type specification.Loss of GCN5 leads to increased neuronal apoptosis by upregulating E2F1- and Egr-1-dependent BH3-only protein Bim.Bromodomains as therapeutic targets.Ochratoxin a and mitotic disruption: mode of action analysis of renal tumor formation by ochratoxin A.
P2860
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P2860
Loss of Gcn5 acetyltransferase activity leads to neural tube closure defects and exencephaly in mouse embryos
description
2007 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի մայիսին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2007
@ast
im Mai 2007 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2007/05/01)
@sk
vědecký článek publikovaný v roce 2007
@cs
wetenschappelijk artikel (gepubliceerd op 2007/05/01)
@nl
наукова стаття, опублікована в травні 2007
@uk
مقالة علمية (نشرت في مايو 2007)
@ar
name
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@ast
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@en
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@nl
type
label
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@ast
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@en
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@nl
prefLabel
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@ast
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@en
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@nl
P2093
P2860
P3181
P356
P1476
Loss of Gcn5 acetyltransferase ...... d exencephaly in mouse embryos
@en
P2093
Guillermina Lozano
Yvonne A Evrard
P2860
P304
P3181
P356
10.1128/MCB.00066-07
P407
P50
P577
2007-02-26T00:00:00Z