Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HDAC1/2 are required for microglia identity during development, homeostasis and neurodegeneration in a context-dependent manner [ChIP inducible knockout on FAD background]

ABSTRACT: HDAC1/2 are required for microglia identity during development, homeostasis and neurodegeneration in a context-dependent manner [ChIP inducible knockout on FAD background]

PROVIDER: PRJNA432994 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6674740_1.fastq.gz	Fastqsanger.gz
	SRR6674740_2.fastq.gz	Fastqsanger.gz
	SRR6674750_1.fastq.gz	Fastqsanger.gz
	SRR6674750_2.fastq.gz	Fastqsanger.gz
	SRR6674741_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Expression data from Hdac1 and 2 knock out microglia in 5X familial Alzheimer's disease (FAD) background

Project description:Epigenetic alterations has been implicated in the pathology of several neurodegenerative diseases. To investigate the role of microglial Hdac1 and 2 in the pathogenesis of Alzheimer's disease (AD), we created microglia specific compound Hdac1 and Hdac2 knock out mice in 5X FAD background. Genetic ablation of Hdac1 and 2 from microglia reduced amyloid plaque burden and improved spatial learning and memory function. To study how Hdac1 and 2 knock out in microglia alters gene expression profile in 5X FAD mice we carry out microarray analysis using 24-28 weeks animals

2018-03-14 | GSE96622 | GEO

HDAC1/2 are required for microglia identity during development, homeostasis and neurodegeneration in a context-dependent manner [ChIP inducible knockout on FAD background]

Project description:Microglia as tissue macrophages of the central nervous system (CNS) provide immunological defense and contribute to the establishment and maintenance of CNS homeostasis. Several transcription factors have been described that regulate microglia development and its steady state form, however little is known about the epigenetic signals that control microglia function in vivo. Here, we employed constitutive and inducible mutagenesis in microglia to delete two class I histone deacetylases (HDACs), Hdac1 and 2. Prenatal ablation of Hdac1 and 2 from microglia drastically impaired microglial development with reduced cell number, altered morphology and induction of apoptosis. Comparative transcriptomic profiling revealed an essential role of Hdac1/2 in the regulation of microglia survival and expansion. Mechanistically, hyperacetylation at H3K9 and H3K27 was found at the promoters of pro-apoptotic and cell cycle genes in the absence of Hdac1/2. In contrast, Hdac1/2 were not required in adult microglia during homeostasis. In a mouse model of Alzheimer’s disease, suppression of Hdac1/2 in microglia, but not in neuroectodermal cells, remarkably displayed substantial decrease in amyloid load and improved cognitive impairment by enhancing microglial amyloid phagocytosis. Collectively, we report a previously unknown role of epigenetic factors that differentially affect microglia development, homeostasis and disease that could potentially be utilized therapeutically.

2018-03-14 | GSE110166 | GEO

HDAC1/2 are required for microglia identity during development, homeostasis and neurodegeneration in a context-dependent manner [ChIP-seq constitutive knockout]

2018-03-14 | GSE107436 | GEO

HDAC1/2 are required for microglia identity during development, homeostasis and neurodegeneration in a context-dependent manner [ChIP-seq constitutive knockout]

Project description:HDAC1/2 are required for microglia identity during development, homeostasis and neurodegeneration in a context-dependent manner [ChIP-seq constitutive knockout]

| PRJNA420076 | ENA

Hepatitis C virus RNA is 5’ flavin adenine dinucleotide (FAD) capped

Project description:RNA viruses have developed elaborate strategies for 5’ capping and protection of their genomes. However, so far no 5’ RNA cap has been identified for Hepatitis C virus (HCV), which cause chronic infection, liver cirrhosis and cancer in humans4. Here, we demonstrate that the cellular metabolite flavin adenine dinucleotide (FAD) is used as noncanonical initiating nucleotide by the viral RNA-dependent RNA polymerase resulting in a 5’ FAD cap on the HCV RNA. FAD capping is completely conserved for the HCV replication intermediate negative RNA strand and partially for the positive RNA strand. The prototype strain J6/JFH1 RNA is FAD capped when isolated from the liver and serum of a human liver chimeric mouse model and in vitro the FAD capping frequency is ~75 %, which is the highest metabolite RNA capping frequency observed. Furthermore, we show that 5’ FAD capping protects RNA from cell-intrinsic innate immune recognition but has limited effect on HCV RNA stability. These results establish capping with cellular metabolites, such as FAD, as a novel viral RNA capping and immune evasion strategy, which potentially could be used by many viruses for protection of their intermediate RNA strands and thereby affect viral treatment outcomes and persistency.

2022-07-31 | GSE180956 | GEO

Transcriptome analysis using Arabidopsis leaves after exogenous FAD treatment

Project description:Riboflavin (RF) and its cofactors (FMN and FAD) are essential molecules for vital metabolic processes in all organisms. Thus, the flavin metabolism must be tightly regulated in the cells. We previously demonstrated that the intracellular levels of flavins were tightly maintained by the enzymes involved in their synthesis and degradation, inducing a plastidic FAD hydrolase (AtNUDX23), in Arabidopsis. However, information of regulatory factors involved in the flavin homeostasis and transporters in each organelle are mostly limited. Terefore, we tried to identify novel factors involved in the flavin metabolism, such as transcription factors and transporters by a transcriptome analysis after exogenous FAD treatment.

2021-03-18 | GSE169061 | GEO

Pseudomonas sp. ZH-FAD

Project description:Pseudomonas sp. ZH-FAD Genome sequencing and assembly

| PRJNA417872 | ENA

Identification of FAD subtypes in mouse HCC models

Project description:In this study, we identified and validated a molecular classification of hepatocellular carcinoma (HCC) based on 42 fatty acid degradation (FAD) genes in clinical samples. We further searched PubMed for the RNA sequencing datasets of mouse models to identify the FAD subtypes in mouse HCC models. A total of 90 samples were collected from five publicly available datasets including 11 mouse HCC models. In addition, the transcriptome sequencing data of 8 samples from our two mouse models (NRAS.MYC.ND and AKT1.MYC.KD) were also included. This dataset aims to explore the transcriptomic characteristics of these two models.

2023-05-01 | GSE202070 | GEO

Bacillus amyloliquefaciens strain:Fad 108

Project description:Bacillus amyloliquefaciens strain:Fad 108 Genome sequencing

| PRJNA1066400 | ENA

The interactome of flavin adenine dinucleotide (FAD) with RNA-binding proteins

Project description:We explored the interactome of flavin adenine dinucleotide (FAD) and the matrix of UV-immobilised FAD bound more than 3,000 proteins from SW-620 lysate. GO enrichment analysis showed that about 600 RNA-binding proteins were bound to FAD beads and, surprisingly, more than 40 proteins showed clear dose-dependent binding competition with nanomolar affinities indicating that their direct or indirect interaction with free FAD is both specific and strong. Among the few known consensus sequences for RNA-binding proteins, we selected the PUF motif 5'-UGUANAUA-3' to investigate whether FAD is binding the Pumilio homologs PUM1 and PUM2 in their RNA-binding pocket, as both these proteins showed dose-response behaviour in the FAD versus FAD-beads. Immobilisation of an oligomer containing the consensus sequence on NHS-activated Sepharose beads yielded PUM-beads that did enrich the Pumilio homologs. Oligomer vs FAD-beads and FAD vs PUM-beads together with the FAD vs FAD-beads dose-response competition indicated that the binding of FAD does not seem to influence the binding of the RNA. It is therefore most likely that FAD binding is allosteric for PUMs.

2022-10-06 | PXD036953 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data