Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed Q175 mice.

ABSTRACT: WT and Q175 heterozygous (het) mice treated orally twice a day with vehicle (10% HPβCD), and Q175 mice treated with either 30 or 100 mg/kg orally twice a day CHDI-00390576. CHDI-00390576 is a Class IIa HDAC inhibitor. Mice were dosed from 4 weeks to 6 months of age.

ORGANISM(S): Mus musculus

PROVIDER: GSE104064 | GEO | 2017/09/23

SECONDARY ACCESSION(S): PRJNA408141

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed R6/2 mice.

Project description:R6/2 and WT mice treated orally twice a day with vehicle (10% HPβCD), and R6/2 mice treated with either 30 or 100 mg/kg orally twice a day CHDI-00390576. CHDI-00390576 is a Class IIa HDAC inhibitor. Mice were dosed from 4 - 12 weeks of age.

2017-09-23 | GSE104086 | GEO

RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed Q175 mice.

Project description:RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed Q175 mice.

| PRJNA408141 | ENA

RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed R6/2 mice.

Project description:RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed R6/2 mice.

| PRJNA408174 | ENA

miRNASeq of z_Q175 knock-in mouse lines with and without neo cassette

Project description:In order to determine the effect of neoR gene in Q175 locus, miRNASeq was performed to compare the transcriptional signatures of zQ175 knock-in neo-in (z_Q175 KI) (CHDI-81003003) and zQ175 KI neo-out (Z_Q175 (neo -) KI) (CHDI-81003019) mouse lines. The z_Q175 KI is a knock-in mouse line with humanized exon 1 (190-200 pure CAG repeats) derived from Q140 KI colony. It contains floxed neo cassette upstream of exon 1. The Z_Q175 KI (neo -) KI was generated by crossing the Z-Q175 KI line with a zp3-cre transgenic line to delete out the neo cassette.

2018-12-19 | GSE123664 | GEO

mRNASeq of z_Q175 knock-in mouse lines with and without neo cassette

Project description:In order to determine the effect of neoR gene in Q175 locus, mRNASeq was performed to compare the transcriptional signatures of zQ175 knock-in neo-in (z_Q175 KI) (CHDI-81003003) and zQ175 KI neo-out (Z_Q175 (neo -) KI) (CHDI-81003019) mouse lines. The z_Q175 KI is a knock-in mouse line with humanized exon 1 (190-200 pure CAG repeats) derived from Q140 KI colony. It contains floxed neo cassette upstream of exon 1. The Z_Q175 KI (neo -) KI was generated by crossing the Z-Q175 KI line with a zp3-cre transgenic line to delete out the neo cassette.

2018-12-19 | GSE123657 | GEO

Reduced Representation Bisulfite Sequencing from HD knock-in mouse model

Project description:We generated two types of DNA methylation datasets (Reduced Representation Bisulfite Sequencing [RRBS] and custom methylation array) from a heterozygous HD knock-in mouse model. The heterozygous Htt knock-in line expressed one wildtype endogenous Htt allele and a second Htt allele with knock-in of human mHTT exon 1 with either approximately 190 CAG repeats (Q175) or 20 CAG repeats (Q20). For each genotype (Q175 and Q20) we analyzed two brain regions (striatum and cerebellum) from 8 mice each on the RRBS platform (N=32 RRBS samples). Our EWAS of mutant Htt gene status (i.e. Q175 status) across the two brain regions identified two genome-wide significant CpGs in Htt region. contributor: CHDI foundation

2020-07-02 | GSE147156 | GEO

Transcriptomic analysis of myosin IIa-deficient B cells

Project description:Myosin IIa-deficient follicular B cells have a hyperactivated phenotype. To identify what pathways are regulated by myosin IIa, we performed RNA-seq of coding RNA on flow cytometry sorted follicular B cells from CD23Cre+Myh9fl/fl and CD23Cre+Myh9wt/fl mice.

2018-04-14 | GSE113114 | GEO

Effect of group IIA phospholipase A2 deletion on gene expression in the small intestine

Project description:Besides promoting inflammation by mobilizing lipid mediators, secreted phospholipase A2 group IIA (sPLA2-IIA) prevents bacterial infection by degrading bacterial membranes. Here we show that despite the restricted intestinal expression of sPLA2-IIA in BALB/c mice, its genetic deletion leads to amelioration of cancer and exacerbation of psoriasis in distal skin. Intestinal expression of sPLA2-IIA is reduced after antibiotics treatment or under germ-free conditions, suggesting its upregulation by gut microbiota. Metagenome, transcriptome and metabolome analyses have revealed that sPLA2-IIA deficiency alters the gut microbiota, accompanied by notable changes in the intestinal expression of genes related to immunity and metabolism as well as the levels of various blood metabolites and fecal bacterial lipids, suggesting that sPLA2-IIA contributes to shaping of the gut microbiota. The skin phenotypes in Pla2g2a–/– mice are lost when they are co-housed with littermate wild-type mice, resulting in mixing of the microbiota between the genotypes, or when they are housed in a more stringent pathogen-free facility, where Pla2g2a expression in wild-type mice is low and the gut microbial compositions in both genotypes are nearly identical. Thus, our results highlight a new aspect of sPLA2-IIA as a modulator of gut microbiota, perturbation of which affects distal skin responses.

2022-01-01 | GSE182283 | GEO

Gene expression profiling using RNA-Seq data of MMTV-Wnt1 tumor tissue from mice treated with E7386

Project description:We conducted an RNA-Seq analysis using total RNA extracted from MMTV-Wnt1 tumor tissues resected from mice orally administered E7386 at 25 or 50 mg/kg twice daily, or vehicle, for 3 days (Day 4) or 7 days (Day 8) and examined the differentially expressed gene levels compared with vehicle at days 4 and 8.

2020-12-21 | GSE158713 | GEO

The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammation

Project description:Secreted phospholipase A2-IIA (sPLA2-IIA) hydrolyzes phospholipids to liberate lysophospholipids and fatty acids. Given its poor activity toward eukaryotic cell membranes, its role in the generation of proinflammatory lipid mediators is unclear. Conversely, sPLA2-IIA efficiently hydrolyzes bacterial membranes. Here, we show that sPLA2-IIA impacts on the immune system by acting on the intestinal microbial flora. Using mice overexpressing transgene-driven human sPLA2-IIA, we found that the intestinal microbiota was critical for both induction of an immune phenotype and promotion of inflammatory arthritis. The expression of sPLA2-IIA led to alterations of the intestinal microbiota composition, but housing in a more stringent pathogen-free facility revealed that its expression could affect the immune system in the absence of changes to the composition of this flora. In contrast, untargeted lipidomic analysis focusing on bacteria-derived lipid mediators revealed that sPLA2-IIA could profoundly alter the fecal lipidome. The data suggest that a singular protein, sPLA2-IIA, produces systemic effects on the immune system through its activity on the microbiota and its lipidome.

2021-11-25 | GSE189441 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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