Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular and phenotypic changes in FLExDUX4 mice

ABSTRACT: Molecular and phenotypic changes in FLExDUX4 mice

PROVIDER: PRJNA978063 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24780803.fastq.gz	Fastqsanger.gz
	SRR24780804.fastq.gz	Fastqsanger.gz
	SRR24780805.fastq.gz	Fastqsanger.gz
	SRR24780806.fastq.gz	Fastqsanger.gz
	SRR24780807.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Monitoring RAS Phenotypic Changes Based on ctDNA to Predict the Efficacy of Cetuximab in Metastatic Colorectal Cancer

Project description:Interventions: Gold Standard:Clinical outcome;Index test:RAS phenotypic changes in ctDNA Primary outcome(s): RAS gene phenotype;SEN, SPE, ACC, AUC of ROC Study Design: Sequential

| 2687923 | ecrin-mdr-crc

Characterization of molecular changes at meiotic initiation in mice

Project description:Characterization of molecular changes at meiotic initiation in mice

| PRJNA476515 | ENA

Molecular and phenotypic changes in FLExDUX4 mice

Project description:We investigated differences in the quadriceps transcriptome of 13-week-old heterozygous B6(Cg)-Gt(ROSA)26Sortm1.1(DUX4*)Plj/J (FLExDUX4) mouse model of Facioscapulohumeral Muscular Dystrophy (FSHD) and their wild type (WT) littermates to determine if there were characterize the structural/functional adaptations to aerobic exercise training and their molecular foundations using RNA sequencing

2023-07-31 | GSE233832 | GEO

Molecular and Phenotypic Changes in FLExDUX4 Mice.

Project description:Facioscapulohumeral muscular dystrophy (FSHD) is caused by the aberrant expression of the double homeobox 4 (DUX4) gene. The FLExDUX4 mouse model carries an inverted human DUX4 transgene which has leaky DUX4 transgene expression at a very low level. No overt muscle pathology was reported before 16 weeks. The purpose of this study is to track and characterize the FLExDUX4 phenotypes for a longer period, up to one year old. In addition, transcriptomic changes in the muscles of 2-month-old mice were investigated using RNA-seq. The results showed that male FLExDUX4 mice developed more severe phenotypes and at a younger age in comparison to the female mice. These include lower body and muscle weight, and muscle weakness measured by grip strength measurements. Muscle pathological changes were observed at older ages, including fibrosis, decreased size of type IIa and IIx myofibers, and the development of aggregates containing TDP-43 in type IIb myofibers. Muscle transcriptomic data identified early molecular changes in biological pathways regulating circadian rhythm and adipogenesis. The study suggests a slow progressive change in molecular and muscle phenotypes in response to the low level of DUX4 expression in the FLExDUX4 mice.

| S-EPMC10381554 | biostudies-literature

BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss

Project description:BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss

| PRJNA1019260 | ENA

E-GEOD-37218

Project description:Gene expression changes in Ahnak knockout mice

2015-09-28 | E-GEOD-37218 | ExpressionAtlas

E-GEOD-106937

Project description:Molecular Changes of Lung Malignancy in HIV Infection

2020-03-31 | E-GEOD-106937 | ExpressionAtlas

Mineralized collagen induces phenotypic changes in MDA-MB-231

Project description:Mineralized collagen induces phenotypic changes in MDA-MB-231

| PRJNA952893 | ENA

Early cardiac ageing: Phenotypic and transcriptional transitions in young to middle-aged mice

Project description:While much research has focussed on advanced stages (and mechanisms) of ageing, this fundamental process may commence at a relatively early age, impacting organ function and resilience throughout the adult lifespan. In male C57BL/6 mice, multiple phenotypic and transcriptional features of cardiovascular ageing were evident from 16 weeks of age, well in advance of 'middle age'. Phenotypic changes include declining cardiac and coronary reserves and resistance to ischaemic insult. Gene changes support early constitutive stress together with a plateau in transcriptome responsiveness to ischaemia, and declining induction of cardioprotective and quality control pathways vs. increasing induction of genes promoting signalling dysfunction, hypertrophy and cell death. These findings support cardiac ageing from early adulthood. Molecular changes reflect declining adaptive capacity/quality control, consistent with evolutionary theories of biological ageing.

2021-12-31 | GSE179286 | GEO

A broad phenotypic screen identifies novel dominant phenotypes in Huntington’s disease CAG knock-in mice

Project description:Huntington’s disease (HD) is a dominantly inherited neurodegenerative disorder characterized by abnormal voluntary and involuntary movements, cognitive impairment and psychiatric disturbances. In order to identify phenotypic changes in the mouse that are most likely to be relevant to events triggered by the CAG repeat expansion in HD patients, we are interested in the earliest events that are triggered by expression of a single allele’s worth of full-length mutant huntingtin in the mouse, whether at the molecular, cellular or whole animal level. To this end, we have undertaken a broad-based, unbiased phenotypic screen in heterozygous HdhQ111/+ C57BL/6J mice. For expression profiling analysis, four male mice at the age of 18 weeks were analysed versus a pool of four male wildtype mice (reference) at the same age. For each single mouse, two chip hybridizations, including a dye-swap experiment, were performed per tissue. Using our genome-wide microarray platform, we performed transcriptome analysis of liver and brain.

2011-09-30 | E-GEOD-28232 | biostudies-arrayexpress

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