Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Plasma DNA profile in DNASE1L3 deficiency-Mouse AAV samples

ABSTRACT: Plasma DNA profile in DNASE1L3 deficiency-Mouse AAV

PROVIDER: EGAS00001004409 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Plasma DNA profile in DNASE1L3 deficiency

Project description:Plasma DNA profile in DNASE1L3 deficiency

| EGAS00001004342 | EGA

ena-DATASET-DCPTCUHK-12-06-2020-14:07:24:130-345 - samples

Project description:Human dnase1l3 deficiency-Mouse AAV samples

| EGAD00001006215 | EGA

Nuclease deficiencies alter plasma cell-free DNA methylationprofiles (mouse)

Project description:The effects of DNASE1L3 or DNASE1 deficiency on cfDNA methylation was explored in plasma of mice deficient in these nucleases and in DNASE1L3-deficient humans. Compared to wildtype cfDNA, cfDNA in Dnase1l3-deficient mice was significantly hypomethylated, while cfDNA in Dnase1-deficient mice was hypermethylated. The cfDNA hypomethylation in Dnase1l3-deficient mice was due to increased fragmentation and representation from open chromatin regions (OCRs) and CpG islands (CGIs). These findings were absent in Dnase1-deficient mice.

| EGAS00001004696 | EGA

Plasma DNA end analysis (mouse)

Project description:Plasma DNA end analysis (mouse)

| EGAS00001006700 | EGA

Molecular pathways modifying progranulin deficiency phenotypes in mouse models

Project description:Haploinsufficiency of the progranulin (PGRN) protein is a leading cause of frontotemporal lobar degeneration (FTLD). Mouse models have been developed to study PGRN functions. However, PGRN deficiency in the commonly used C56BL/6 mouse strain background leads to very mild phenotypes, and pathways regulating PGRN deficiency phenotypes remain to be elucidated. We generated PGRN-deficient mice in the FVB/N background and compared PGRN deficiency phenotypes between C56BL/6 and FVB/N background via immunostaining, western blot, RNA-seq, and proteomics approaches. We also identified sPLA2-IIA as a novel binding partner of PGRN and demonstrated the importance of sPLA2-IIA in modifying PGRN deficiency phenotypes using inhibitor treatment and AAV-mediated overexpression in mouse models. We report that PGRN loss in the FVB/N mouse strain results in earlier onset and stronger FTLD-related and lysosome-related phenotypes. We found that PGRN interacts with sPLA2-IIA, a member of the secreted phospholipase A2 (sPLA2) family member and a key regulator of inflammation that is expressed in FVB/N but not C56BL/6 background. sPLA2-IIA inhibition rescues PGRN deficiency phenotypes and sPLA2-IIA overexpression drives enhanced gliosis and lipofuscin accumulation in PGRN-deficient mice. Additionally, RNA-seq and proteomics analysis revealed that mitochondrial pathways are upregulated in the PGRN-deficient C57BL/6 mice but not in the FVB/N mice. Our studies establish a better mouse model for FTLD-GRN and uncover novel pathways modifying PGRN deficiency phenotypes.

2025-03-20 | MSV000097392 | MassIVE

ena-DATASET-DCPTCUHK-12-06-2020-14:15:10:066-348 - samples

Project description:Plasma DNA profile in DNASE1L3 deficiency

| EGAD00001006216 | EGA

Jagged ends of plasma DNA (mouse)

Project description:Jagged ends of plasma DNA (mouse)

| EGAS00001005563 | EGA

Nuclease deficiencies alter plasma cell-free DNA methylationprofiles (Human)

| EGAS00001004897 | EGA

Functional characterization of hGRÎ² Isoform in mouse liver

Project description:We used AAV as a vector to deliver hGRÎ² to C57BL/6 mouse liver. We collected liver samples for microarray analysis to investigate any phenotype as well as the underlying specific signaling pathway. In particular, we would like to determine if and how hGRÎ² overexpression in liver affects mGRÎ±âs gene transcription profile in C57BL/6 mice. Three replicates for each group: untreated WT liver, AAV-GFP treated liver, and AAV-hGRB treated liver.

2015-12-11 | E-GEOD-75740 | biostudies-arrayexpress

Genetic Model of iron deficiency in the Mouse Liver

Project description:Iron overload causes the generation of reactive oxygen species, which can lead to lasting damage to the liver and other organs. We studied the effects of iron deficiency and iron overload on the hepatic transcriptional and metabolomic profile in mouse models.

2018-02-13 | GSE86292 | GEO

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