Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell sequencing of hypothalamus tissues in IDOL KO

ABSTRACT: Single cell sequencing of hypothalamus tissues in IDOL KO

PROVIDER: PRJNA490830 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7829281_1.fastq.gz	Fastqsanger.gz
	SRR7829281_2.fastq.gz	Fastqsanger.gz
	SRR7829282_1.fastq.gz	Fastqsanger.gz
	SRR7829282_2.fastq.gz	Fastqsanger.gz
	SRR7829283_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Single cell sequencing of hypothalamus tissues in IDOL KO

Project description:A single cell suspension was generated from IDOL KO and Control mouse hypothalami, and single-cell mRNAseq libraries were generated with Drop-Seq.

2019-10-01 | GSE119960 | GEO

Neuronal Idol deletion ameliorates amyloid pathology

Project description:Earlier studies demonstrated that overexpression of the low-density lipoprotein receptor (LDLR) decreases apolipoprotein E (APOE) levels in the brain and alleviates amyloid-beta (Aβ) pathology. We hypothesized that inhibiting the Inducible Degrader of LDLR (IDOL)- an E3 ubiquitin ligase that ubiquitinates LDLR for degradation- would increase endogenous LDLR levels and decrease amyloid pathology. Previously, we demonstrated that the deletion of Idol increased LDLR levels and reduced amyloid deposition in a transgenic mouse model of Aβ-amyloidosis. However, the cellular mechanisms underlying these beneficial effects were unknown. Here, we investigate the cell-type-specific contribution of Idol deletion to amyloid pathology by generating Idol conditional knock-out mouse models. We demonstrate that deletion of neuronal, but not microglial, Idol reduces amyloid accumulation in the 5XFAD transgenic mouse model. Furthermore, only neuronal Idol deletion alters brain LDLR and APOE levels, pointing to the critical role of the neuronal LDLR-APOE axis in modulating Aβ accumulation.

2025-12-16 | GSE301451 | GEO

Deletion of neuronal Idol ameliorates Alzheimer's disease–related pathologies via APOE receptors

Project description:Overexpression of the low-density lipoprotein receptor (LDLR) is known to decrease apolipoprotein E (APOE) levels and alleviate amyloid beta (Aβ) pathology. We hypothesized that inhibiting the Inducible Degrader of LDLR (IDOL), an enzyme that ubiquitinates LDLR for degradation, would increase endogenous LDLR levels and attenuate amyloid pathology. To investigate the cell-type–specific role of IDOL, we generated Idol conditional knockout mice on an Aβ-amyloidosis mouse model and performed biochemical, histological, and multi-omics analyses. We demonstrated that neuronal, but not microglial, Idol deletion reduced amyloid accumulation and altered brain LDLR and APOE levels, indicating the critical role of neuronal IDOL-LDLR in amyloid pathology. In addition, neuronal Idol deletion increased the levels of Reelin receptors important for synaptic function, and single-nuclei RNA sequencing revealed significant changes associated with synaptic organization.

2025-12-15 | GSE300690 | GEO

RNA-seq analysis of mice hypothalamus tissues.

Project description:RNA-seq analysis of mice hypothalamus tissues.

| PRJNA681412 | ENA

Zanclus cornutus (Moorish idol)

Project description:Zanclus cornutus (Moorish idol) genome, fZanCor1

| PRJEB104044 | ENA

Peptidome analysis of the hypothalamus in a single mouse.

Project description:A 2-mg frozen section of hypothalamus from a single mouse was homogenized in 200 µL of denaturing solution(7 M urea, 2 M thiourea, 20 mM dithiothreitol) containing cOmplete Mini Protease Inhibitor Cocktail (Roche). Peptide extracts equivalent to 135 µg of tissue were analyzed by LC-MS/MS.

2022-01-08 | PXD023475 | JPOST Repository

Neuronal Idol deletion ameliorates amyloid pathology

Project description:Neuronal Idol deletion ameliorates amyloid pathology

| PRJNA1285258 | ENA

Neuronal Idol deletion ameliorates amyloid pathology

Project description:Earlier studies demonstrated that overexpression of the low-density lipoprotein receptor (LDLR) decreases apolipoprotein E (APOE) levels in the brain and alleviates amyloid-beta (Abeta) pathology. We hypothesized that inhibiting the Inducible Degrader of LDLR (IDOL)- an E3 ubiquitin ligase that ubiquitinates LDLR for degradation- would increase endogenous LDLR levels and decrease amyloid pathology. Previously, we demonstrated that the deletion of Idol increased LDLR levels and reduced amyloid deposition in a transgenic mouse model of Abeta-amyloidosis. However, the cellular mechanisms underlying these beneficial effects were unknown. Here, we investigate the cell-type-specific contribution of Idol deletion to amyloid pathology by generating Idol conditional knock-out mouse models. We demonstrate that deletion of neuronal, but not microglial, Idol reduces amyloid accumulation in the 5XFAD transgenic mouse model. Furthermore, only neuronal Idol deletion alters brain LDLR and APOE levels, pointing to the critical role of the neuronal LDLR-APOE axis in modulating Abeta accumulation.

2025-06-16 | MSV000098209 | MassIVE

Single cell analysis of the aging hypothalamus

Project description:Single cell analysis of the aging hypothalamus

| PRJNA779749 | ENA

Therapeutic IDOL reduction ameliorates amyloidosis and improves cognitive function in APP/PS1 mice

Project description:An antisense oligonucleotide (ASO) against E3 ubiquitin ligase IDOL in the brain significantly decreased Aβ pathology, and improved spatial learning and memory in APP/PS1 mice.

2019-12-24 | GSE142535 | 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