Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages [RNA-seq]

PROVIDER: PRJNA317674 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3346250_1.fastq.gz	Fastqsanger.gz
	SRR3346250_2.fastq.gz	Fastqsanger.gz
	SRR3346251_1.fastq.gz	Fastqsanger.gz
	SRR3346251_2.fastq.gz	Fastqsanger.gz
	SRR3346252_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages

Project description:Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages

| PRJNA317673 | ENA

Mus musculus

Project description:Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages [ChIP-seq]

| PRJNA317669 | ENA

Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages [RNA-seq]

Project description:Mononuclear phagocytes are a diverse cell family that occupy all tissues and assume numerous functions to support tissue and systemic homeostasis. Our ability to investigate the roles of individual subsets is limited by an absence of approaches to ablate gene function within specific sub-populations. Using Nr4a1-dependent Ly6Clow monocytes as a representative cell type we show that enhancer deletion addresses these limitations. Combining ChIP-Seq and molecular approaches we identify a single, conserved, sub-domain within the Nr4a1 enhancer that is essential for Ly6Clow monocyte development. Mice lacking this enhancer lack Ly6Clow monocytes but retain Nr4a1 gene expression in macrophages during steady state and in response to LPS. Nr4a1 is a key negative regulator of inflammatory gene expression and decoupling these processes allows Ly6Clow monocytes to be studied without confounding influences. Enhancer targeting possesses greater specificity than cre recombinase-mediated gene deletion, providing a route to generate loss-of-function models in closely related cell types.

2016-11-02 | GSE80036 | GEO

Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages [ChIP-seq]

2016-11-02 | GSE80031 | GEO

Transcriptional analysis on the impact of anti-PD-L1 mAb on murine lung tumor sorted myeloid populations.

Project description:Targeted gene expression on Lewis lung carcinoma (LLC) sorted MHC-IIlow macrophages (M2), Ly6Chigh inflammatory (IM) and Ly6Clow residential (RM) monocytes to investigate the effect of anti-PD-L1 mAb on specific myeloid subsets in the lung tumor microenvironment performed using the nCounter Myeloid Innate Immunity Panel by Nanostring .

2022-03-04 | GSE165517 | GEO

Triggering of NOD2 receptor converts inflammatory Ly6Chigh into Ly6Clow monocytes with patrolling properties.

Project description:In the present study, we demonstrate that NOD2 receptor triggering by muramyl dipeptide converts blood inflammatory Ly6Chigh monocytes into patrolling Ly6Clow monocytes. Muramyl dipeptide administration to Nr4a1-/- mice, which lack Ly6Clow monocytes, and to Ly6Clow-depleted mice leads to the emergence of blood patrolling monocytes expressing phenotypic profile of typical Ly6Clow monocytes, including high expression of CX3CR1 and LFA1. Furthermore using intravital microscopy in live animal models of inflammatory diseases, we observed that converted Ly6Chigh monocytes are capable of patrolling the endothelium of blood vessels and their presence contributes to reduce the inflammatory response following muramyl dipeptide injection.

2019-01-14 | GSE101496 | GEO

Dynamic lipid mediator changes support infiltrating macrophage subtype transitions during skeletal muscle injury and regeneration

Project description:Time-dependent profiles were recapitulated in sorted neutrophils and Ly6Chigh and Ly6Clow muscle macrophages, with a distinct pro-resolving signature observed in Ly6Clow reparative macrophages. RNA-seq analysis of macrophages stimulated with resolvin D2 (RvD2) showed similarities to transcriptional changes found during the temporal Ly6Chigh to Ly6Clow phenotypic transition. Importantly, RvD2 promoted the temporal progression from Ly6Chigh to Ly6Clow macrophages in vivo.

2019-02-01 | GSE114291 | GEO

Cripto shapes macrophage plasticity and restricts EndMT in injured and diseased skeletal muscle

Project description:The membrane protein Cripto plays a key role in shaping macrophage plasticity in skeletal muscle during regeneration and disease. Cripto acts as an extrinsic modulator of macrophage plasticity and is required for the proper expansion/maintenance of the CD206+ anti-inflammatory macrophage population. Nevertheless, Cripto deletion does not change the gene expression profile of F4/80+/Ly6CLow macrophages suggesting that Cripto was dispensable to induce/maintain the Ly6CLow phenotype.

2020-02-06 | GSE142072 | GEO

RNA Sequencing Analysis of cultured macrophages harvested from the infarcted heart of WT mice and il21 receptor deficient mice (il21r-/-)

Project description:Ly6Clow macrophages promote scar formation and prevent early infarct expansion after myocardial infarction (MI). Although CD4+ T cells influence the regulation of Ly6Clow macrophages after MI, the mechanism remains largely unknown. Here, we focused on IL-21 and uncovered its physiological relevance in post-MI hearts. CD4+ T cells harvested from the infarcted heart produce IL-21 upon stimulation, and IL-21 receptor was expressed on Ly6Clo macrophages in the infarcted heart. The survival rate after MI was significantly improved in IL-21-deficient mice compared with WT mice. Moreover, transcriptome analysis of infarcted heart tissue demonstrated that inflammation was persistent in WT mice compared with IL-21-deficient mice. The number of neutrophils was significantly decreased, whereas the number of Ly6Clow macrophages was significantly increased in IL-21-deficient mice. Consistently, IL-21 enhanced the apoptosis of Ly6Clow macrophages. Furthermore, RNA-seq analysis of Ly6Chi and Ly6Clo macrophages stimulated with or without IL-21 for 24 hours revealed that IL-21 induces inflammatory responses in both Ly6Chi and Ly6Clo macrophages. Finally, the treatment with IL-21 receptor Fc protein significantly increased the survival after MI. Thus, the deletion of IL-21 improves survival after MI by preventing Ly6Clo macrophage apoptosis.

2021-10-31 | GSE161868 | GEO

Identification of miR-146a target genes in mouse monocyte subsets

Project description:To gain insight into the mechanisms underlying miR-146a-mediated modulation of Ly6Chigh monocyte function, we compared the expression profiles of Ly6Chigh and Ly6Clow monocytes in miR-146a+/+ (WT) versus miR-146a-/- (KO) conditions.

2019-06-01 | GSE77159 | 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