Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of LPS-induced gene expression in NEDD8-sufficient or -deficient primary macrophages

ABSTRACT: Bone marrow-derived macrophages (BMMs) from Nedd8(flox/flox) mice or Nedd8(flox/flox; lyz2-cre) mice were stimulated with or without 100ng/ml LPS for 4 hours. The total RNA was prepared and subjected to microarray.

ORGANISM(S): Mus musculus

PROVIDER: GSE99386 | GEO | 2020/05/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Comparison of LPS-induced gene expression in UBA3-sufficient or -deficient primary macrophages

Project description:Bone marrow-derived macrophages (BMMs) from Uba3(flox/flox) mice or Uba3(flox/flox; lyz2-cre) mice were stimulated with or without 100ng/ml LPS for 4 hours. The total RNA was prepared and subjected to microarray.

2020-05-26 | GSE99376 | GEO

Decreased expression of a subset of TLR-dependent genes by heme-inducible Spi-C

Project description:To determine the functions of Spi-C in innate immune responses, we investigated the overall gene expression patterns in M-CSF-BMDMΦs prepared from Spicflox/flox and Lyz2-cre; Spicflox/flox mice. M-CSF-BMDMΦs were stimulated with or without LPS following heme treatment and used for RNA-seq analysis.

2018-06-27 | GSE100805 | GEO

Comparison of gene expression in NEDD8-sufficient or -deficient neonatal liver

Project description:The total RNA was prepared from the postnatal day 3 NEDD8-sufficient or -deficient liver and subjected to microarray.

2022-06-24 | GSE133215 | GEO

Alternate splicing in Tlr4 pathway in LPS Stimulated BMMs

Project description:Pairwise comparison of expression of alternate splicing in the Tlr4 pathway using custom designed Combimatix oligonucleotide arrays. Bone marrow derived macrophages (BMMs) from C57Bl6/J mice (6 wks male) exposed to LPS (10ng/ml) for 7hrs. Keywords: Response to LPS

2007-01-15 | GSE4044 | GEO

High-throughput sequencing Analysis of mouse BMDM cell Transcriptomes after LPS Challenge

Project description:Purpose: Mouse BMDM is the universal cell type of studying innate immunity.This study was designed to analyze LPS induced innate immune respone and the gene expression in WT and HDAC3 KO BMDMs. Methods: BMDM cells from Hdac3f/f and Lyz2-Cre-Hdac3f/f were treated with or without LPS for 4 hours. Then mRNA profiles of these samles were generated by High-throughput sequencing analysis, in triplicate, using illumina HiSeqTM2000/MiSeq. And the differencial mRNA profiles were analyzed. Results: mRNA profiles were analyzed, and differencial expression profiles were compared . Conclusions: Our study demostrated the transcriptional profiles of BMDMs from Hdac3f/f and Lyz2-Cre-Hdac3f/f mice upon LPS challenge, with biologic replicates, generated by RNA-seq technology.

2021-08-06 | GSE155801 | GEO

Gene expression profiling of mT/mG;Lyz2.Cre vs IKKbetaf/f;Lyz2.Cre mouse bone marrow derived macrophages

Project description:Gene expresion comparison between tomato Lyz2 Cre and IKKbeta flox/flox Lyz2 Cre bone marrow derived macrophages

2019-06-28 | GSE94880 | GEO

TDAG51 is a novel coactivator of FoxO1

Project description:Tight regulation of Toll-like receptor (TLR)-mediated inflammatory responses is important in innate immunity. Here, we show that T cell death-associated gene 51 (TDAG51/PHLDA1) is a novel coactivator of the transcription factor FoxO1, regulating inflammatory mediator production in the lipopolysaccharide (LPS)-induced inflammatory response. TDAG51 induction by LPS stimulation was mediated by the TLR2/4 signaling pathway in bone marrow-derived macrophages (BMMs). LPS-induced inflammatory mediator production was significantly decreased in TDAG51-deficient BMMs. In TDAG51-deficient mice, LPS- or pathogenic Escherichia coli infection-induced lethal shock was reduced by decreasing serum proinflammatory cytokine levels. The recruitment of 14-3-3 to FoxO1 was competitively inhibited by the TDAG51-FoxO1 interaction, leading to blockade of FoxO1 cytoplasmic translocation and thereby strengthening FoxO1 nuclear accumulation. TDAG51/FoxO1 double-deficient BMMs showed significantly reduced inflammatory mediator production compared with TDAG51- or FoxO1-deficient BMMs. TDAG51/FoxO1 double deficiency protected mice against LPS- or pathogenic E. coli infection-induced lethal shock by weakening the systemic inflammatory response. Thus, these results indicate that TDAG51 acts as a coactivator of the transcription factor FoxO1, leading to strengthened FoxO1 activity in the LPS-induced inflammatory response.

2023-06-24 | PXD039815 | Pride

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

RNA-seq in RAW264.7 cells after silence of Synbindin in response to LPS

Project description:RAW264.7 cells were transfected with Synbindin siRNA for 48hours, then 100ng/ml LPS were treated cells for 4 hours. Before and after LPS stimulation, cells were collected and RNA were extracted for RNA-seq.

2022-09-01 | GSE158301 | GEO

Single-cell RNAseq analysis (10X Genomics Chromium) of cMAF- and Mafb-deficent lung monocytes and interstium macrophages

Project description:Lung interstitium macrophages (IMs) are non-alveolar resident tissue macrophages which contribute to the lung homeostasis. These cells were reported to be heterogeneous by our group and other teams, which contains two main distinct subpopulations: CD206+ IMs and CD206- IMs. However, the exact origin of IMs and the transcriptional programs that regulate IM differentiation remains unclear. In recent report, we analyzed the refilled IMs in the course of time after induced IM depletion with single-cell RNA sequencing (10X Genomics Chromium) and bulk RNA sequencing. The lung IMs and monocytes from either Lyz2-Cre Mafflox/flox mice (cMAF-KO), Lyz2-Cre Mafbflox/flox (MAFb-KO), Lyz2-Cre Mafflox/flox Mafbflox/flox (dKO) or control litermate mice without floxp locus (Control) were analyzed and compared using single-cell RNA sequencing. All the main substs, i.e. Ly6C+ classical monocytes, Ly6C- patrolling monocytes, CD206+ IMs, CD206- IMs were found in control sample, while IMs are absent in both MAFb-KO and dKO sample accompied by a new intermediate population independent of Mafb expression. CMAF-KO sample show less impact in cell population composition with a lower freqency of CD206+ IM population.

2023-02-07 | GSE193891 | 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