Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional Profiling in macrophage-specific GR KO mice

ABSTRACT: We generated transcriptional profiles in fasted GRflox; LysM-Cre+/- (GRMAC) mice and littermate controls (GRflox).

ORGANISM(S): Mus musculus

PROVIDER: GSE147924 | GEO | 2022/01/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA -Seq analysis of CD11b+Mac-Spleen from HFD-Mettl3-LysM-Cre mice

Project description:We processed RNA-sequencing on splenic CD11b+ macrophages isolated from 10-week old Mettl3f/f-LysM-Cre KO and littermate WT mice. NO_4-1, NO_4-2 are Mettl3f/f-LysM-Cre KO. NO_5-2, NO_5-3 are WT littermate controls.

2022-01-07 | GSE184318 | GEO

m6A-Epitranscriptomic Microarray analysis of CD11b+Mac-Spleen from HFD-Mettl3-LysM-Cre mice

Project description:We processed m6A-Epitranscriptomic Microarray analysis on splenic CD11b+ macrophages isolated from 10-week old Mettl3f/f-LysM-Cre KO and littermate WT mice.

2022-01-07 | GSE184367 | GEO

Transcriptional Profiling in macrophage-specific GR KO mice

Project description:Transcriptional Profiling in macrophage-specific GR KO mice

| PRJNA622554 | ENA

DICER controls macrophage polarization and tumor response to immunotherapy

Project description:Tumor-associated macrophages (TAMs) have immunosuppressive capacity in mouse models of cancer. Here we show that the genetic deletion of the microRNA (miRNA)-processing enzyme DICER in TAMs broadly programs them to a CD11c+MRC1â/low M1-like immunostimulatory phenotype characterized by activated interferon-Î³ (IFN-Î³)/STAT1/IRF signaling. M1-like TAM programming fostered the recruitment of cytotoxic T-cells (CTLs), including tumor-antigen-specific CTLs, inhibited tumor growth, and enhanced the efficacy of PD1 checkpoint blockade. Bioinformatics analysis of TAM transcriptomes identified a limited set of miRNAs putatively involved in TAM programming. Re-expression of Let-7 in Dicer-deficient TAMs was sufficient to partly rescue the M2-like (protumoral) TAM phenotype and abate tumor CTL infiltration. Targeted suppression of DICER activity in TAMs may, therefore, stimulate antitumor immunity and enhance the efficacy of cancer immunotherapy. To explore the role of DICER in the development, activation and immunological functions of TAMs, we crossed homozygous LysM-Cre (Clausen et al., 1999) with Dicerlox/lox (Harfe et al., 2005) mice to obtain mice with myeloid-cell-specific Dicer1 gene deletion (LysM-Cre;Dicerâ/â, referred to as Dâ/â). These mice were then backcrossed to LysM-Cre to obtain the control LysM-Cre; Dicer+/+ mice (referred to as D+/+). Both LysM-Cre and Dicerlox/lox mutations were always homozygous in our experiment. We then inoculated Lewis lung carcinoma (LLC) cells subcutaneously (s.c.) in Dâ/â and control D+/+ mice. Once the tumors were established, we isolated by fluorescence-activated cell sorting (FACS) tumor-associated macrophages (F4/80+ cells).

2016-06-13 | E-GEOD-76356 | biostudies-arrayexpress

Macrophage specific Mafb deficiency effects brown adipose tissue's cold adaptability

Project description:To investigate the Cold exposure adaptation under macrophage-specific Mafb deficiency, we put the Mafbf/f (Control) mice and Mafbf/f::LysM-cre (Macrophage specific Mafb deficient) under cold exposure for 10 days and collected the interscapular brown adipose tissue (iBAT) of these mice to compare the changes using RNA sequencing.

2024-02-29 | GSE225421 | GEO

Ago2-RIP-chip in Dicer WT and KO macrophages

Project description:To determine the spectrum of miRNA targets regulated following Dicer deletion, we performed argonaute 2 (AGO2)-RNA Immunoprecipitation (RIP)-microarray in bone marrow-derived macrophages (BMDMs) from LysM-Cre/Dicerflox/flox/Apoe–/– and LysM-Cre/Dicerwt/wt/Apoe–/– mice. This analysis combined with miRNA profiling in Dicer wild type (WT) and knockout (KO) BMDMs may help to identify the miRNA targets regulated by Dicer deletion.

2018-05-23 | GSE87717 | GEO

Knockout of the selenocysteine tRNA (Trsp) gene in mouse macrophage

Project description:Comparative analysis of gene expression in bone marrow-derived macrophages (BMDM) from trsp knockout mice (Trspfl/fl-LysM-Cre+/-) and Control (Trspfl/fl-LysM-Cre-/-) mice. Selenium, a micronutrient whose deficiency in the diet causes immune dysfunction and inflammatory disorders, exerts its physiological effects partly in the form of selenium-containing proteins (selenoproteins). Incorporation of selenium into the amino acid selenocysteine (Sec), and subsequently into selenoproteins, is mediated by Sec tRNA[Ser]Sec. To identify macrophage-specific selenoprotein function, we generated mice with the Sec tRNA[Ser]Sec gene specifically deleted in myeloid cells. These mutant mice were devoid of the selenoproteome in macrophages, yet exhibited largely normal inflammatory responses. However, selenoprotein deficiency led to aberrant expression of extracellular matrix-related genes, and diminished migration of macrophages in a protein gel matrix. Therefore, selenium status may affect immune defense and tissue homeostasis through its effect on selenoprotein expression and the trafficking of tissue macrophages. We have generated mice in which we have selectively removed the selenocysteine tRNA gene (trsp) in macrophages under the control of LysM-Cre promoter. Microarray analysis was performed on RNA samples taken from bone marrow-derived macrophages in knockout and control mice. 1. Control unstimulated 2. Knockout unstimulated 3. Control lipopolysaccharide (LPS) stimulated (4h) 4. Knockout LPS stimulated (4h). Three replicates for each condition. Thus, a total of 12 samples.

2009-12-21 | E-GEOD-15610 | biostudies-arrayexpress

Global hepatic gene expression data from PPARa liver-specific KO and PPARa liver wild-type male mice fed ad libitum

Project description:To identify genes whose expression is under the strict dependence of hepatocyte PPARa activity, we used a mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to their liver WT littermates (albumin-Cre-/- Pparaflox/flox or LWT) fed ad libitum or fasted for 24 hours.

2017-12-16 | GSE96559 | GEO

RNA-seq of IL-4 complex treated tissue resident macrophages vs. monocytic macrophages from LysM Cre+ (WT litermate control) and LysM Cre+ RICTOR KO (myeloid specifically RICTOR deleted) mice

Project description:RNA-seq was performed on sorted peritoneal tissue resident macrophages (CD11b+F4/80hiTIM4+) and monocytic macrophages (CD11b+F4/80loTIM4-) from IL-4c (recombinant IL-4 (5µg) and anti-IL-4 ab (12.5µg) IP injection on days 0 and 2 and sorted on day 4) treated 6-8wks old LySM Cre+ and LysM Cre+ RICTOR KO (C57BL/6 background) for expression profiling

2017-10-01 | GSE94965 | GEO

Myod1 and GR coordinate myofiber-specific transcriptional enhancers.

Project description:Skeletal muscle is a dynamic tissue the size of which can be remodeled through the concerted actions of various cues. Here, we investigated the skeletal muscle transcriptional program and identified key tissue-specific regulatory genetic elements. Our results show that Myod1 is bound to numerous skeletal muscle enhancers in collaboration with the glucocorticoid receptor (GR) to control gene expression. Remarkably, transcriptional activation controlled by these factors occurs through direct contacts with the promoter region of target genes, via the CpG-bound transcription factor Nrf1, and the formation of Ctcf-anchored chromatin loops, in a myofiber-specific manner. Moreover, we demonstrate that GR negatively controls muscle mass and strength in mice by down-regulating anabolic pathways. Taken together, our data establish Myod1, GR and Nrf1 as key players of muscle-specific enhancer-promoter communication that orchestrate myofiber size regulation.

| S-EPMC8096230 | biostudies-literature

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