Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of genetic deletion of Slc37a2 on gene expression of mouse bone marrow macrophage-derived osteoclasts

ABSTRACT: To investigate the mechanism(s) by which Slc37a2 regulates osteoclasts, we performed gene expression profiling analysis using data obtained from RNA-seq of osteoclasts derived from wild-type and Slc37a2-knockout mice (C57BL/6N-SLC37A2 tm2a(KOMP)Wtsi)

ORGANISM(S): Mus musculus

PROVIDER: GSE219216 | GEO | 2023/01/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of genetic deletion of Slc37a2 on gene expression of mouse bone marrow macrophage-derived osteoclasts

Project description:Effect of genetic deletion of Slc37a2 on gene expression of mouse bone marrow macrophage-derived osteoclasts

| PRJNA907740 | ENA

RNA sequencing data of osteoclasts subtypes in bone

Project description:Flow cytometrically sorted bone marrow osteoclasts from tibia of 2-weeks-old C57Bl/6 mice were used for generating this dataset. VAO and BAO represent RANK+ 2 nucleated and RANK+ 4 (and >4) nucleated osteoclasts from bone marrow respectively.

2019-02-07 | E-MTAB-6857 | biostudies-arrayexpress

Microarray analysis of Macrophages and Osteoclasts

Project description:Comparaison of genes expression between bone marrow derived macrophages and osteoclasts in C57BL/6J mice

2016-09-17 | GSE86998 | GEO

Expression array of mouse bone marrow-derived macrophages and osteoclasts

Project description:In response to the cytokines, macrophage colony-stimulating factor and receptor activator of NF-kB ligand, monocyte precursors differentiate into bone marrow-derived macrophages (BMDMs) that ultimately fuse to form multi-nucleated osteoclasts, following a tightly controlled genetic program where specific sets of genes are differentially expressed. We used microarrays to examine the gene expression profile underlying mouse osteoclast differentiation.

2019-10-03 | GSE138324 | GEO

Effect of Dnmt3a deletion on the global DNA methylation status of osteoclasts

Project description:Epigenetic regulation is a fundamental mechanism mediating various cellular processes. However, epigenetic mechanisms in osteoclastogenesis remain to be elucidated. We performed MBD-seq analysis to investigate DNA methylation in osteoclasts derived from wild-type and osteoclast-specific Dnmt3a knockout mice. Examination of DNA methylation in 2 cell types.

2015-02-23 | E-GEOD-59388 | biostudies-arrayexpress

Real-time microRNA quantitative PCR array of mouse bone marrow-derived osteoclasts

Project description:Mouse bone marrow-derived OSCAR+CTR+ osteoclasts were harvested from mice with anterior cruciate ligament transection (ACLT) or sham operation by magnetic-activated cell sorting. The cells were lysated by Trizol reagent for total RNA extraction. The miRNA were profiled using the QuantiMir RT Kit (System Biosciences)

2021-03-01 | GSE166776 | GEO

Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts

Project description:The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the non-selective S1P receptor agonist FTY720 causes increased bone formation in wildtype, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo, and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts. Osteoclasts of wildtype and Calcr-/- C57Bl/6 mice were treated with Calcitonin and compared to the non-treated osteoclasts of wildtype or Calcr-/- mice, respectively.

2014-10-19 | E-GEOD-60761 | biostudies-arrayexpress

Effect of Dnmt3a deletion on the global DNA methylation status of osteoclasts

2015-02-23 | GSE59388 | GEO

Expression data of bone marrow-derived osteoclasts expressing wild-type or mutant PSS1

Project description:Phosphatidylserine (PS) is an acidic phospholipid that is involved in various cellular events. Heterologous dominant mutations have been identified in the gene encoding PS synthase 1 (PSS1) in patients of a congenital disease called Lenz-Majewski syndrome (LMS). LMS patients show various symptoms, including craniofacial/distal-limb bone dysplasia and progressive hyperostosis. The LMS-causing gain-of-function mutants of PSS1 (PSS1-LMS) have been shown to synthesize PS without control, but why the uncontrolled synthesis would lead to LMS is unknown. We investigated the effect of PSS1-LMS(Q353R) on osteoclasts to elucidate the causative mechanism of LMS and found that PSS1-LMS inhibited the formation, multinucleation, and activity of osteoclasts. We used microarrays to comprehensively examine the effects of PSS1-LMS on osteoclast gene expression.

2022-07-04 | GSE207351 | GEO

Real-time microRNA quantitative PCR array of mouse bone marrow-derived osteoclasts II

Project description:Mouse bone marrow-derived OSCAR+CTR+ osteoclasts were harvested from osteoclast-miRNA knockdown (OCmiR-KD) mice or osteoclast-miRNA intact (OCmiR-Intact) mice at 2w after anterior cruciate ligament transection (ACLT) by magnetic-activated cell sorting. The cells were lysated by Trizol reagent for total RNA extraction. The miRNA were profiled using the QuantiMir RT Kit (System Biosciences)

2021-03-01 | GSE167161 | 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