Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ga13 functions as a cytoskeletal and mitochondrial regulator to restrain osteoclast function

ABSTRACT: We performed RNA-seq experiments, one with the WT control and Ga13ΔM/ΔM osteoclast precursors at baseline and after RANKL stimulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE116550 | GEO | 2019/03/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

G-protein G?13 functions as a cytoskeletal and mitochondrial regulator to restrain osteoclast function.

Project description: Not available

| S-EPMC6414604 | biostudies-literature

Ga13 functions as a cytoskeletal and mitochondrial regulator to restrain osteoclast function

Project description:Ga13 functions as a cytoskeletal and mitochondrial regulator to restrain osteoclast function

| PRJNA478996 | ENA

M-CSF priming of osteoclast precursors can cause osteoclastogenesis-insensitivity, which can be prevented and overcome on bone

Project description:Comparison of gene expression of the osteoclast precursor myeloid blast seeded on plastic and on bone, primed with M-CSF for 4 days and culture with M-CSF and RANKL for 1 day. Osteoclasts and macrophages share progenitors that must receive decisive lineage signals driving them into their respective differentiation routes. Macrophage colony stimulation factor M-CSF is a common factor; bone is likely the stimulus for osteoclast differentiation. To elucidate the effect of both, shared mouse bone marrow precursor myeloid blast was pre-cultured with M-CSF on plastic and on bone. M-CSF priming prior to stimulation with M-CSF and osteoclast differentiation factor RANKL resulted in a complete loss of osteoclastogenic potential without bone. This coincided with a steeply decreased expression of osteoclast genes TRACP and DC-STAMP, but an increased expression of the macrophage markers F4/80 and CD11b. Compellingly, M-CSF priming on bone accelerated the osteoclastogenic potential: M-CSF primed cells that had received only one day M-CSF and RANKL and were grown on bone already expressed an array of genes that are associated with osteoclast differentiation and these cells differentiated into osteoclasts within 2 days. This implies that adhesion to bone dictates the fate of osteoclast precursors. Common macrophage-osteoclast precursors may become insensitive to differentiate into osteoclasts and regain osteoclastogenesis when bound to bone or when in the vicinity of bone. Two conditions: Osteoclast precursors on plastic and on bone, n=4, dye swap

2014-06-02 | E-GEOD-58146 | biostudies-arrayexpress

Bone protection by inhibition of microRNA-182

Project description:We performed RNA-seq experiments, one with the WT control and Mir182ΔM/ΔM osteoclast precursors at baseline and after RANKL stimulation, the other with miR-182 gain of function approach using the control and Mir182mTg BMMs, to identify genes regulated by miR-182 in osteoclast precursors.

2018-09-04 | GSE108721 | GEO

M-CSF priming of osteoclast precursors can cause osteoclastogenesis-insensitivity, which can be prevented and overcome on bone

2014-06-02 | GSE58146 | GEO

miR-155 role in osteoclast differentiation

Project description:We used microarrays to understand the effect miR-155 has on osteoclast differentiation. RAW264.7 cells were grown in a-MEM supplemented with 10% FBS and antibiotics. mRNA extracted from wild-type RAW264.7 cells and miR-155 mis-expressing cells either before or after 72 hr of stimulation with 20ng/ml RANKL and M-CSF to induce osteoclast differentiation.

2010-07-30 | E-GEOD-16749 | biostudies-arrayexpress

Effect of RANKL on gene expression during osteoclast differentiation

Project description:To investigate effect of RANKL on osteoclast differentiation, bone marrow cells were cultured with M-CSF and RANKL.

2023-11-08 | GSE225883 | GEO

STING-dependent interferon signatures restrict osteoclast differentiation and bone loss in mice

Project description:Stimulator of Interferon Genes (STING) is a key mediator of type-I interferon (IFN-I) signaling in response to a variety of stimuli, but the contribution of STING to homeostatic processes is not fully characterized. Previous studies showed ligand activation of STING limits osteoclast differentiation in vitro through the induction of IFN and IFN-I Interferon Stimulated Genes (ISGs). In a disease model (SAVI) driven by the V154M gain-of-function mutation in STING, fewer osteoclasts form from SAVI precursors in response to RANKL in an IFN-I-dependent manner. Due to the described role of STING-mediated regulation of osteoclastogenesis in activation settings, we sought to determine whether basal STING signaling contributes to bone homeostasis, an unexplored area. Using whole-body and myeloid-specific deficiency, we show that STING signaling prevents trabecular bone loss in mice over time and that myeloid-restricted STING activity is sufficient for this effect. STING-deficient osteoclast precursors differentiate with greater efficiency than wildtypes. RNA sequencing of wildtype and STING-deficient osteoclast precursor cells and differentiating osteoclasts reveals novel clusters of ISGs including a previously undescribed ISG set expressed in RANKL naïve precursors (tonic expression) and downregulated during differentiation. We identify a 50 gene tonic ISG signature that is STING-dependent and shapes osteoclast differentiation. From this list, we identify Interferon Stimulated Gene 15 (ISG15) as a tonic STING-regulated ISG that limits osteoclast formation. Thus, STING is an important upstream regulator of tonic IFN-I signatures shaping the commitment to osteoclast fates, providing evidence for a nuanced and novel role for this pathway in bone homeostasis.

2023-04-19 | GSE226625 | GEO

Transcription profiling of mouse osteoclastogenesis

Project description:Expressions of mRNA in osteoclast precursors treated with RANKL and M-CSF for 0, 24, and 72 h. We used DNA microarray to analyze the changes in mRNA expressions during osteoclastogegesis. Experiment Overall Design: Osteoclast precursors were induced from mouse bone marrow cells by M-CSF for 3 days and treated with RANKL. WE extracted total RNA and analyzed by DNA microarray.

2009-09-05 | E-GEOD-17563 | biostudies-arrayexpress

Identification of a novel role for FoxO3 isoform2 in osteoclastic inhibition

Project description:We performed RNA-seq experiments, one with the WT control and Foxo3KO osteoclast precursors after RANKL stimulation to identify genes regulated by Foxo3 in osteoclast precursors.

2019-09-25 | GSE135479 | 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