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Expression data from 48 h incubation of RAW264.7 cells with 50 ng/ml RANK Ligand

ABSTRACT: A variety of genes are responsible for regulating osteoclastogenesis in response to RANK Ligand. Microarray analysis was used to identify genes sensitive to RANKL-induced osteoclastogenesis in RAW264.7 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE74847 | GEO | 2015/11/11

SECONDARY ACCESSION(S): PRJNA301670

REPOSITORIES: GEO

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Expression data from 48 h incubation of RAW264.7 cells with 50 ng/ml RANK Ligand

Project description:A variety of genes are responsible for regulating osteoclastogenesis in response to RANK Ligand. Microarray analysis was used to identify genes sensitive to RANKL-induced osteoclastogenesis in RAW264.7 cells. RAW264.7 cells were incubated with 50 ng/mL RANKL or vehicle control (3 replicates each). After 48 h, total RNA were harvested by an RNeasy Plus Mini Kit (QIAGEN).

2015-11-11 | E-GEOD-74847 | biostudies-arrayexpress

Uridine Modulates Gene Expression Programs During RANKL-Induced Osteoclastogenesis in RAW264.7 Cells

Project description:Uridine has been implicated in the regulation of metabolic and redox processes, yet its transcriptional effects during osteoclast differentiation remain unclear. This dataset profiles global gene expression in RAW264.7 cells under three conditions: untreated control, RANKL-induced osteoclastogenesis, and RANKL combined with uridine treatment. The results reveal uridine-responsive transcriptional changes involving osteoclast differentiation, oxidative stress regulation, and PI3K/Akt–FoxO–related pathways, providing mechanistic insight into uridine-mediated modulation of osteoclastogenesis.

2026-04-09 | GSE311708 | GEO

Folliculin deficiency effect on Raw264.7 cells

Project description:Osteoclast differentiation is a dynamic differentiation process, which is accompanied by dramatic changes in metabolic status as well as in gene expression. Recent findings have revealed an essential connection between metabolic reprogramming and dynamic gene expression changes during osteoclast differentiation. However, the upstream regulatory mechanisms that drive these metabolic changes in osteoclastogenesis remain to be elucidated. We demonstrate that induced deletion of a tumor suppressor gene, Folliculin (Flcn), in mouse osteoclast precursors causes severe osteoporosis in 3 weeks through excess osteoclastogenesis. Flcn deficient osteoclast precursors (Raw264.7 cells) reveal cell autonomous accelerated osteoclastogenesis. For the purpose of elucidating the molecular mechanism of accelerated osteoclastogenesis in Flcn deficient Raw264.7 cells, we performed DNA microarray analysis.

2018-07-30 | GSE115084 | GEO

RAW264.7 cells: RANKL vs Bone Metastasis Tumor Cell Condidtioned Media

Project description:Transcriptional profiling of differential miRNA expression in mouse RAW264.7 preosteoclast cells comparing control untreated cells with RAW264.7 cells treated for 6 days. Treatment conditiones tested included 50ng/mL RANKL or indicated bone metastasis tumor cell conditioned media from 4T1, 4T1.2, TSU-PR1, and TSU-PR1-B2 cell lines. Two-condition experiment, Control cells vs. treated cells.

2013-10-14 | E-GEOD-44936 | biostudies-arrayexpress

Expression of RAW264.7 cells stimulated with RANKL and treated with supernatant from Lactobacillus reuteri

Project description:Analysis of gene expression in RAW264.7 cells stimulated for osteoclastogenesis and then treated with cell culture supernatant from Lactobacillus reuteri. Results will offer insight into targeted mechanisms suppressing osteoclastogenesis

2019-08-13 | GSE135755 | GEO

The RANK IVVY Motif-regulated Genes in Osteoclastogenesis

Project description:By carrying out a systematic structure/function study of the RANK cytoplasmic domain, we previously identified a specific 4-a.a. RANK motif (IVVY535-538) which plays a critical role in osteoclastogenesis by mediating commitment of macrophages to the osteoclast lineage. We have recently validated the role of this IVVY motif in osteoclastogenesis in vivo by generating knockin (KI) mice bearing inactivating mutations in the RANK IVVY motif. This microarray experiment was performed to determine whether the IVVY motif is involved in regulating gene expression in osteoclastogenesis. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Bone marrow macrophages isolated from wild-type (WT) or knockin (KI) mice were plated in 60-mm tissue culture dishes and treated with M-CSF (44ng/ml) and RANKL (100ng/ml) for 24 hours. Each genotype has three triplicates. Total RNA was isolated for microarray analysis using mouse chips (type 430.2.0) at the Microarray Shared Facility at the University of Alabama at Birmingham.

2011-07-05 | E-GEOD-30160 | biostudies-arrayexpress

Proteomic Study of Different Culture Medium Serum Volume Fractions on RANKL-dependent Differentiating into Osteoclasts of RAW264.7 Cells

Project description:Supplemental data for the article: Proteomic Study of Different Culture Medium Serum Volume Fractions on RANKL-dependent Differentiating into Osteoclasts of RAW264.7 Cells

2015-06-02 | PXD001935 | Pride

RAW264.7 cells: RANKL vs Bone Metastasis Tumor Cell Condidtioned Media

2013-10-14 | GSE44936 | GEO

RNA-seq in Cpeb4 knockdown RAW264.7 cells three days after RANKL stimulation

Project description:To identify the changes of mRNA expressions by Cpeb4 knockdown in RAW264.7 cells treted with RANKL for three days, we performed RNA-sequencing.

2024-08-31 | GSE241811 | GEO

Transcriptomic Profiling of RAW264.7 Cells During RANKL-Induced Osteoclast Differentiation

Project description:Osteoclast differentiation is primarily driven by RANKL stimulation, yet the transcriptional remodeling associated with this process remains incompletely characterized. This dataset profiles global gene expression changes in RAW264.7 macrophages under two conditions: untreated control and RANKL-induced osteoclast differentiation. The transcriptomic comparison reveals key pathways associated with osteoclast formation, including osteoclast-related gene activation, metabolic remodeling, and oxidative stress–related signaling. These data serve as the baseline reference for subsequent uridine-intervention analyses.

2026-04-09 | GSE311709 | GEO

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