Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE241811 | GEO | 2024/08/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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

| PRJNA1010145 | ENA

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

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

2013-10-14 | GSE44936 | GEO

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

Cpeb4-mediated Translational Regulatory Circuitry Controls Terminal Erythroid Differentiation

Project description:Erythropoiesis is essential to mammals and is regulated at multiple steps by both extracellular and intracellular factors. Many transcriptional regulatory networks in erythroid differentiation have been well characterized. However, our understanding of post-transcriptional regulatory circuitries in this developmental process is still limited. Using genomic approaches, we identified a sequence-specific RNA-binding protein, Cpeb4, which is dramatically induced in terminal erythroid differentiation (TED) by two erythroid important transcription factors, Gata1/Tal1. Cpeb4 belongs to the cytoplasmic polyadenylation element binding (CPEB) protein family that regulates translation of target mRNAs in early embryonic development, neuronal synapse, and cancer. Using primary mouse fetal liver erythroblasts, we found that Cpeb4 is required for terminal erythropoiesis by repressing the translation of a set of mRNAs highly expressed in progenitor cells. This translational repression occurs by the interaction with a general translational initiation factor, eIF3. Interestingly, Cpeb4 also binds its own mRNA and represses its translation, thus forming a negative regulatory circuitry to limit Cpeb4 protein level. This mechanism ensures that the translation repressor, Cpeb4, does not interfere with the translation of other mRNAs in differentiating erythroblasts. Our study characterized a translational regulatorycircuitry that controls TED and revealed that Cpeb4 is required for somatic cell differentiation. We used microarray to identify mRNAs associated with Cpeb4 in mouse fetal liver erythroblasts. Cpeb4 associated mRNAs were isolated from mouse fetal liver erythroblasts using anti-Cpeb4 antibody for immunoprecipitation followed by RNA extraction. Then Affymetrix microarrays were used to identify and quantify the mRNAs associated with Cpeb4.

2015-12-09 | E-GEOD-57004 | biostudies-arrayexpress

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

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

2015-11-11 | GSE74847 | GEO

Identification of Cpeb4 binders in cardiomyocyte

Project description:Mutations or decreased expression of RNA-binding proteins (mRBPs) can lead to cardiomyopathies in humans. Here we defined RBPs in healthy and diseased primary cardiomyocytes at a system-wide level by RNA Interactome Capture. This identified 67 novel cardiomyocyte specific RBPs including several contractile proteins. Furthermore, we identified Cytoplasmic polyadenylation element binding protein 4 (Cpeb4) as a dynamic mRBP in diseased cardiomyocytes, regulating cardiac growth both in vitro and in vivo. To study Cpeb4 in cardiomyocytes, we identified mRNAs bound to and regulated by Cpeb4. Cpeb4 regulates cardiac remodeling by differential expression of transcription factors. Among Cpeb4 target mRNAs, two Zinc finger transcription factors (Zeb1 and Zbtb20) were identified. We show that Cpeb4 regulates the translation of these mRNAs and that Cpeb4 depletion increases their expression. Thus, Cpeb4 emerges as critical regulator of cardiomyocyte function by differential binding of specific mRNAs in response to pathological growth stimulation.

2020-06-29 | GSE153409 | GEO

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

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

| PRJNA559903 | ENA

CPEB4 prevents hepatic steatosis [RIP-Seq]

Project description:The Cytoplasmic Polyadenylation Element Binding (CPEB)-family of RNA-binding proteins regulates pre-mRNA processing and translation of CPE-containing mRNAs in early embryonic development and synaptic activity. However, the specific functions of each CPEB in the adult organism are poorly understood. Here we show that CPEB4 is required to suppress high fat diet- and aging-induced endoplasmic reticulum (ER) stress, and its subsequent hepatic steatosis. Stress-activated expression of CPEB4 in the liver is controlled through a double layer of regulation. First, Cpeb4 is transcriptionally regulated by the circadian clock and then, its mRNA translation is regulated by the Unfolded Protein Response (UPR) through the upstream Open Reading Frames (uORFs) present in its 5’ UTR. Thus, CPEB4 is synthesized only upon ER-stress but the amplitude of the induction is circadian. In turn, CPEB4 activates a second wave of UPR-translation required to maintain ER and mitochondrial homeostasis. Our results suggest that combined transcriptional and translational regulation of CPEB4 generates a “circadian mediator”, which coordinates the hepatic UPR activity with periods of high ER protein-folding demand preventing non-alcoholic fatty liver disease (NAFLD).

2017-01-16 | GSE81876 | 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