Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

14-3-3ζ controls adipocyte progenitor cell cycle and differentiation via Gli3-dependent p27Kip expression

ABSTRACT: 14-3-3 proteins facilitate cytoplasmic-nuclear shuttling of transcription factors.Adipocyte differentiation requires the function of critical transcription factors to drive the development of a mature adipocyte. The aim of the study was to investigate if 14-3-3ζ is required for the adipogenic transcriptional program.

ORGANISM(S): Mus musculus

PROVIDER: GSE60745 | GEO | 2015/07/23

SECONDARY ACCESSION(S): PRJNA259415

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

14-3-3ζ controls adipocyte progenitor cell cycle and differentiation via Gli3-dependent p27Kip expression

Project description:14-3-3 proteins facilitate cytoplasmic-nuclear shuttling of transcription factors.Adipocyte differentiation requires the function of critical transcription factors to drive the development of a mature adipocyte. The aim of the study was to investigate if 14-3-3ζ is required for the adipogenic transcriptional program. Examination of the transcriptome in siCon- and si14-3-3ζ-transfected 3T3-L1 cells undergoing differentiation at t=0, 24, and 48 hours.

2015-07-23 | E-GEOD-60745 | biostudies-arrayexpress

Role of 14-3-3ζ in the adipogenesis program and the differentiation of healthy adipose tissue

Project description:Obesity is an independent risk factor for diabetes and cardiovascular disease. Before effective anti-obesity therapies can be developed, understanding of what governs the production of healthy versus unhealthy fat tissue is required, as not all types confer equal risk. Adipogenesis requires the precise transduction of signals and coordination of transcription factor cascades. Molecular adaptor proteins of the 14-3-3 family are known to coordinate signaling events from multiple cues, but whether specific isoforms have unique, non-redundant roles in adipogenesis remains unclear. RNAi screening revealed 14-3-3ζ as the critical isoform for in vitro adipocyte differentiation. This study aims to understand the role of 14-3-3ζ in adipogenesis program and the differentiation in health adipose tissue.

2022-03-01 | PXD001215 | Pride

14-3-3ζ overexpression-induced gene signature in MCF-10A cells

2013-11-05 | GSE52032 | GEO

Thermogenic differentiation of adipocyte progenitors

Project description:FACS-purified adipocyte progenitors from murine subcutaneous adipose tissue were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with cPGI2). Time course expression profiling was performed during differentiation. In addition, some cultures of differentiated adipocytes were stimulated with norepinephrine for 3 hours. In parallel, differentiation and norepinephrine stimulation of progenitors from interscapular brown fat was performed and profiled.

2015-08-20 | E-MTAB-3693 | biostudies-arrayexpress

14-3-3ζ overexpression-induced gene signature in MCF-10A cells

Project description:To study the function of 14-3-3ζ, we established MCF-10A human mammary epithelial cells transduced with 14-3-3ζ (10A.ζ) and vector (10A.Vec) We performed gene expression profiling on 10A.ζ cells and 10A.Vec cells, and normalized to profiling of MCF-10A parental cells Total mRNA were extracted from 10A.Parental cells, 10A.Vec cells, 10A.ζ cells which were cultured in 3D culture model for 16 days, and subjected to Affymetrix microarray analysis

2013-11-05 | E-GEOD-52032 | biostudies-arrayexpress

Jak kinase inhibition in mouse adipocyte progenitors

Project description:FACS-purified adipocyte progenitors from murine subcutaneous adipose tissue were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with cPGI2) in the presence of absence of Jak inhibitor I (JakiI), which targets all Jak family members. The cells were harvested 24 hours after induction of differentiation.

2018-04-24 | E-MTAB-6029 | biostudies-arrayexpress

14-3-3ζ promotes TGF-β-induced bone metastasis program in 231 cells

Project description:To explore the regulatory role of 14-3-3ζ in TGF-β induced bone metastasis program in 231 cells, we generated MDA-MB-231 human breast cancer cell sublines with 14-3-3ζ shRNA knockdown (231.ZKD-4 and 231.ZKD-5) and scrambled shRNA (231.Scr) We performed cDNA microarray analysis on these cells treated with vehicle or TGF-β (5ng/ml, 2 hours) respectively in vitro

2013-11-05 | GSE52066 | GEO

Regulation of adipocyte differentiation by IRF3

Project description:The hypothesis tested is that IRF3 regulates adipogenesis and adipocyte function. Global gene expression of IRF3 wildtype (WT) and knockout (KO) adipocytes at different days during differentiation was compared. The results provide evidence on how IRF3 controls PPARg -regulated adipogenic program thereby regulate adipocyte differentiation.

2021-04-22 | GSE172491 | GEO

Transcriptional response to Rosiglitazone in adipocyte progenitors isolated from WT and Cited4-KO scWAT

Project description:Lin-Sca-1+ adipocyte progenitors from subcutaneous adipose tissue of wild-type and Cited4-/- female mice were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with Rosi). Cells were harvested 48 post-induction of differentiation.

2018-07-04 | E-MTAB-6796 | biostudies-arrayexpress

SRSF10 regulates alternative splicing and is required for adipocyte differentiation.

Project description:During adipocyte differentiation, significant alternative splicing changes occur in association with the adipogenic process. However, little is known about roles played by splicing factors in this process. We observed that mice deficient for the splicing factor SRSF10 exhibit severely impaired development of subcutaneous white adipose tissue as a result of defects in adipogenic differentiation. To identify splicing events responsible for this, RNA-seq analysis was performed using embryonic fibroblast cells. Several SRSF10-affected splicing events that are implicated in adipogenesis have been identified. Skipping of lipin1 exon 7 is controlled by SRSF10-regulated cis-element located in the constitutive exon 8. The activity of this element depends on the binding of SRSF10 and correlates with the relative abundance of lipin1a mRNA. A series of experiments demonstrated that SRSF10 controls the production of lipin1a and thus promotes adipocyte differentiation. Indeed, lipin1a expression could rescue SRSF10-mediated adipogenic defects. Taken together, our results identify SRSF10 as an essential regulator for adipocyte differentiation and also provide new insights into splicing control by SRSF10 in lipin1 pre-mRNA splicing. RNA-seq for wide type (WT) and SRSF10-deficient (KO) mouse MEF cells

2014-05-12 | E-GEOD-54226 | biostudies-arrayexpress

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