Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

41 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAi knockdown of Tip60 and Usp7 in mouse 3T3-L1 adipocytes

ABSTRACT: Knockdown of Tip60 or Usp7 in differentiated 3T3-L1 adipocytes

ORGANISM(S): Mus musculus

SUBMITTER: M Groot Koerkamp

PROVIDER: E-TABM-1145 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Early adipogenesis is regulated through USP7-mediated deubiquitination of the histone acetyltransferase TIP60.

Gao Yuan Y Koppen Arjen A Rakhshandehroo Maryam M Tasdelen Ismayil I van de Graaf Stan F SF van Loosdregt Jorg J van Beekum Olivier O Hamers Nicole N van Leenen Dik D Berkers Celia R CR Berger Ruud R Holstege Frank C P FC Coffer Paul J PJ Brenkman Arjan B AB Ovaa Huib H Kalkhoven Eric E

Nature communications 20130101

Transcriptional coregulators, including the acetyltransferase Tip60, have a key role in complex cellular processes such as differentiation. Whereas post-translational modifications have emerged as an important mechanism to regulate transcriptional coregulator activity, the identification of the corresponding demodifying enzymes has remained elusive. Here we show that the expression of the Tip60 protein, which is essential for adipocyte differentiation, is regulated through polyubiquitination on ...[more]

PMID: 24141283

Similar Datasets

Proteome dynamics during differentiation of 3T3-L1 adipocytes

Project description:Here, we identified temporal dynamics in the proteome during adipocyte differentiation of the murine 3T3-L1 cells, applying untargeted proteomics. Samples were taken at initiation of differentiation, at an intermediate and terminal time point.

2024-06-13 | PXD045772 | Pride

Acetylome dynamics during differentiation of 3T3-L1 adipocytes

Project description:Here, we identified temporal dynamics of the acetylome during adipocyte differentiation in the murine 3T3-L1 cells, applying untargeted proteomics in combination with immunoaffinity purification of acetylated peptides. Samples were taken at initiation of differentiation, at an intermediate and terminal time point.

2024-06-13 | PXD045776 | Pride

Phosphoproteome dynamics during differentiation of 3T3-L1 adipocytes

Project description:Here, we identified temporal dynamics of the phosphoproteome during adipocyte differentiation in the murine 3T3-L1 cells, applying untargeted proteomics in combination with enrichment strategies for phosphorylated peptides. Samples were taken at initiation of differentiation, at an intermediate and terminal time point.

2024-06-13 | PXD045778 | Pride

Characterising the transcriptional profile of murine 3T3-L1 adipocytes with altered expression of IRF3.

Project description:The chronic inflammatory state that accompanies obesity is a major contributor to insulin resistance and other metabolic dysfunction features. Despite recent advances in our understanding of the cellular and secreted factors that promote the inflammatory milieu of obesity, we have much less insight into the transcriptional pathways that drive these processes. While most attention has focused on the canonical inflammatory transcription factor NF-KB, other potentially important factors exist, including members of the interferon regultory factor (IRF) family. Here we show that IRF3 expression is upregulated in the adipocytes of obese mice and humans. TLR3/TLR4 activation induces insulin resistance in adipocytes, which can be prevented by IRF3 knockdown. Furthermore, Irf3KO mice display improved insulin sensitivity, associated with reduced intra-adipose and systemic inflammation in the high-fat fed state, enhanced browning of subcutaneous fat, and increased adipose expression of Glut4. Taken together, our data indicates that IRF3 is a major transcriptional regulator of adipose inflammation to maintain systemic glucose and energy homeostasis. Transcriptional profiling of murine 3T3-L1 adipocytes with altered expression of IRF3. Overexpression or knockdown of IRF3 was achieved by lentivirus transduction for 6 days. 3T3-L1 adipocytes with IRF3 knockdown were further treated in the absence or presence of LPS for 6 days. Samples consist of triplicate replica with appropriate control.

2016-05-31 | E-GEOD-81193 | biostudies-arrayexpress

Transcriptional co-factor TBLR1 controls lipid mobilization in white adipose tissue

Project description:Lipid mobilization (lipolysis) in white adipose tissue (WAT) critically controls lipid turnover and adiposity in humans. While the acute regulation of lipolysis has been studied in detail, the transcriptional determinants of WAT lipolytic activity remain still largely unexplored. Here we show that the genetic inactivation of transcriptional co-factor transducin beta-like-related (TBLR) 1 blunts the lipolytic response of white adipocytes through the impairment of cAMP-dependent signal transduction. Indeed, mice lacking TBLR1 in adipocytes are defective in fasting-induced lipid mobilization and when placed on a high fat diet show aggravated adiposity, glucose intolerance and insulin resistance. TBLR1 levels are found to increase under lipolytic conditions in WAT of both human patients and mice, correlating with serum free fatty acids (FFA). As a critical regulator of WAT cAMP signaling and lipid mobilization, proper activity of TBLR1 in adipocytes may thus represent a critical molecular checkpoint for the prevention of metabolic dysfunction in subjects with obesity-related disorders. We used microarrays to identify global gene expression in 3T3-L1 adipocytes lacking TBLR1 and compared gene expression to control shRNA treated cells in both basal and isoproterenol stimulated states. We analyzed 12 RNA samples extracted from 3T3-L1 adipocytes that were treated with either control or TBLR1 specific shRNAs and with or without 10 ÂµM isoproterenol for 3 hrs. Three replicates of each condition.

2013-04-01 | E-GEOD-43658 | biostudies-arrayexpress

Molecular architecture of transcription factor hotspots in early adipogenesis

Project description:Here, we have used digital genomic footprinting to precisely define protein localization for several adipogenic transcription factors at a genome-wide level. In combination with ChIP-seq data, these analyses reveal novel molecular insight into the organization of transcription factors at hotpot regions, which provides a new framework for understanding transcription factor cooperativity on chromatin. Digital genomic footprinting and gene expression in 3T3-L1 pre-adipocytes by high throughput sequencing.

2014-05-08 | E-GEOD-57415 | biostudies-arrayexpress

Gene expression analysis of cultured adipocytes treated with different types of asbestos fibers

Project description:We hypothesized that adipocytes can be triggered by asbestos fibers to produce an inflammatory response. Microarray-based gene expression analysis was thus carried out to identify potential inflammation-related candidates with altered expression in adipocytes following asbestos exposure. We found changes in the expression of some inflammation-related genes in adipocytes treated with the different types of asbestos fibers Cultured adipocytes were treated with 3 different types of asbestos fibers: chrysotile, crocidolite and amosite fibers at 10 mg/cm2 for 72 hours. Physiological saline was used as a control. Microarray was performed with duplicate for each sample.

2013-09-03 | E-GEOD-42330 | biostudies-arrayexpress

RNAi profiling of mouse 3T3-L1 adipocytes knocked down for PPAR gamma returned the expression of most adipocyte genes towards preadipocyte levels

Project description:The nuclear receptor PPAR gamma is required for adipocyte differentiation, but its role in mature adipocytes is less clear. Here we report that knockdown of PPAR gamma expression in 3T3-L1 adipocytes returned the expression of most adipocyte genes towards preadipocyte levels. Consistently, down regulated but not up regulated genes showed strong enrichment of PPAR gamma binding. Surprisingly, not all adipocyte genes were reversed and the adipocyte morphology was maintained for an extended period after PPAR gamma depletion. To explain this, we focused on transcriptional regulators whose adipogenic regulation was not reversed upon PPAR gamma depletion. We identified GATA2, a transcription factor whose down-regulation early in adipogenesis is required for preadipocyte differentiation, remaining low after PPAR gamma knockdown. Forced expression of GATA2 in mature adipocytes complemented PPAR gamma depletion and impaired adipocyte functionality with a more preadipocyte- like gene expression profile. Ectopic expression of GATA2 in adipose tissue in vivo had similar effect on adipogenic gene expression. These results suggest that PPAR gamma-independent down regulation of GATA2 prevents reversion of mature adipocytes after PPAR gamma depletion. Experiment Overall Design: This dataset consists of three sample groups: preadipocytes, control siRNA treated adipocytes, and PPAR gamma siRNA treated adipocytes. Each sample group consists of three replicates samples. Each sample was hybridized to a separate array for a total of nine arrays. Experiment Overall Design: Technical replicates: Pread 1, Pread 2, Pread 3 Experiment Overall Design: Technical replicates: Cont siRNA 1, Cont siRNA 2, Cont siRNA 3 Experiment Overall Design: Technical replicates: PPAR gamma siRNA 1, PPAR gamma siRNA 2, PPAR gamma siRNA 3

2009-01-29 | E-GEOD-14004 | biostudies-arrayexpress

Time-resolved adipocyte FGF21 phosphoproteome

Project description:To elucidate the signalling network responsible for mediating the effects of FGF21, we quantified the dynamic phosphoproteome of adipocytes following acute exposure to this hormone. A major FGF21-regulated signalling node was mTORC1/S6K. In contrast to insulin, we find that FGF21 activates mTORC1 via MAPK signalling rather than through the canonical PI3K/AKT pathway. This study provides a systems view of FGF21 signalling and reveals a new role for mTORC1 in maintaining nutrient homeostasis.

2016-08-15 | PXD003631 | Pride

Genome-wide maps of TCF7L1 binding during early adipogenesis

Project description:Here we show through genome-wide binding studies that transcription factor 7-like 1 (TCF7L1) represses structure-related genes during adipogenesis. Intriguingly, TCF7L1 is induced in a cell contact-dependent manner by confluency in preadipocytes and is required for adipocyte differentiation by repressing transcription of cell structure genes. TCF7L1 is also sufficient to bestow adipogenic potential upon non-adipogenic cells. These results implicate TCF7L1 as a novel adipogenic competency factor that uniquely determines adipogenic fate through cell structure organization required for adipocyte gene activation. Examination of TCF7L1 binding in preadipocytes treated for 24 hours with adipogenic stimuli.

2011-09-02 | E-GEOD-31867 | 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