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Acetylome dynamics during differentiation of 3T3-L1 adipocytes

ABSTRACT: 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.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Fibroblast

SUBMITTER: Alix Sarah Aldehoff

LAB HEAD: Kristin Schubert

PROVIDER: PXD045776 | Pride | 2024-06-13

REPOSITORIES: Pride

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			Action	DRS
	125_3T3L1_d0_1_IP.raw	Raw
	125_3T3L1_d0_2_IP.raw	Raw
	125_3T3L1_d0_3_IP.raw	Raw
	125_3T3L1_d10_1_IP.raw	Raw
	125_3T3L1_d10_2_IP.raw	Raw

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Publications

Unveiling the dynamics of acetylation and phosphorylation in SGBS and 3T3-L1 adipogenesis.

Aldehoff Alix Sarah AS Karkossa Isabel I Goerdeler Cornelius C Krieg Laura L Schor Jana J Engelmann Beatrice B Wabitsch Martin M Landgraf Kathrin K Hackermüller Jörg J Körner Antje A Rolle-Kampczyk Ulrike U Schubert Kristin K von Bergen Martin M

iScience 20240410 6

Obesity, characterized by enlarged and dysfunctional adipose tissue, is among today's most pressing global public health challenges with continuously increasing prevalence. Despite the importance of post-translational protein modifications (PTMs) in cellular signaling, knowledge of their impact on adipogenesis remains limited. Here, we studied the temporal dynamics of transcriptome, proteome, central carbon metabolites, and the acetyl- and phosphoproteome during adipogenesis using LC-MS/MS combi ...[more]

PMID: 38840842

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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

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

Proteome dynamics during differentiation of SGBS adipocytes

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

2024-06-13 | PXD045767 | Pride

Acetylome dynamics during differentiation of SGBS adipocytes

Project description:Here, we identified temporal dynamics of the acetylome during adipocyte differentiation in human SGBS 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 | PXD045768 | Pride

Phosphoproteome dynamics during differentiation of SGBS adipocytes

Project description:Here, we identified temporal dynamics of the phosphoproteome during adipocyte differentiation in the human SGBS 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 | PXD045770 | Pride

Comparative proteomic profiling of 3T3-L1 adipocyte differentiation using SILAC quantification

Project description:Comparative proteomic profiling of 3T3-L1 adipocyte differentiation using SILAC quantification

2020-10-26 | PXD019716 | Pride

Preadipocytes of T2DM patients display an intrinsic gene expression profile of decreased differentiation capacity

Project description:Insulin resistance and Type 2 Diabetes Mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. To identify the underlying molecular processes in preadipocytes of T2DM patients that are a characteristic of the development of T2DM, preadipocyte cell cultures were prepared from subcutaneous fat biopsies of T2DM patients and compared with age- and BMI matched control subjects. Gene expression profiling showed changed expression of transcription factors involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were down-regulated, and inflammation/apoptosis was up-regulated in T2DM preadipocytes. The down-regulation of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage. 7 T2DM preadipocyte samples and 9 age- and BMI-matched control samples were hybridized using 70-mer oligonucleotide microarrays. Samples were labeled with either Cy3 or Cy5. A total of 20 arrays were used including dye swop. Per array, a T2DM sample was hybridized with a control sample of the same gender and matched based on age and BMI. To ensure hybridization of two samples with the same gender, three T2DM (5064, 5128, 5395) and one control sample (5616) were used twice and listed as technical replicates.

2010-05-16 | E-GEOD-15790 | biostudies-arrayexpress

Genome-wide RING1B binding in Fbxl10 overexpressing 3T3-L1 cells at day 2 of differentiation

Project description:We analyzed RING1B binding regions in 3T3-L1 cell lines transduced with the retroviral vector for V5-tagged Fbxl10 or its dF-box mutant. RING1B ChIP-seq in empty, Fbxl10-1, and dF-box mutant vector transduced 3T3-L1 preadipocytes, in duplicate, and V5-Fbxl10 ChIP-seq in Fbxl10 overexpressing 3T3-L1 cells

2015-03-04 | E-GEOD-64312 | biostudies-arrayexpress

Effects of bisphenol A on gene expression in adipocytes from lean children: association to metabolic disorders

Project description:Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1beta, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ER? and ERR?, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders. Three prototypic situations were analyzed (5 replication each): untreated cells (C), 10 nM BPA treated cells (BPA), 1 nM 17-beta Estradiol treated cells (ES).

2015-07-09 | E-GEOD-58516 | 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

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