Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-CBIL-26
PROVIDER: PRJNA92167 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Insulin and IGF-1 promote adipocyte differentiation via complex and overlapping signalling networks. Here we used microarray analysis of brown preadipocytes derived from wild-type and insulin receptor substrate (IRS) knockout (KO) animals, which exhibited progressively impaired differentiation, to define the set of genes that predict adipogenic potential in these cells. 374 genes/ESTs were identified whose expression in preadipocytes correlated with their ultimate ability to differentiate. Many of these genes were related to early adipogenic events, including genes involved in extracellular matrix, cytoskeletal organization, growth arrest, post-mitotic clonal expansion, and inhibitors of adipogenesis, including preadipocyte factor-1 and multiple members of the Wnt-signalling pathway. Reconstitution of IRS-1 KO cells with IRS-1 reversed these changes and restored the ability to differentiate. Several of these genes showed concordant changes in brown adipose tissue in vivo. Necdin was markedly increased in IRS-1 KO cells that could not differentiate, and knockdown of necdin restored brown adipogenesis with down-regulation of Pref-1 and Wnt10a expression. We demonstrated a necdin-E2F4 interaction repressing PPARg transcription. IRS proteins regulated necdin via a CREB dependent pathway, defining a signalling network involved in brown preadipocyte determination.
2007-08-04 | E-GEOD-2556 | biostudies-arrayexpress
Project description:Insulin and IGF-1 promote adipocyte differentiation via complex and overlapping signalling networks. Here we used microarray analysis of brown preadipocytes derived from wild-type and insulin receptor substrate (IRS) knockout (KO) animals, which exhibited progressively impaired differentiation, to define the set of genes that predict adipogenic potential in these cells. 374 genes/ESTs were identified whose expression in preadipocytes correlated with their ultimate ability to differentiate. Many of these genes were related to early adipogenic events, including genes involved in extracellular matrix, cytoskeletal organization, growth arrest, post-mitotic clonal expansion, and inhibitors of adipogenesis, including preadipocyte factor-1 and multiple members of the Wnt-signalling pathway. Reconstitution of IRS-1 KO cells with IRS-1 reversed these changes and restored the ability to differentiate. Several of these genes showed concordant changes in brown adipose tissue in vivo. Necdin was markedly increased in IRS-1 KO cells that could not differentiate, and knockdown of necdin restored brown adipogenesis with down-regulation of Pref-1 and Wnt10a expression. We demonstrated a necdin-E2F4 interaction repressing PPARg transcription. IRS proteins regulated necdin via a CREB dependent pathway, defining a signalling network involved in brown preadipocyte determination. Keywords = brown fat Keywords = preadipocyte Keywords = adipogenesis Keywords = mouse Keywords: parallel sample
2005-06-01 | GSE2556 | GEO
Project description:Brown adipose tissue (BAT) has in recent times been rediscovered in adult humans, and together with work from preclinical models, shown to have the potential of providing a variety of positive metabolic benefits. These include improved insulin sensitivity and reduced susceptibility to obesity and its various co-morbidities. As such, its continued study could offer insights to therapeutically modulate this tissue to improve metabolic health. It has been reported that adipose-specific deletion of the gene for protein kinase D1 (Prkd1) enhances mitochondrial respiration and improves whole-body glucose homeostasis. We sought to determine whether these effects were mediated specifically through brown adipocytes using a Prkd1 brown adipose tissue (BAT) Ucp1-Cre-specific knockout mouse model, Prkd1BKO. We unexpectedly observed that upon both cold exposure and beta-3-AR agonist administration, Prkd1 loss in BAT did not alter canonical thermogenic gene expression or adipocyte morphology. We took an unbiased approach to assess whether other signaling pathways were altered. RNAs from cold-exposed control and Prkd1BKO were subjected to RNA-Seq analysis. These studies revealed that myogenic gene expression is altered in Prkd1BKO BAT after both acute (8 hr) and extended (4 day) cold exposure. Given that brown adipocytes and skeletal myocytes share a common precursor cell lineage expressing myogenic factor 5 (Myf5), these data suggest that loss of Prkd1 in BAT may alter the biology of preadipocytes in this depot. The data presented herein clarify the role of Prkd1 in BAT thermogenesis and present new avenues for the further study of Prkd1 function in BAT.
2023-09-01 | E-MTAB-12170 | biostudies-arrayexpress
Project description:Expression data from mouse primary brown preadipocytes
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Project description:The experiment was designed to determine the gene expression changes cultured brown adipocytes in response to the inflammatory stimulus of LPS treatment. Both wild type and TLR4 knockout cells were applied to enable assessment of the contribution of TLR4 to the response.
2024-03-21 | E-MTAB-12834 | biostudies-arrayexpress
Project description:Brown preadipocytes were grown to confluence and synchronized by overnight serum starvation. Four independent RNA samples were analyzed from each IRS KO cell line and three independent clones of WT cells were separately analyzed as controls. Splitting of the samples resulted in a total 28 microarrays. 15 mg of adjusted cRNA were hybridized to Affymetrix U74A-v2 arrays.
2007-04-06 | E-CBIL-26 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description: Not available
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