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Mus musculus
8 Downloadable Samples
Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPAR ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPAR ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPAR agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes.
Publication Title
PPARγ agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
KLF7 null mice show profound axonal growth defects in the olfactory epithelium. The goal of this study was the identification of potential KLF7 target genes in olfactory sensory neurons.
Publication Title
Identification of genes regulated by transcription factor KLF7 in differentiating olfactory sensory neurons.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors.
Publication Title
Initiation of myoblast to brown fat switch by a PRDM16-C/EBP-beta transcriptional complex.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The aim of this study was to identify genes expressed selectively in brown adipose tissue as compared to white adipose tissue from the same animals. This analysis provides a gene set that is brown and white adipose selective.
Publication Title
Transcriptional control of brown fat determination by PRDM16.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Comparing gene expression profiles of murine subcutaneous vs. visceral adipose tissue. Gene expression was analyzed in two subcutaneous depots (inguinal and axillary) and two visceral depots (epididymal and mesenteric) from male C57Bl/6 mice.
Publication Title
Ablation of PRDM16 and beige adipose causes metabolic dysfunction and a subcutaneous to visceral fat switch.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The current studies show that JMJD1A is phosphorylated at S265 by protein kinase A (PKA), and this is pivotal to activate expression of the b1-adrenergic receptor gene (Adrb1) and downstream targets including Ucp1. Phosphorylation of JMJD1A increases its interaction with the SWI/SNF nucleosome remodeling complex and DNA-bound PPARg. This complex conferred b-adrenergic-induced JMJD1A recruitment to target sites throughout the genome. Phospho-JMJD1A also facilitated long-range chromatin looping to recruit PPARg-bound distal-enhancers, SWI/SNF, and RNA polymerase close to the Adrb1 locus to activate transcription. Mutation of the PKA-phosphorylation site on JMJD1A abolished interactions with SWI/SNF without affecting demethylase activity suggesting the two functions are independent of each other. Our results show that JMJD1A demethylase is also a signal-sensing scaffold that regulates cAMP-responsive transcription via interactions with SWI/SNF and hormone stimulated higher-order chromatin conformational changes.
Publication Title
JMJD1A is a signal-sensing scaffold that regulates acute chromatin dynamics via SWI/SNF association for thermogenesis.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
To examine function of PKCh for atherosclerosis, we compared the gene expression profiles of control Apoe-/- and Prkch-/-Apoe-/- mice by microarray analysis.
Publication Title
PKCη deficiency improves lipid metabolism and atherosclerosis in apolipoprotein E-deficient mice.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa.
Publication Title
Neuronal GPCR controls innate immunity by regulating noncanonical unfolded protein response genes.
Sample Metadata Fields
Specimen part
View Samples
GSE37305- Caenorhabditis elegans
- 12 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The Sexual Dimorphism of Dietary Restriction Responsiveness in Caenorhabditis elegans.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Caenorhabditis elegans
- 4 Downloadable Samples
Description
Many species undergo sexual reproduction to distribute the parental genomes and increase the genomic diversity of the progeny. Among such species, sexual dimorphism is often displayed through morphology, size, behavior, and life-span, depending on the survival and reproduction strategies of the species. The nematode Caenorhabditis elegans has two sexes, hermaphrodite and male, and only the hermaphrodites, which produce both oocytes and sperm, are essential for the perpetuation of the species. In this study, we found that dietary restriction, which is the most reproducible way to retard aging in many species, extends the life-span of C. elegans hermaphrodites but not that of males. Our analysis revealed that fasting induces male-enriched genes in hermaphrodites and that the sex determination pathway affects life-span regulation, even after the completion of development, and is regulated by food availability. Furthermore, fasting activates the entire X-chromosome only in hermaphrodites. Our tiling array analysis identified a fasting-inducible, X-linked non-coding RNA for which expression positively correlated with the activation level of the X-chromosome and longevity. These links between the sex determination mechanism and dietary restriction at multiple levels may give priority to the survival of hermaphrodites during food shortages in C. elegans.
Publication Title
The Sexual Dimorphism of Dietary Restriction Responsiveness in Caenorhabditis elegans.
Sample Metadata Fields
No sample metadata fields
View Samples