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SRP047124
Homo sapiens
1 Downloadable Sample
IlluminaGenomeAnalyzerII
Description
Recently a genome of Russian individual (somatic DNA from blood) was sequenced (Skryabin et al. 2009). That study was continued to find a linkage between genetic differences in parental alleles and bias in biallelic expression of genes.
Publication Title
Individual genome sequencing identified a novel enhancer element in exon 7 of the CSFR1 gene by shift of expressed allele ratios.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-beta/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3 deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3-/- white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3-/- adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-alpha1 expression. We observe significant correlation between TGF-beta1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-beta1 signaling protects mice from obesity, diabetes and hepatic steatosis. Together, these results demonstrate that TGF-beta signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-beta1 activity might be an effective treatment strategy for obesity and diabetes.
Publication Title
Protection from obesity and diabetes by blockade of TGF-β/Smad3 signaling.
Sample Metadata Fields
Treatment
View Samples- Rattus norvegicus
- 18 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Hepatic cancer (HC), as one of the common malignancies in the world, is characterized by malignant cell prolifeHCion and growth, and hepatocarcinogenesis covers the stages of non-specific liver injury, liver fibrosis, liver cirrhosis, dysplasia nodules and finally liver carcinoma
Publication Title
Correlation between liver cancer occurrence and gene expression profiles in rat liver tissue.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Nonalcoholic fatty liver disease (NAFLD) is a common disorder characterized by excessive hepatic fat accumulation, and potentially resulting in non-alcoholic steatohepatitis (NASH), liver cirrhosis (LC) and end-stage liver disease
Publication Title
Correlation analysis between gene expression profile of rat liver tissues and high-fat emulsion-induced nonalcoholic fatty liver.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 20 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) and C57BL/6 (B6-apoe) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE).
Publication Title
Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
PTEN loss or PI3K/AKT signaling pathway activation correlates with human prostate cancer progression and metastasis. However, in preclinical murine models, deletion of Pten alone fails to mimic the significant metastatic burden that frequently accompanies the end stage of human disease. To identify additional pathway alterations that cooperate with PTEN loss in prostate cancer progression, we surveyed human prostate cancer tissue microarrays and found that the RAS/MAPK pathway is significantly elevated both in primary and metastatic lesions. In an attempt to model this event, we crossed conditional activatable K-rasG12D/WT mice with the prostate conditional Pten deletion model we previously generated. Although RAS activation alone cannot initiate prostate cancer development, it significantly accelerated progression caused by PTEN loss, accompanied by epithelial-to-mesenchymal transition (EMT) and macrometastasis with 100% penitence. A novel stem/progenitor subpopulation with mesenchymal characteristics was isolated from the compound mutant prostates, which was highly metastatic upon orthotopic transplantation. Importantly, inhibition of RAS/MAPK signaling by PD325901, a MEK inhibitor, significantly reduced the metastatic progression initiated from transplanted stem/progenitor cells. Collectively, these data indicate that activation of RAS/MAPK signaling serves as a potentiating second hit to alteration of the PTEN/PI3K/AKT axis and co-targeting both pathways is highly effective in preventing the development of metastatic prostate cancers.
Publication Title
Pten loss and RAS/MAPK activation cooperate to promote EMT and metastasis initiated from prostate cancer stem/progenitor cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE).
Publication Title
Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a C57BL/6 genetic background (B6-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE).
Publication Title
Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Arabidopsis thaliana
- 10 Downloadable Samples
- Illumina HiSeq 2000
Description
To understand how atypical bHLH, INCREASED LEAF INCLINATION1 (ILI1)-BINDING bHLH-1 (IBH1) (At2g43060), and close homologue, IBH1-like1 (IBL1) (At4g30410), interact to regulate cell elongation, genome-wide RNA-Seq expression analyses of IBH1 and IBL1 gain-(IBH1OE, IBL1OE) and loss-of-function (ibh1 (SALK 049177), ibl1(SALK 119457)) mutants were conducted. Overall design: For loss-of-function mutant, homozygous ibh1(SALK 049177) and ibl1(SALK 119457) were compared to wild type (Col). For gain-of-function mutant, homozygous 35Spro:IBH1-GFP and 35Spro:IBL1-GFP were compared to wild type (Col). Total RNAs were extactced from seedling of each genotypes. For each genotype two biological replicates were sequenced.
Publication Title
Helix-loop-helix/basic helix-loop-helix transcription factor network represses cell elongation in Arabidopsis through an apparent incoherent feed-forward loop.
Sample Metadata Fields
Specimen part, Subject
View Samples