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GSE53006
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
- 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- 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- 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
- 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- 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- Homo sapiens
- 4 Downloadable Samples
- Ion Torrent Proton
Description
Background: Cantharidin, an active constituent of mylabris, is believed to have anti-tumor activity. Cantharidin selectively inhibit protein phosphatase 2A (PP2A), a repressor of oncogenic kinase pathways (ERK, JNK, NF-?B, and PKC). Cantharidin represses the growth and metastasis of pancreatic cancer cells in vitro. In the present study, we investigated the effects of cantharidin on pancreatic cancer xenografts in vivo. Methods: Cells stably expressing luciferase were used to establish xenograft models. Xenograft growth was evaluated by living imaging. Gene expression was determined using a microarray, real-time PCR, a RayBiotech antibody array, and the Milliplex assay. Results: Surprisingly, cantharidin significantly accelerated xenograft growth. Living imaging showed a rapid distribution of D-luciferin in cantharidin-treated xenografts, suggesting a rich blood supply. Immunohistochemistry confirmed increased angiogenesis. Microarray and antibody array identified upregulated pro-angiogenic and downregulated anti-angiogenic factors. The Milliplex assay suggested elevated secretion of IL-6, IL-8, TNF-a, and VEGF. ERK, JNK, NF-?B, and PKC pathway inhibitors attenuated the cantharidin-induced changes to pro-angiogenic gene expression. PKC pathway-inhibiting tamoxifen or antiangiogenic therapeutics, including Ginsenoside Rg3, bevacizumab, Apatinib, and Endostar antagonized the pro-angiogenic effect of cantharidin or its derivatives. These regimens presented remarkable synergistic antitumor effects in vivo. Conclusion: Although cantharidin presents anti-tumor effects in vitro and has been applied in clinical practice, we revealed an unfavorable pro-angiogenic side effect. We recommend that the clinical application of cantharidin should be performed on the premise of anti-vascularization therapy. Overall design: Examination of gene expression profiles after treatment with Ginsenoside Rg3 or tamoxifen in PANC-1 cells
Publication Title
The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic cancer.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples