Four mature, non-lactating dairy cattle were transitioned from a high forage diet (HF; 0% grain) to a high grain diet (HG; 65% grain) that was fed for three weeks. Rumen papillae biopsies were performed during the HF baseline (week 0) and after the first (week 1) and third week (week 3) of the grain challenge to create a transcript profile for the the short and long-term adaption of the rumen epithelium during ruminal acidosis.
Bovine rumen epithelium undergoes rapid structural adaptations during grain-induced subacute ruminal acidosis.
Specimen part, Time
View SamplesAssessment of mRNA expression levels in fat biopsies from subcutaneous adipose tissue from unrelated individuals.
A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.
Specimen part
View SamplesMicroRNAs are small, non-coding RNAs that post-transcriptionally regulate gene expression by binding to 3UTRs of target mRNAs. Kaposis sarcoma-associated herpesvirus (KSHV), a virus linked to malignancies including primary effusion lymphoma (PEL), encodes 12 miRNA genes, but only a few regulatory targets are known. We found that KSHV-miR-K12-11 shares 100% seed-sequence homology with hsa-miR-155, a miRNA frequently found up-regulated in lymphomas and critically important for B cell development. Based on this seed-sequence homology, we hypothesized that both miRNAs regulate a common set of target genes and as a result, could have similar biological activities.
Kaposi's sarcoma-associated herpesvirus encodes an ortholog of miR-155.
No sample metadata fields
View SamplesOverexpression of USF1 in HEK293T cells in vitro to ascertain the genes downstream of USF1. Will identify direct targets as well as indirect targets of USF1.
A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.
Cell line
View SamplesAlteration of the PTEN/PI3K pathway is associated with late stage and castrate resistant prostate cancer (CRPC). However, how PTEN loss involves in CRPC development is not clear. Here we show that castration-resistant growth is an intrinsic property of Pten-null prostate cancer (CaP) cells, independent of cancer development stage.PTEN loss suppresses androgen-responsive gene expressions by modulating androgen receptor (AR) transcription factor activity. Conditional deletion of AR in the epithelium promotes the proliferation of Pten-null cancer cells, at least in part, by down-regulating androgen-responsive gene FKBP5 and preventing PHLPP-mediated AKT inhibition. Our findings identify PI3K and AR pathway crosstalk as a mechanism of CRPC development, with potentially important implications for CaP etiology and therapy
Cell autonomous role of PTEN in regulating castration-resistant prostate cancer growth.
Specimen part, Time
View SamplesTo elucidate the mechanism(s) underlying the synergistic interaction between ETV6 and NFKB1, we analyzed the genome-wide transcriptional consequences of single and double knock-downs of the two TFs in U251 cells.
Causal Mechanistic Regulatory Network for Glioblastoma Deciphered Using Systems Genetics Network Analysis.
Cell line
View SamplesOxidized phospoholipids are a pro-inflammatory component of minimally modified lipoproteins that get trapped in the subendothelial space of atherosclerotic plaques of large arteries. To model the response of endothelial cells in a pro-atherosclerotic enviroment we measured the expression in primary endothelial cells with and without treatment with oxidized phsopolipids from 96 genetically identical donors of anonymous origin.
Systems genetics analysis of gene-by-environment interactions in human cells.
Sex, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
KSHV-encoded miRNAs target MAF to induce endothelial cell reprogramming.
Sex, Specimen part
View SamplesKaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognisable by its distinctive red skin lesions. The lesions are KSHV-infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. The effects of KSHV infection of both LEC and BEC were assayed using Affymetrix hgu133plus2 chips at 72 hours post infection.
KSHV-encoded miRNAs target MAF to induce endothelial cell reprogramming.
Specimen part
View SamplesKaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognisable by its distinctive red skin lesions. The lesions are KSHV-infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. The KSHV virus expresses multiple microRNA in a single cluster. Here we test the effects of this KSHV microRNA cluster in LEC cells using Affymetrix hgu133plus2 chips.
KSHV-encoded miRNAs target MAF to induce endothelial cell reprogramming.
Specimen part
View Samples