The estrogen receptor-alpha (ER) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ER function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ER function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription.
Estrogen-dependent gene transcription in human breast cancer cells relies upon proteasome-dependent monoubiquitination of histone H2B.
Cell line
View Samples[original title] Tissue-specific silencing of C2TA reveals the autonomous role of medullary thymic epithelial cells in central CD4 T cell tolerance.
Autonomous role of medullary thymic epithelial cells in central CD4(+) T cell tolerance.
Sex, Specimen part
View SamplesThe aim of this study was to assess the relative gene expression in human AAA and AOD.
Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease.
Specimen part, Disease, Disease stage
View SamplesAnalysis of differential gene expression for rutured vs stable abdominal aortic aneurysms (AAA) and for intermediate size (55mm) vs large (>70mm) AAA.
Molecular Fingerprint for Terminal Abdominal Aortic Aneurysm Disease.
Specimen part
View SamplesPolycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which characterizes many silenced genes including those on the inactive X-chromosome. Here we interrogate the role of core PRC2 protein EED in X-linked gene silencing by assessing allele-specific X-linked gene expression in WT and Eed-/- hybrid mouse trophoblast stem cells (TSCs) harboring a 129/S1-derived maternal X-chromosome and a JF1/Ms-derived paternal X-chromosome. This study generates mRNA-seq data for WT and Eed-/- TSCs, which undergo imprinted inactivation of the paternal X-chromosome. RNA-seq data was mapped allele-specifically to in silico strain-specific maternal and paternal reference genomes, generated based on known single nucleotide polymorphisms. We find that EED loss abrogates H3K27me3 and expression of Xist lncRNA, which is required for X-inactivation, however, despite the absence of H3K27me3 and Xist, only a subset of PRC2 target genes are derepressed in Eed-/- TSCs. Overall design: RNA-seq profiles of four WT (Eed +/+ and Eed fl/fl) and three EED null (Eed -/-) female TS cell lines were generated through strand-specific 100 bp paired-end sequencing on the Illumina HiSeq2000
PRC2 represses transcribed genes on the imprinted inactive X chromosome in mice.
Specimen part, Subject
View SamplesmRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated Overall design: mRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated
Murine Norovirus Infection Induces T<sub>H</sub>1 Inflammatory Responses to Dietary Antigens.
Age, Specimen part, Cell line, Subject
View SamplesKlotho-deficient mice develop aortic valve annulus calcification by 6 weeks of age. Understanding the molecular basis by which aortic valve calcification is initiated will help define potential molecular targets which may be inhibited to reduce or prevent aortic valve calcification.
COX2 inhibition reduces aortic valve calcification in vivo.
Specimen part
View SamplesThe initial segment of the epididymis is vital for male fertility, therefore, it is important to understand the mechanisms that regulate this important region. Deprival of testicular luminal fluid factors/lumicrine factors from epididymis, a subset of cells within the initial segment undergo apoptosis. In this study, microarray analyses was used to examine early changes in the downstream signal transduction pathways following the loss of lumicrine factors, and we discovered the following cascade of events leading to loss of protection and eventual apoptosis. First, mRNA expression of several key components of ERK pathway decreased sharply after 6 hours of loss protection from testicular lumicrine factors. After 12 hours, the levels of mRNA expression of STAT and NF-B pathways components increased, mRNA expression of genes encoding cell cycle inhibitors increased. After 18 hours of loss protection from testicular lumicrine factors, apoptosis was observed in the initial segment. In conclusion, testicular lumicrine factors protect the cells of the initial segment by activating ERK pathway, repressing STAT and NF-B pathways, and preventing a cascade of reactions leading to apoptosis.
Testicular lumicrine factors regulate ERK, STAT, and NFKB pathways in the initial segment of the rat epididymis to prevent apoptosis.
Sex, Specimen part, Time
View SamplesHyperhomocysteinemia (HHcy) causes cardiovascular dysfunction and is associated with many complications during pregnancy related to reduced NO bioactivity. The mechanisms of HHcy on the NO-dependent control of myocardial metabolism was compared with L-NAME, which directly inhibits NO bioavailability, treated animals.
Long-term methionine-diet induced mild hyperhomocysteinemia associated cardiac metabolic dysfunction in multiparous rats.
Sex, Specimen part
View SamplesThere is cardiac dysfunction in male eNOS (-/-) with age and 50% mortality at 21M. It was of interest to investigate the gene expression profile of aged eNOS (-/-) male in comparison to (+/+) in order to explore the genetic markers and molecular mechanisms leading to heart failure. RNA was extracted from the left ventricle from male (-/-) (n=3) and (+/+) (n=4) at the age of 21M.
Transcriptional basis for exercise limitation in male eNOS-knockout mice with age: heart failure and the fetal phenotype.
No sample metadata fields
View Samples