We were interested in determining what genes might be controlled by TFAP2C and/or TFAP2A, either directly or indirectly through regulation of ER-alpha and potentially other signaling pathways. We performed an microarray analysis in MCF7 cells with elimination of either TFAP2C or TFAP2A. The patterns of gene expression with alteration of TFAP2 activity were compared to changes in expression induced by estrogen exposure. Knock-down of TFAP2C in the presence of estrogen altered the pattern of several known ERalpha-regulated genes and a number of genes outside the estrogen-regulated pathways.
TFAP2C controls hormone response in breast cancer cells through multiple pathways of estrogen signaling.
Specimen part
View SamplesTissue-specific comparison of gene expression levels in T65H translocation mice, either with or without uniparental duplications of Chrs 7 & 11. Identification of highly differentially expressed transcripts.
Chromosome-wide identification of novel imprinted genes using microarrays and uniparental disomies.
Specimen part
View SamplesComparison of gene expression levels between MatDp(dist2) and PatDp(dist2) mice (newborn whole head). Identification of highly differentially expressed transcripts.
Transcript- and tissue-specific imprinting of a tumour suppressor gene.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
WAMIDEX: a web atlas of murine genomic imprinting and differential expression.
Age, Specimen part
View SamplesComparison of gene expression levels between matUPD12 and patUPD12 15.5 dpc whole embryo or placenta samples (maternal versus paternal uniparental disomy of Chr 12). Identification of highly differentially expressed transcripts.
WAMIDEX: a web atlas of murine genomic imprinting and differential expression.
Age, Specimen part
View SamplesDuring oogenesis, DNA methyltransferase 3-like (Dnmt3l) is required for the establishment of the maternal germline DNA methylation imprints that in the offspring, govern the parent-of-origin-specific expression of most known imprinted genes (Science 2001, 294:2536-9). Dnmt3l-deficient dams were crossed with wildtype sires to obtain Dnmt3l-/+ embryos that lack maternal methylation imprints. Gene expression was measured in Dnmt3l-/+ and wildtype embryos and is expected to differ for imprinted genes that are under the control of a maternal methylation mark.
WAMIDEX: a web atlas of murine genomic imprinting and differential expression.
Sex, Age, Specimen part
View SamplesComparison of gene expression levels between matUPD18 and patUPD18 8.5 dpc whole embryo samples (maternal versus paternal uniparental disomy of Chr 18). Identification of highly differentially expressed transcripts.
WAMIDEX: a web atlas of murine genomic imprinting and differential expression.
Age, Specimen part
View SamplesWhereas DNA methylation is essential for genomic imprinting, the importance of histone methylation in the allelic repression of imprinted genes is unclear. Imprinting control regions (ICRs), however, are consistently marked by histone H3 K9 methylation on their DNA-methylated allele. In the placenta, the paternal silencing along the Kcnq1 domain on distal chromosome 7 also correlates with the presence of H3-K9 methylation, but imprinted repression at these genes is maintained independently of DNA methylation. To explore which histone methyltransferase (HMT) could mediate the allelic H3-K9 methylation on distal chromosome 7, and at ICRs, we generated mouse conceptuses deficient for the SET-domain protein G9a. We find that in the embryo and placenta, the differential DNA methylation at ICRs and imprinted genes is maintained in the absence of G9a. Accordingly, in embryos, imprinted gene expression is unchanged at the domains analysed, in spite of a global loss of H3-K9 di-methylation (H3K9me2). In contrast, the placenta-specific imprinting of genes on distal chromosome 7 is lost in the absence of G9, and this correlates with a loss of H3K9me2 and H3K9me3. These findings provide the first in vivo evidence for the involvement of a SET domain protein in imprinting and highlight the importance of histone lysine methylation rather than DNA methylation in the maintenance of imprinting in the trophoblast lineage.
G9a histone methyltransferase contributes to imprinting in the mouse placenta.
Age, Specimen part
View SamplesConsider the problem of designing a panel of complex biomarkers to predict a patient's health or disease state when one can pair his or her current test sample, called a target sample, with the patient's previously acquired healthy sample, called a reference sample. As contrasted to a population averaged reference, this reference sample is individualized. Automated predictor algorithms that compare and contrast the paired samples to each other could result in a new generation of test panels that compare to a person's healthy reference to enhance predictive accuracy. This study develops such an individualized predictor and illustrates the added value of including the healthy reference for design of predictive gene expression panels. The objective is to predict each subject's state of infection, e.g., neither exposed nor infected, exposed but not infected, pre-acute phase of infection, acute phase of infection, post-acute phase of infection. Using gene microarray data collected in a large-scale serially sampled respiratory virus challenge study, we quantify the diagnostic advantage of pairing a person's baseline reference with his or her target sample.
An individualized predictor of health and disease using paired reference and target samples.
Specimen part, Subject, Time
View SamplesArabidopsis fc2-1 mutants fail to properly de-etiolate after a prolonged period in the dark. Our goal was to monitor whole genome expression during the first 2 hours of de-etiolation to determine the cuase of this growth arrest.
Ubiquitin facilitates a quality-control pathway that removes damaged chloroplasts.
Specimen part
View Samples