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GSE9397
Homo sapiens
18 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant disorder linked to contractions of the D4Z4 repeat array in the subtelomeric region of chromosome 4q. By comparing genome-wide gene expression data from muscle biopsies of patients with FSHD to those of 11 other neuromuscular disorders, we intend to identify disease-specific changes which are more likely to be involved in the early stages of the disease progression. The data will help to identify pathological mechanisms involved in FSHD.
Publication Title
DUX4, a candidate gene of facioscapulohumeral muscular dystrophy, encodes a transcriptional activator of PITX1.
Sample Metadata Fields
Disease, Disease stage
View Samples- Sus scrofa
- 12 Downloadable Samples
- Porcine Gene 1.0 ST Array (porgene10st)
Description
Expression data from valvular interstitial cells cultured in 2D or 3D PEG hydrogel systems compared to culture on tissue culture polystyrene and freshly isolated cells
Publication Title
Transcriptional profiles of valvular interstitial cells cultured on tissue culture polystyrene, on 2D hydrogels, or within 3D hydrogels.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 33 Downloadable Samples
Illumina HiSeq 2000
Description
During transcription initiation, the TFIIH-kinase Kin28/Cdk7 marks RNA polymerase II (Pol II) by phosphorylating the C-terminal domain (CTD) of its largest subunit. Here we describe a structure-guided chemical approach to covalently and specifically inactivate Kin28 kinase activity in vivo. This method of irreversible inactivation recapitulates both the lethal phenotype and the key molecular signatures that result from genetically disrupting Kin28 function in vivo. Inactivating Kin28 impacts promoter release to differing degrees and reveals a “checkpoint” during the transition to productive elongation. While promoter-proximal pausing is not observed in budding yeast, inhibition of Kin28 attenuates elongation-licensing signals, resulting in Pol II accumulation at the +2 nucleosome and reduced transition to productive elongation. Furthermore, upon inhibition, global stabilization of mRNA masks different degrees of reduction in nascent transcription. This study resolves long-standing controversies on the role of Kin28 in transcription and provides a rational approach to irreversibly inhibit other kinases in vivo. Overall design: Total RNA was collected from wild-type and analog-sensitive Kin28 strains treated with reversible inhibitor 1-NAPP-1, irreversible inhibitor CMK, and solvent control DMSO. Equivalent ratios of S. pombe : S. cerevisiae cells were added to each sample before RNA extraction for normalization of read counts after sequencing. Nascent RNA was purified from total RNA by 4-thiouracil labeling, biotinylation, and streptavidin-pulldown. As a negative control, nascent RNA was also extracted from total RNA from cells that had not been treated with 4-thiouracil.
Publication Title
Engineered Covalent Inactivation of TFIIH-Kinase Reveals an Elongation Checkpoint and Results in Widespread mRNA Stabilization.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
In order to elucidate the molecular mechanism giving rise to the rare In(Lu) type of Lu(a-b-) blood group phenotype we compared the transcriptome of normal and In(Lu) erythroblasts at different stages of maturation. Many erythroid-specific genes had reduced transcript levels suggesting the phenotype resulted from a transcription factor abnormality. A search for mutations in erythroid transcription factors revealed mutations in the promoter or coding sequence of EKLF in 21 of 24 individuals with the In(Lu) phenotype. In all cases the mutant EKLF allele occurred in the presence of a normal EKLF allele. Individuals with the In(Lu) phenotype have no reported pathology indicating that one functional EKLF allele is sufficient to sustain human erythropoiesis. These data provide the first description of inactivating mutations in human EKLF and the first demonstration of a blood group phenotype resulting from mutations in a transcription factor.
Publication Title
Mutations in EKLF/KLF1 form the molecular basis of the rare blood group In(Lu) phenotype.
Sample Metadata Fields
No sample metadata fields
View Samples- Sus scrofa
- 12 Downloadable Samples
- Affymetrix Porcine Genome Array (porcine)
Description
Fibrotic diseases have significant health impact and have been associated with differentiation of the resident fibroblasts into myofibroblasts. In particular, stiffened extracellular matrix and TGF-1 in fibrotic lesions have been shown to promote pathogenic myofibroblast activation and progression of fibrosis in various tissues. To better understand the roles of mechanical and chemical cues on myofibroblast differentiation and how they may crosstalk, we cultured primary valvular interstitial cells (VICs) isolated from porcine aortic valves and studied how traditional TCPS culture, which presents a non-physiologically stiff environment, and TGF-1 affect native VIC phenotypes.
Publication Title
Hydrogels preserve native phenotypes of valvular fibroblasts through an elasticity-regulated PI3K/AKT pathway.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 25 Downloadable Samples
- Illumina HiSeq 2500
Description
Polycomb repressive complex 2 (PRC2-EZH2) methylates histone H3 at lysine 27 (H3K27) and is required to maintain gene repression during development. Misregulation of PRC2 is linked to a range of neoplastic malignancies, which is believed to involve methylation of H3K27. However, the full spectrum of non-histone substrates of PRC2 that might also contribute to PRC2 function is not known. We characterized the target recognition specificity of PRC2 and used the resultant data to screen for novel potential targets. The RNA polymerase II (Pol II) transcription factor, Elongin A (EloA), is methylated by PRC2 in vivo. Mutation of the methylated EloA residue decreased repression of many, but not all, PRC2 target genes as measured by both steady state and nascent RNA levels. We propose that PRC2 regulates transcription of a subset of target genes in part via methylation of EloA. Overall design: We examined the transcripitonal profile of EEDnull, EloAnull, EloA mutant, and parental mouse embryonic stem cells by RNAseq. Please note that the .bw processed data file was generated from the *mESC replicate samples together and linked to the corresponding *rep1 sample records.
Publication Title
Polycomb Repressive Complex 2 Methylates Elongin A to Regulate Transcription.
Sample Metadata Fields
Specimen part, Subject
View Samples- Saccharomyces cerevisiae
- 21 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Gene expression was compared for wild type yeast (BY4741) and yeast lacking Gal11/Med15 and Med3, or from a gal11-myc med3 strain. The gal11-myc allele shows a partial loss of function when combined with med3. Expression was analyzed for yeast grown in YPD as well as in CSM.
Publication Title
Distinct role of Mediator tail module in regulation of SAGA-dependent, TATA-containing genes in yeast.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina HiSeq 2500
Description
Polycomb repressive complex 2 (PRC2-EZH2) methylates histone H3 at lysine 27 (H3K27) and is required to maintain gene repression during development. Misregulation of PRC2 is linked to a range of neoplastic malignancies, which is believed to involve methylation of H3K27. However, the full spectrum of non-histone substrates of PRC2 that might also contribute to PRC2 function is not known. We characterized the target recognition specificity of PRC2 and used the resultant data to screen for novel potential targets. The RNA polymerase II (Pol II) transcription factor, Elongin A (EloA), is methylated by PRC2 in vivo. Mutation of the methylated EloA residue decreased repression of many, but not all, PRC2 target genes as measured by both steady state and nascent RNA levels. We propose that PRC2 regulates transcription of a subset of target genes in part via methylation of EloA. Overall design: We examined the nascent transcripiton profile of mES cells by adding 5-Bromouridine (BrU) to the media for 10 min. Following RNA isolation, BrU-labelled nascent RNA species were affinity purified using BrdU antibody and sequenced after library preparation. Please note that each .bw file was generated from two replicate samples together and linked to the corresponding *rep1 sample records.
Publication Title
Polycomb Repressive Complex 2 Methylates Elongin A to Regulate Transcription.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Lymphatic endothelial cells were grown under normoxia, hypoxia (1% 0xygen) and conditioned medio from NSLCN growth under normoxia or hypoxia. Gene expression was measured and comparition between samples performed
Publication Title
Hypoxia alters the adhesive properties of lymphatic endothelial cells. A transcriptional and functional study.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
We investigated the ability of monoclonal B cells to restore primary and secondary antibody responses in adoptive immune-deficient hosts. Priming induced B cell activation and expansion, AID expression, antibody production and the generation of IgM+IgG- and IgM-IgG+ antigen-experienced B-cell subsets that persisted in the lymphopenic environment by cell division. Using RNA sequencing, we compared the gene expression profil of memory B cells subpopulations and activated B cells. These data showed a clear discrimination of naïve and activated/memory cells while indicating only minor differences between both subsets of memory cells. Overall design: mRNA profiles of B cell subtypes (activated, memory IgM+, memory IgG+) were generated by deep sequencing, in triplicate, using Illumina
Publication Title
Regulation and Maintenance of an Adoptive T-Cell Dependent Memory B Cell Pool.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples