Primary Sjgrens syndrome (pSS) is a chronic autoimmune disease with complex etiopathogenesis. Here we use Affymetrix U133 plus 2.0 microarray gene expression data from human parotid tissue. Parotid gland tissues were harvested from 17 pSS and 14 14 non-pSS sicca patients and 18 controls. The data were used in the following article: Nazmul-Hossain ANM, Pollard RPE, Kroese FGM, Vissink A, Kallenberg CGM, Spijkervet FKL, Bootsma H, Michie SA, Gorr SU, Peck AB, Cai C, Zhou H, Horvath S, Wong DTW (2012) Systems Analysis of Primary Sjgrens Syndrome Pathogenesis in Salivary Glands: Comparative Pathways and Molecular Events in Humans and a Mouse Model.
Systems analysis of primary Sjögren's syndrome pathogenesis in salivary glands identifies shared pathways in human and a mouse model.
Disease
View SamplesNMJ Junction various time points normal C57BL10 LCM mRNA
Intracellular expression profiling by laser capture microdissection: three novel components of the neuromuscular junction.
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View SamplesWe investigated transcriptional responses of different lung macrophage lineages during M.tuberculosis infection by RNAseq. Our data revealed that different lineages of macrophages respond differentially to M.Tuberculosis infection. Overall design: Alveolar macrophage (AM) and interstitial macrophages (IM) with or without Mtb were FACS-sorted from Mtb infected mice for RNAseq.
Growth of <i>Mycobacterium tuberculosis</i> in vivo segregates with host macrophage metabolism and ontogeny.
Specimen part, Cell line, Subject
View SamplesGene expression in mice skin stimulated with 3 different cytokines
Thymic stromal lymphopoietin is up-regulated in the skin of patients with systemic sclerosis and induces profibrotic genes and intracellular signaling that overlap with those induced by interleukin-13 and transforming growth factor β.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
RNA sequencing and transcriptome arrays analyses show opposing results for alternative splicing in patient derived samples.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Correlated alterations in genome organization, histone methylation, and DNA-lamin A/C interactions in Hutchinson-Gilford progeria syndrome.
Sex, Specimen part, Disease, Cell line
View SamplesHere we compared the performance of Affymetrix HTA 2.0 microarray and Illumina 2000 RNA-sequencing techniques on the clinical samples collected from patients with lung squamous cell carcinoma.
RNA sequencing and transcriptome arrays analyses show opposing results for alternative splicing in patient derived samples.
Specimen part
View SamplesLoss of function of the tumor suppressor BRCA1 (Breast Cancer 1) protein is responsible for numerous familial and sporadic breast cancers. We previously identified PABP1 as a novel BRCA1 partner and showed that BRCA1 modulates translation through its interaction with PABP1. We showed that the global translation was diminished in BRCA1-depleted cells and increased in BRCA1-overexpressing cells. Our findings raised the question whether BRCA1 affects translation of all cytoplasmic cellular mRNAs or whether it specifically targets a subset of mRNAs.
BRCA1-Dependent Translational Regulation in Breast Cancer Cells.
Cell line
View SamplesHutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease that is frequently caused by a de novo point mutation at position 1824 in LMNA. This mutation activates a cryptic splice donor site in exon 11, and leads to an in-frame deletion within the prelamin A mRNA and the production of a dominant negative lamin A protein, known as progerin. Here we show that HGPS cells experience genome-wide alterations in patterns of H3K27me3 deposition, changes in the associations of genomic loci with nuclear lamin A/C, and, at late passages, genome-wide loss of spatial compartmentalization of active and inactive chromatin domains that characterizes chromosome folding in normal cells. We further demonstrate that the H3K27me3 changes associate with gene expression alterations in HGPS cells. Our results support a model that the accumulation of progerin in the nuclear lamina leads to altered H3K27me3 marks in heterochromatin, possibly through the down-regulation of EZH2, and disrupts heterochromatin-lamina interactions. These changes may then lead to the genomic disorganization and changes in transcriptional regulation we observe in HGPS fibroblasts.
Correlated alterations in genome organization, histone methylation, and DNA-lamin A/C interactions in Hutchinson-Gilford progeria syndrome.
Sex, Specimen part, Disease, Cell line
View SamplesT-cell clones were obtained by limiting dilution culture of PBMC of HTLV-1 carriers. Exon expression profiling was performed using Affymetrix exon array (Affymetrix Human Exon 1.0 ST Array) according to the manufacturer's instructions.
HTLV-1 bZIP factor HBZ promotes cell proliferation and genetic instability by activating OncomiRs.
Specimen part
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