To understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq analysis of JunB-deficient and control Treg cells (CD4+ CD25hi). Overall design: Gene expresson profiles in WT and JunB-deficient Treg cells.
JunB regulates homeostasis and suppressive functions of effector regulatory T cells.
Specimen part, Cell line, Subject
View SamplesProgressive myoclonus epilepsy of Unverricht-Lundborg type (EPM1) is an inherited neurodegenerative disease with myoclonus, seizures and ataxia, caused by the mutations in cystatin B (CSTB) gene. In an approach towards understanding the molecular basis of pathogenic events in EPM1 we have utilized the cystatin B deficient mice (Cstb-/-), a model for the disease. We have characterized the gene expression changes from the cerebellum of Cstb-/- mouse at postnatal day 7 (P7) and P30 as well as in cultured cerebellar granule cells using a pathway-based approach. A marked upregulation of immune response genes was seen at P30, reflecting the ongoing neuropathology, however, the observed alterations in complement cascade genes could also imply defects in synaptic plasticity. Differentially expressed genes in pre-symptomatic Cstb-/- animals at P7 were connected to synaptic function and plasticity and in cultured cerebellar granule cells to cellular biogenesis, cytoskeleton and intracellular transport. Especially GABAergic pathways were affected.
Gene expression alterations in the cerebellum and granule neurons of Cstb(-/-) mouse are associated with early synaptic changes and inflammation.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion.
Specimen part, Cell line
View SamplesGene-expression in siRNA treated U2OS and hTERT-RPE1 cells showed that CASP8AP2, NPAT and HINFP do not regulate expression of each other, and do not have any common target genes, except histones. Most histone genes are downregulated in U2OS cells following loss of CASP8AP2, NPAT or HINFP. In normal cells, highly-expressed histone genes were downregulated, albeit less than in tumor cells following loss of CASP8AP2. The p53 target genes were upregulated relatively late, clearly after the changes in expression of histone genes were observed.
Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion.
Cell line
View SamplesTF binding clusters in promoter correlate well with gene expression. We used ChIP-seq to map binding sites of the majority of highly expressed TFs in the cell. The size of clusters of TFs in the promoters of genes were found to correlate well with gene expression.
Transcription factor binding in human cells occurs in dense clusters formed around cohesin anchor sites.
Cell line
View SamplesGene expression profiles of 10 uterine leiomyomas and their matched normal myometrium specimens were studied using Affymetrix GeneChip Human Genome U133 Plus 2.0 gene expression arrays. Four tumors displayed a codon 44 mutation, four carried a intron 1 mutation, and the remaining two displayed no MED12 mutation.
MED12, the mediator complex subunit 12 gene, is mutated at high frequency in uterine leiomyomas.
Specimen part, Subject
View SamplesTo identify downstream targets of Jak/Stat3 pathways without being distracted by differentiation signalings from MEK/ERK pathway, we exploited a engineered B6 cells, which stably stably expressing a chimeric receptor (GRgp-Y118F). The chimeric receptor can induce the phosphorylation of Stat3 by GCSF without activating the MEK/ERK pathway. To mimic the effect of GCSF, the chimeric B6 cells were also treated with LIF plus a selective MEK chemical inhibitor, PD0325901, to induce LIF/Jak/Stat3 but MEK/ERK pathways.
Gbx2, a LIF/Stat3 target, promotes reprogramming to and retention of the pluripotent ground state.
Cell line
View SamplesAnalysis of ovarian cancer cell lines after knockdown of FGFRL1 using SiRNA.
FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling.
Cell line
View SamplesAnalyze the effect of TLR9 deficiency on immue cell function at the gene expression level. Our hypothesis was that TLR9 deficiency promotes CD73 expression in T cells thus regulates autoimmune diabetes development in NOD mice.
TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in nonobese diabetic mice.
Specimen part
View SamplesA data set of normal epithelium, serous ovarian surface epithelial-stromal tumors (benign and type II malignancies), stroma distal to tumor, and stroma adjacent to tumor (50 samples total). Additional cel files are included which represent replicate sampling from patients, and cel files that failed quality control but may be bioinformatically interesting. Additional replicate or failed cel files were not included in the final analysis (and so these samples were not included in the matrix).
Dysregulation of AKT3 along with a small panel of mRNAs stratifies high-grade serous ovarian cancer from both normal epithelia and benign tumor tissues.
Specimen part, Subject
View Samples