Transcript dynamics in mitotic exit mutants in the S. cerevisiae BF264-15D strain background. We examined the extent to which periodic cell-cycle transcription persisted in cells arrested in anaphase with intermediate level of B-cyclins.
Reconciling conflicting models for global control of cell-cycle transcription.
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View SamplesYeast cell cycle transcript dynamics in three S. cerevisiae strains grown at 30 degrees Celsius: cdc20 GALL-CDC20 (persistent mitotic CDK activity; CDK on), cdc8-ts (DNA replication checkpoint), GAL-cse4-353 (spindle assembly checkpoint), cdc8-ts cdc20 (DNA replication checkpoint, CDK on), and cdc8-ts cdc20, rad53-1 (DNA replication checkpoint without Rad53 activity, CDK on) in a BF264-15DU background. We compared transcript levels of genes previously shown to be periodically expressed in wild-type cells and in cells lacking all mitotic cyclins (clb1,2,3,4,5,6; CDK off).
Checkpoints couple transcription network oscillator dynamics to cell-cycle progression.
No sample metadata fields
View SamplesMycobacterium avium infection in mice induces granuloma necrosis in the lung which is dependent on IFNg. IRF1 is a transcription factor activated by IFNg signaling. The effect of IFNg and IRF1 on immunopathology and transcriptional changes in the lung were analysed using gene-deficient mice.
Mycobacteria-induced granuloma necrosis depends on IRF-1.
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View SamplesWe analyzed anti-proliferative dominant-negative Brd4 mutants that compete with the function of distinct Brd4 domains. We used these Brd4 mutants to compare the Brd4-specific transcriptome with the transcriptome of JQ1 treated cells. Overall design: We performed polyA RNA-seq of Raji cells expressing Brd4 constructs f3 and f9 (dnBrd4_f3/f9) and Raji cell expressing the luciferase control vector treated with JQ1 (luc_JQ1) or DMSO as control (luc_DMSO).
Transcriptome analysis of dominant-negative Brd4 mutants identifies Brd4-specific target genes of small molecule inhibitor JQ1.
Cell line, Treatment, Subject
View SamplesHere we demonstrate by the use of extensive controls and stringent statistical analysis that dendritic cells differentially regulate hundreds of different genes based upon sequence similarity of endogenously- and exogenously-loaded antigens and in a T-cell independent fashion. When endogenously and exogenously-derived antigens are identical, dendritic cells upregulate many different components of the Th-1 response, favoring the priming of CD8+ effectors and promulgating cellular immunity.
Th-1 polarization is regulated by dendritic-cell comparison of MHC class I and class II antigens.
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View SamplesBaseline gene expression for two primary and two recurrent tumor cell lines derived from MTB;TAN transgenic mice. Microarrays were performed in biological duplicate to determine differential gene expression between primary and recurrent tumor cell cohorts.
Epigenetic silencing of tumor suppressor Par-4 promotes chemoresistance in recurrent breast cancer.
Cell line
View SamplesMesenchymal stromal cells are a critical component of the bone marrow hematopoietic stem cell niche. In myelofibrosis, these cells are the major source of fibrosis in the bone marrow. We performed gene expression analysis using microarrays to systematically elucidate the mechanisms leading to fibrogenic conversion of these cells.
Leptin-receptor-expressing bone marrow stromal cells are myofibroblasts in primary myelofibrosis.
Specimen part, Disease, Disease stage
View SamplesGEP of the murine cell line BAL17 (BALB/c)
Mechanisms of intracerebral lymphoma growth delineated in a syngeneic mouse model of central nervous system lymphoma.
Specimen part
View SamplesMetastatic relapse of breast cancer and other tumor types usually occurs several years after surgical resection of the primary tumor. Early dissemination of tumor cells followed by an extended period of dormancy is thought to explain this prevalent clinical behavior. By using a gain-of-function retroviral cDNA screen in the mouse, we found that Coco, a secreted antagonist of TGF-beta ligands, induces solitary mammary carcinoma cells that have extravasated in the lung stroma to exit from dormancy. Mechanistic studies demonstrate that Coco awakens dormant metastasis-initiating cells by blocking stroma-derived Bone Morphogenetic Proteins. Inhibition of canonical BMP signaling reverses the commitment to differentiation of these cells and enhances their self-renewal and tumor-initiation capacity. Expression of Coco induces a discrete gene expression signature strongly associated with metastatic relapse to the lung but not to the bone or brain in primary patients samples. Accordi ngly, silencing of Coco does not inhibit metastasis to the bone or brain in mouse models. These findings suggest that metastasis-initiating cells require the self-renewal capability typically associated with stem cells in order to exit from dormancy and identify Coco as a master regulator of this process.
The BMP inhibitor Coco reactivates breast cancer cells at lung metastatic sites.
Cell line
View SamplesHuman T-cell Acute lymphoblastic Leukemia cell line CEM was transfected with either shRNA against ZMIZ1 or scrambled shRNA. Four (non-paired) biological replicates of each condition had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets. A supplementary Excel workbook holding the same processed data as the series matrix file is provided, with some probe set annotation, and a simple statistical comparison. The raw (.CEL) files are also provided.
Convergence of the ZMIZ1 and NOTCH1 pathways at C-MYC in acute T lymphoblastic leukemias.
Cell line
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