Primary mammary gland stromal fibroblasts from pubertal SHARPIN-deficient cpdm/cpdm -mice and their littermate controls Overall design: mRNA seq data from 3 wt and 3 Sharpincpdm mouse mammary gland stromal fibroblast cell samples
SHARPIN regulates collagen architecture and ductal outgrowth in the developing mouse mammary gland.
Age, Specimen part, Cell line, Subject
View SamplesWe performed microarrays to identify change of gene expression under NR, CR, and RM and found differentially expressed genes between each condition.
Caloric Restriction and Rapamycin Differentially Alter Energy Metabolism in Yeast.
No sample metadata fields
View SamplesMost human tumors have abnormal numbers of chromosomes, a condition known as aneuploidy. The mitotic checkpoint is an important mechanism that prevents aneuploidy through restraining the activity of the anaphase-promoting complex (APC). USP44 was identified as a key regulator of APC activation that maintains the association of MAD2 with the APC co-activator Cdc20. However, the physiological importance of USP44 and its impact on cancer biology are unknown. Here, we show that USP44 is required to prevent tumors in mice and is frequently down-regulated in human lung cancer. USP44 inhibits chromosome segregation errors independently of its role in the mitotic checkpoint by regulating proper centrosome separation, positioning, and mitotic spindle geometry, functions that require direct binding to the centriole protein, centrin. These data reveal a new role for the ubiquitin system in mitotic spindle regulation and underscore the importance of USP44 in the pathogenesis of human cancer.
USP44 regulates centrosome positioning to prevent aneuploidy and suppress tumorigenesis.
Sex, Disease, Disease stage
View SamplesSexual dimorphism of the behaviors or physiological functions in mammals is mainly due to the sex difference of the brain. The goal of this study is to identify genes mediating sexaul dimorphism of the brain.
Microarray analysis of perinatal-estrogen-induced changes in gene expression related to brain sexual differentiation in mice.
Sex, Specimen part
View SamplesThe goal of this experiment was to identify transcripts that are differentially expressed in dCAP-D3 mutant tissues. Overall design: RNA was isolated from wing discs and salivary glands of wild type (w1118) or dCap-D3 homozygous mutant (dCap-D3c07081/c07081) larvae. Directional (wing disc) or nondirectional (salivary gland) cDNA libraries (50 bp, paired end) were made at the University of Chicago Genomics Core and sequenced on an Illumina HiSeq2500, according to standard protocols.
Comparing and Contrasting the Effects of <i>Drosophila</i> Condensin II Subunit dCAP-D3 Overexpression and Depletion <i>in Vivo</i>.
Specimen part, Cell line, Subject
View SamplesSecretion of insulin by pancreatic cells in response to glucose is central for glucose homeostasis, and dysregulation of this process is a hallmark of the early stages of diabetes. We utilized a tetracycline-inducible approach to investigate the immediate impact of a pulse of Sox17 expression on the insulin secretory pathway. Sox17 gain-of-function animals (Sox17-GOF) were generated using an Ins2-rtTA mouse line and a line in which Sox17 expression is regulated by the tetracycline transactivator (tetO-Sox17). Administering doxycycline to 16-week old mice resulted in Sox17 overexpression in mature cells in the islets.
Sox17 regulates insulin secretion in the normal and pathologic mouse β cell.
Age, Specimen part
View SamplesMicroarrays were used to detail the global programme of gene expression comparing wild-type and RNAi knock-down plants of SPT4-1 and SPT4-2
The transcript elongation factor SPT4/SPT5 is involved in auxin-related gene expression in Arabidopsis.
Age, Specimen part
View SamplesWe used microarrays to compare gene expression across different murine tissues.
Using ribosomal protein genes as reference: a tale of caution.
No sample metadata fields
View SamplesThe number of long-term survivors of high-risk neuroblastoma remains discouraging, with 10-year survival as low as 20%, despite decades of considerable international efforts to improve outcome. Major obstacles remain and include managing resistance to induction therapy, which causes tumor progression and early death in high-risk patients, and managing chemotherapy-resistant relapses, which can occur years after the initial diagnosis. Identifying and validating novel therapeutic targets is essential to improve treatment. Delineating and deciphering specific functions of single histone deacetylases in neuroblastoma may support development of targeted acetylome-modifying therapeutics for patients with molecularly defined high-risk neuroblastoma profiles. We show here that HDAC11 depletion in MYCN-driven neuroblastoma cell lines strongly induces cell death, mostly mediated by apoptotic programs. Genes necessary for mitotic cell cycle progression and cell division were most prominently enriched in at least two of three time points in whole-genome expression data combined from two cell systems, and all nine genes in these functional categories were strongly repressed, including CENPA, KIF14, KIF23 and RACGAP1. Enforced expression of one selected candidate, RACGAP1, partially rescued the induction of apoptosis caused by HDAC11 depletion. High-level expression of all nine genes in primary neuroblastomas signicantly correlated with unfavorable overall and event-free survival in patients, suggesting a role in mediating the more aggressive biological and clinical phenotype of these tumors. Our study identied a group of cell cycle-promoting genes regulated by HDAC11, being both predictors of unfavorable patient outcome and essential for tumor cell viability. The data indicates a signicant role of HDAC11 for mitotic cell cycle progression and survival of MYCN-amplified neuroblastoma cells, and suggests that HDAC11 could be a valuable drug target.
Neuroblastoma cells depend on HDAC11 for mitotic cell cycle progression and survival.
Cell line, Time
View SamplesPurpose: Identifying target genes of the two human chromatin remodeling enzymes CHD3 and CHD4 Methods: see below in protocols Results: Libraries were sequenced on Illumina HiSeq2000 platform resulting in 37-71 Mio 50 bp paired-end reads per sample. We identified 16 (i) and 115 (ii) distinctly regulated genes when CHD3-GFP (i) or CHD4-GFP (ii) were overexpressed. Nine genes seem to be commonly regulated by CHD3 and CHD4. We successfully validated four genes from our RNA-seq via qPCR with two new (independent from those, used for RNA-seq) biological replicates. Conclusion: CHD3 and CHD4 regulate distinct genes. Overall design: Total RNA was prepared from 24 hours induced (1 ng/µl Dox) and non-induced Flp-In™ T-REx™ 293 cells, expressing GFP, hCHD3-GFP (UniProt: Q12873) or hCHD4-GFP(UniProt Q14839). Library preparation and Illumina Sequencing was perfprmed by EMBL GeneCore facility in Heidelberg (Germany: Dr. Vladimir Benes)
CHD3 and CHD4 form distinct NuRD complexes with different yet overlapping functionality.
Cell line, Subject
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