Latent HIV-1 infection represents a barrier to virus eradication as latent HIV-1 is impervious to the effects of antiretroviral drugs and can avoid detection by the host immune system. Strategies to clear latent HIV-1 infection in patients have so far failed in clinical trials to increase the decay rate of the latent reservoir underscoring the need for continued study of HIV-1 latency. In this study, a genome-wide RNAi screen was performed to probe cellular factors involved in maintaining HIV-1 latency in HeLa cells latently infected with an HIV-1 reporter virus.
No associated publication
Specimen part, Cell line
View SamplesRNA from wt and SIN1 knock-out MEF cell lines were compared
mTORC2 Responds to Glutamine Catabolite Levels to Modulate the Hexosamine Biosynthesis Enzyme GFAT1.
Specimen part
View SamplesMice lacking topoisomerase II (Top II) are known to exhibit a perinatal death phenotype. In the current study, transcription profiles of the brains of wild type and top2 knockout mouse embryos were generated. Surprisingly, only a small number (1-4%) of genes were affected in top2 knockout embryos. However, the expression of nearly 30% of developmentally regulated genes was either up- or down-regulated.
Role of topoisomerase IIbeta in the expression of developmentally regulated genes.
Sex, Specimen part
View SamplesThe present study was to investigate the differentially expressed genes in 24-hour-old (containing proliferative cardiomyocytes), 7-day-old (containing the burst of proliferative cardiomyocytes), and 10-week-old (containing growth-arrested cardiomyocytes) C57BL/6 mouse hearts using global gene expression profiles.
Global gene expression analysis combined with a genomics approach for the identification of signal transduction networks involved in postnatal mouse myocardial proliferation and development.
Specimen part
View SamplesCharacterization of the global transcriptome of bacterial strains carrying IncA/C plasmids, mapping of fitness compensatory mutations in strains carrying IncA/C plasmids and targeted pull-downs of DNA associated with proteins of interest.
No associated publication
None
Specimen part, Disease, Cell line
View SamplesMED1 is a transcriptional coactivator for gene-specific activators involved in growth and development, we were interested in identifying MED1 target genes potentially involved in prostate development by cDNA microarray. Med1 was conditional knocked out in mice prostate. We performed cDNA microarray with two sets: (1) RNA isolated from three WT ventral prostates and three MT ventral prostates; (2) RNA isolated from three WT lateral prostates and three MT lateral prostates.
No associated publication
Age, Specimen part
View SamplesTo understand molecular mechanisms underlying the synergy of Rb loss and E2F8 loss, we used gene expression profiling to assess molecular changes in Mx1-Cre-mediated knockout (KO) mice using RNA isolated from sorted Ter119+CD71high Erythroblasts.
Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation.
Specimen part
View SamplesTumor associated mutant p53 proteins often gain new functions for tumorigenesis and tumor progression. It has been shown that mutant p53 can transcriptionally regulate a group of genes, which in turn contributes to mutant p53 gain of function. A mutant p53 interacting protein Pontin binds to mutant p53 and promotes its gain of function. This experiment tests whether the interaction of Pontin with mutant p53 regulates the transcriptional activity of mutant p53.
No associated publication
Specimen part, Cell line
View SamplesAnalysis of the transcriptome of mouse models of prostate cancer to assemble a mouse prostate cancer interactome.
Cross-species regulatory network analysis identifies a synergistic interaction between FOXM1 and CENPF that drives prostate cancer malignancy.
Treatment
View SamplesTo investigate the role of NKX3.1 in prostate differentiation, we employed transcriptome analysis of mouse seminal vesicle (from 15-month-old Nkx3.1+/+ mice); mouse prostate (from 4-month-old Nkx3.1+/+ and Nkx3.1-/- mice); human prostate cells (RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression); and tissue recombinants (generated from combining engineered mouse epithelial cells (seminal vesicle epithelial cells or prostate epithelial cells from 2-month-old mice) and rat UGS mesenchymal cells). Mouse tissue or human cells were snap frozen for subsequent molecular analysis.
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Cell line
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