This SuperSeries is composed of the SubSeries listed below.
Phytochrome interacting factors 4 and 5 control seedling growth in changing light conditions by directly controlling auxin signaling.
Age, Specimen part, Treatment
View SamplesAs sessile organisms plants developed a veriety of adaptive responses to the ever changing environment. One of these responses is the shade avoidance syndrome which is composed of different responses like elongation growth, hyponastic leafs or early flowering to shade (low R/FR). Phytochrcome Interacting Factor 4 and 5 are bHLH transcription factors reported to activate gene expression upon perception of low R/FR. Using this miroarray experiment we identified new genes regulated by PIF4 and PIF5 in response to shade and investigated their genome wide role.
Phytochrome interacting factors 4 and 5 control seedling growth in changing light conditions by directly controlling auxin signaling.
Age, Specimen part, Treatment
View SamplesPlants with decreased SWC4 expression levels displayed several pleiotropic phenotypic alterations, suggesting that this gene participates in the regulation of different developmental processes. To evaluate genes whose expression was misregulated in SCW4 RNAi line, we performed RNA-seq differential expression analysis.
Arabidopsis SWC4 Binds DNA and Recruits the SWR1 Complex to Modulate Histone H2A.Z Deposition at Key Regulatory Genes.
Age, Specimen part
View SamplesWe performed a transcriptomic analysis of Pi-starvation and recovery after resupplying Pi in Arabidopsis thaliana (Columbia-0) wild type plants and double mutant spx1,spx2. Results show that SPX1 is a Pi-dependent inhibitor of the transcription factor PHR1, a central regulatory protein in the control of transcriptional responses to Pi starvation.
SPX1 is a phosphate-dependent inhibitor of Phosphate Starvation Response 1 in Arabidopsis.
Age, Specimen part
View SamplesThe main objective of this study is to identify the list of genes differentially expressed between infected with Leishmania braziliensis and non-infected macrophage cultures based on gene expression microarray profiling
Changes in Macrophage Gene Expression Associated with Leishmania (Viannia) braziliensis Infection.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
No sample metadata fields
View SamplesTwo rat hepatic cell lines, WB-F344 and WB311, were characterized for the effect of rapamycin on gene expression. The WB311 cell line, which is tumorigenic and resistant to the growth inhibitory effects of rapamycin, was originally derived from the WB-F344 parental hepatic epithelial cell line. The goal of this experiment was to identify genes that responded to rapamycin in the sensitive cells but not the resistant cells, thereby providing insight into the mechanism of rapamycin resistance.
Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
No sample metadata fields
View SamplesLung alveolarization is a complex process that involves interactions between several cell types and leads to considerable increase in gas-exchange surface area. The step designated secondary septation includes elastogenesis from interstitial fibroblasts.
Gene expression profiling in lung fibroblasts reveals new players in alveolarization.
No sample metadata fields
View SamplesThe interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNFa, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ERa), the pioneer factor FoxA1 and the p65 subunit of the NF-?B transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between estrogen and TNFa signaling at the gene level is also evident in the patterns of ERa and NF-?B binding, which relocalize to new binding sites that are not occupied by either treatment alone. Interestingly, the chromatin accessibility of classical ERa binding sites is predetermined prior to estrogen treatment, whereas ERa binding sites gained upon co-treatment with TNFa require NF-?B and FoxA1 to promote chromatin accessibility de novo. Our data suggest that TNFa signaling recruits FoxA1 and NF-?B to latent ERa enhancer locations and directly impact ERa enhancer accessibility. Binding of ERa to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response. This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer. Overall design: Using GRO-seq and ChIP-seq (ER, FoxA1 and p65) to assay the molecular crosstalk of MCF-7 cells treated with E2, TNFa or both E2+TNFa.
TNFα signaling exposes latent estrogen receptor binding sites to alter the breast cancer cell transcriptome.
No sample metadata fields
View SamplesInfection of RAW264.7 cells with RHku80 parasites or mock-infection for 24 hours
Infection by Toxoplasma gondii specifically induces host c-Myc and the genes this pivotal transcription factor regulates.
Cell line
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