Carrying out both RNA-seq and Smad1/5 genome-wide chromatin immunoprecipitation and sequencing (ChIP-seq) analyses of mESCs in the naïve or primed states, we revisit the roles of BMP signaling in mESCs. Overall design: RNA-seq analysis in 2 cell types; mESCs and ES-derived EpiSC (ESD-EpiSCs).
BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.
No sample metadata fields
View SamplesDusp5 regulates ERK phosporylation following IL-33 receptor ligation in cultured eosinophils. Dusp5 deficient eosinophils show increased ERK phosphorylation, and as a result are less apoptotic. Since ERK stimulation results in downstream activation of transcription factors, we are utilizing a microarray approach to find alterations in gene expression to uncover potential mechanisms for increased cell survival.
Dusp5 negatively regulates IL-33-mediated eosinophil survival and function.
Specimen part, Treatment
View SamplesSeveral different mechanical signals have been proposed to control the extent and pattern of myocardial growth and remodeling, though this has largely been studied using in vitro model systems that are not representative of intact myocardium or in vivo models in which isolating the effects of individual candidate stimuli is exceedigly difficult. We used a unique tissue culture system that allows the simultaneous control of multiple mechanical inputs and other potentially confounding stimuli (e.g., hormonal).
Effects of stretch and shortening on gene expression in intact myocardium.
Sex, Age
View SamplesAnalysis of expression profiles of human pDC cell line (CAL1) compared to an immature T cell line (MOLT4)
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
No sample metadata fields
View SamplesAnalysis of expression profiles of pDCs from wild type and heterozygous E2-2 mice. Results show the control by E2-2 of the expression of pDC-enriched genes.
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
FOXA1 is a key determinant of estrogen receptor function and endocrine response.
Cell line, Treatment
View SamplesEstrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts.
FOXA1 is a key determinant of estrogen receptor function and endocrine response.
Cell line, Treatment
View SamplesEstrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts.
FOXA1 is a key determinant of estrogen receptor function and endocrine response.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of human germinal center light and dark zone cells and their relationship to human B-cell lymphomas.
Specimen part
View SamplesBevacizumab induces glioblastoma resistance in two in vivo xenograft models. Two cell lines were developed with acquired resistance to bevacizumab. Gene expression difference were analyzed between treated and untreated tumors.
Acquired resistance to anti-VEGF therapy in glioblastoma is associated with a mesenchymal transition.
Specimen part, Treatment
View Samples