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SRP132366
Homo sapiens
12 Downloadable Samples
Illumina HiSeq 4000
Description
We used Illumina-HiSeq4000 to sequence 4sU-labelled RNA samples isolated from unchallenged and DNA damaged HeLa Flp-In cells, which revealed the nature of transcriptional response folowing genotoxic stress and the contribution of P-TEFb kinase in DNA damage-induced gene transcription. Overall design: We mock treated or treated HeLa Flp-In cells for 1 or 2 hr with DMSO, 4-NQO, or 4-NQO + flavopiridol (FP) as indicated below. During the last 30 minutes of the treatments, we labeled the RNA or not with the nucleoside analogue 4-thiouridine (500µM 4sU) for 30 minutes.
Publication Title
P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We used gene array analysis of cortical bone to identify Phex-dependent gene transcripts regulating Fgf23 production and mineralization in Hyp mice. We discovered that activation of Fgf receptor- and Wnt-pathways contribute to increased Ffg23 gene transcription in Hyp bone. We found evidence in Hyp bone for increased expression of Fgf1, Fgf7, and Egr2 in the Fgf-signaling pathway and decrements in Sost and Cpz and increments in Sfrp1 and 4 in the Wnt-signaling pathway. Moreover, activation of Fgf and Wnt-signaling stimulated, whereas Tgf inhibited Fgf23 promoter activity in osteoblasts. We also observed reductions in Bmp1, a metalloproteinase that metabolizes the Fgf23 regulatory extracellular matrix protein Dmp1. These findings suggest that elevation of Fgf23 expression in osteocytes is regulated by interactions between cell surface expression of Phex, extracellular matrix proteins and paracrine effects of Fgf and Wnt. Alterations were also found in enzymes regulating the posttranslational processing and stability of Fgf23, including decrements in the glycosyltransferase Galnt3 and the proprotein convertase Pcsk5. In addition, we found that the Pcsk5 and the glycosyltransferase Galnt3 were decreased in Hyp bone, suggesting that reduced post-translational processing of FGF23 may also contribute to increased Fgf23 levels in Hyp mice. With regards to mineralization, we identified additional candidates to explain the intrinsic mineralization defect in Hyp osteoblasts, including increases in the mineralization inhibitors Mgp and Thbs4, as well as increases in local pH altering factors, carbonic anhydrase 12 (Car12) and 3 (Car3) and the sodium-dependent citrate transporter (Slc13a5). These studies demonstrate the complexity of gene expression alterations in bone that accompanies inactivating Phex mutations and identify novel pathways that may coordinate Fgf23 expression and mineralization of extracellular matrix in Hyp bone.
Publication Title
Novel regulators of Fgf23 expression and mineralization in Hyp bone.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 27 Downloadable Samples
- Illumina HiSeq 3000
Description
We recently reported that single-cell derived isogenic subclones of SKMEL5 cells have differential initial sensitivity to BRAF-inhibitors. In order to probe differences among these subclones, we selected three subclones with unique drug responses: progressing (SK-MEL-5 SC10), stationary (SK-MEL-5 SC07), and regressing (SK-MEL-5 SC01) and performed RNASeq. This study examines differentially expressed genes (DEGs) among the subclones to identify the molecular basis for initial differences in drug sensitivity. Overall design: Transcriptomics analysis between single-cell derived isogenic subclones of BRAF-mutated melanoma cell line, SK-MEL-5
Publication Title
A Nonquiescent "Idling" Population State in Drug-Treated, BRAF-Mutated Melanoma.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 24 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This study compares cardiac induction time-courses using (i) wild-type hESCs subjected to a standard directed differentiation protocol, (ii) EOMES knockout hESCs subjected to the same protocol, and (iii) EOMES KO / TET-ON hESCs subjected to a TET-ON protocol.
Publication Title
Cardiogenic programming of human pluripotent stem cells by dose-controlled activation of EOMES.
Sample Metadata Fields
Cell line, Time
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Ovarian cancer is the fifth leading cause of cancer death among US women. Evidence supports the hypothesis that high-grade serous ovarian cancers (HGSC) may originate in the distal end of the fallopian tube. Although a heterogeneous disease, 96% of HGSC contain mutations in p53. In addition, the p53 signature, or overexpression of p53 protein (usually associated with mutation), is a potential precursor lesion of fallopian tube derived HGSC suggesting an essential role for p53 mutation in early serous tumorigenesis. To further clarify p53-mutation dependent effects on cells, murine oviductal epithelial cells (MOE) were stably transfected with a construct encoding for the R273H DNA binding domain mutation in p53, the most common mutation in HGSC. Mutation in p53 was not sufficient to transform MOE cells, but did significantly increase cell migration. A similar p53 mutation in murine ovarian surface epithelium (MOSE), another potential progenitor cell for serous cancer, was not sufficient to transform the cells nor change migration suggesting tissue specific effects of p53 mutation. Microarray data confirmed expression changes in pro-migratory genes in p53R273H MOE compared to parental cells, which could be reversed by suppressing Slug expression. Combining p53R273H with KRASG12V activation caused transformation of MOE into high-grade sarcomatoid carcinoma when xenografted into nude mice. Elucidating the specific role of p53R273H in the fallopian tube will improve understanding of changes at the earliest stage of transformation and could help develop chemopreventative strategies to prevent the accumulation of additional mutations and reverse progression of the p53 signature thereby, improving survival rates.
Publication Title
Mutant p53 expression in fallopian tube epithelium drives cell migration.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Human ES cells respond to activation of the BMP and WNT signaling by upregulating target genes. A 4h time-point following signaling factor stimulation was chosen to reveal immediate-early induced genes which are likely to be direct targets.
Publication Title
Cardiogenic programming of human pluripotent stem cells by dose-controlled activation of EOMES.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 24 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This study compares directed cardiac differentiation time-courses using (i) HuES6 cells with endogenous ISL1 knockout + inducible ISL1 transgene, and (ii) wild-type HuES6 cells.
Publication Title
Revised roles of ISL1 in a hES cell-based model of human heart chamber specification.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Illumina HiSeq 2500
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling.
Publication Title
Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Saccharomyces cerevisiae
- 23 Downloadable Samples
- Illumina HiSeq 2500
Description
RNA-seq was used to assess mRNA transcript abundance in wild type and fra2? S. cerevisiae (BY4741) cells treated with 2-(6-benzyl-2-pyridyl)quinazoline (BPQ) and CuSO4. BPQ potentiates copper toxicity and in yeast, in common with other organisms, a major cause of copper toxicity is damage of iron-sulphur clusters. Iron sensing within yeast relies on mitochondrial iron-sulphur cluster biosynthesis and therefore treatment with BPQ and copper can be used to mimic iron deficiency. Fra2 is known to be a key component of the iron sensing mechanism; however, this mechanism can operate, to an extent, independently of Fra2. BPQ (+CuSO4) treatment was used with the aim of probing the regulation of the iron regulon of S. cerevisiae and the role of Fra2 in the suppression of the low iron response. This study has uncovered nine new Cth2 target-transcripts, plus a new Aft1 target-gene and paralogous non-target. Fra2 dominates basal repression of the iron regulon in iron-replete cultures, however, Fra2-independent control of the iron regulon is also observed with CTH2 appearing to be atypically Fra2-dependent. Transcripts from untreated and CuSO4 treated cells were included as controls. Overall design: Three independent biological replicates were analysed for each condition (BPQ and CuSO4 treated wild type and fra2? cells, CuSO4 treated wild type and fra2? cells and untreated wild type and fra2? cells)
Publication Title
A chemical potentiator of copper-accumulation used to investigate the iron-regulons of Saccharomyces cerevisiae.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples