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SRP158979
Homo sapiens
6 Downloadable Samples
Illumina HiSeq 2500
Description
We found that CITED2 is highly expressed in metastatic prostate cancer, and its expression is correlated with poor survival in pateints. In this study, we used an siRNA to decrease CITED2 expression in PC3 cells. A RNA-seq approach was utilized in order to determine global gene expression changes in CITED2 knockdown cells compared to control cells. Overall design: PC3 cells transfected with control siRNAs were used as controls. Cells transfected with siRNAs targeting CITED2 were used as experimental group. Cells were transfected for 72 hr and the analyses were done.
Publication Title
Aberrant expression of CITED2 promotes prostate cancer metastasis by activating the nucleolin-AKT pathway.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 50 Downloadable Samples
Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Altered gene expression in the sphingosine 1-phosphate receptor 2 (S1P2)-deficient or sphingosine 1-phosphate receptor 3 (S1P3)-deficient brain.
Publication Title
Frequent spontaneous seizures followed by spatial working memory/anxiety deficits in mice lacking sphingosine 1-phosphate receptor 2.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 11 Downloadable Samples
- Illumina Genome Analyzer II
Description
We conditionally inactivated mouse Cdx2, a dominant regulator of intestinal development, and mapped its genome occupancy in adult intestinal villi. Although homeotic transformation, observed in Cdx2-null embryos, was absent in mutant adults, gene expression and cell morphology were vitally compromised. Lethality was accelerated in mice lacking both Cdx2 and its homolog Cdx1, with exaggeration of defects in crypt cell replication and enterocyte differentiation. Cdx2 occupancy correlated with hundreds of transcripts that fell but not with equal numbers that rose with Cdx loss, indicating a predominantly activating role at intestinal cis-regulatory regions. Integrated consideration of a mutant phenotype and cistrome hence reveals the continued and distinct requirement in adults of a master developmental regulator that activates tissue-specific genes.
Publication Title
Essential and redundant functions of caudal family proteins in activating adult intestinal genes.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens, Trypanosoma cruzi
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity.
Publication Title
Transcriptome profile of Trypanosoma cruzi-infected cells: simultaneous up- and down-regulation of proliferation inhibitors and promoters.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
DNA methylation plays critical roles in the nervous system and has been traditionally considered to be restricted to CpG dinucleotides in metazoan genomes. Here we show that the single-base resolution neuronal DNA methylome from the adult mouse dentate gyrus consists of both CpG (~75%) and CpH (~25%) methylation (H = A/C/T). Neuronal CpH methylation is conserved in human brains, enriched in low CpG-density regions, depleted at protein-DNA interaction sites, and anti-correlated with gene expression. Functionally, both mCpGs and mCpHs can repress transcription in vitro and are recognized by MeCP2 in vivo. Unlike most CpG methylation, CpH methylation is established de novo during neuronal maturation and requires DNMT3A for active maintenance in post-mitotic neurons. These characteristics of CpH methylation suggest a significantly expanded proportion of the neuronal genome under cytosine methylation regulation and provide a new framework for understanding the roles of this key epigenetic modification in neuronal identity, maturation, plasticity and neurological disorders. Overall design: Three biological replicates (dentate gyrus samples from C57Black6 mice) were analyzed by mRNA-seq
Publication Title
Distribution, recognition and regulation of non-CpG methylation in the adult mammalian brain.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 121 Downloadable Samples
- IlluminaHiSeq2500
Description
Clear cell renal cell carcinoma (ccRCC) initiated from the renal epithelium is the most prevalent histological type of adult kidney cancers. Dissecting intratumoral heterogeneity (ITH) of ccRCC has leveraged to extend our knowledge on how primary tumors harboring driver mutations evolve and spread to other sites. The cellular fractions within and across the primary (pRCC) and metastatic RCC (mRCC) are heterogeneous in both their genetic and biological features determining the variability in clinical aggressiveness and sensitivity to the therapy. To achieve sustainable therapeutic benefit with targeted agents in mRCC, the effective target should focus on signaling pathways that are related to driver mutations occurred early in the clonal evolution of the disease and thus should be common to primary tumor and metastatic sites. Considering that extensive genetic heterogeneity may result in drug response variability among patients and treatment resistance, the tailored strategies for metastatic RCC is urgently needed. Here, we analyze single-cell RNA-seq (scRNA-seq) data from a matched primary RCC (pRCC) and lung metastasis (mRCC) to dissect ITH at the highest resolution to date with the objective of discovering the better therapeutic regimen. Overall design: In order to identify successful clonal propagation from patient to PDX samples and understand pathogenesis from primary to metastatic RCC, we performed whole-exome sequencing (WES, n=4) and matched aCGH (n=4) on bulk tumor samples. And we utilized single-cell RNA sequencing (scRNA-seq) to model and dissect functional heterogeneity acroass primary and metastatic RCC tumors. We checked whether of capturing live one cell, not more cells, in microfluidics by fluorescent microscopic observation. To construct RNA sequencing libraries, we performed further quality controls including adequate quantities and qualities of amplified transcriptomes respectively from single cells. Tumor cells from the parental mRCC (n=34), PDX-mRCC (n=36) and PDX-pRCC (n=46) were finally analyzed in this study after filtering out poor quality cells.
Publication Title
Application of single-cell RNA sequencing in optimizing a combinatorial therapeutic strategy in metastatic renal cell carcinoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Transcriptome profile was obtained from a set of human embryonic stem cell (hESCs) line (WA09: H9) with different passage numbers (P1: 40s, P2: 100s, P3: 200s, P4: 300s passage). Culture adaptation occurs in hESCs during repeated in vitro culture to acquire survival advantage to be highly resistant to various stresses. In special, difference in gene expression profile of cell death or apoptotic gene signature was evident between P1/P2 and P3/P4 hESCs.
Publication Title
Selective Elimination of Culture-Adapted Human Embryonic Stem Cells with BH3 Mimetics.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Intestinal master transcription factor CDX2 controls chromatin access for partner transcription factor binding.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We established whether partner transcription factor binding, chromatin structure, or gene expression is compromised upon loss of partner factors cdx2 or hnf4a in mouse intestinal villi
Publication Title
Intestinal master transcription factor CDX2 controls chromatin access for partner transcription factor binding.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
Description
Our independent analyses using mRNA-Seq, quantitative RT-PCR, and in situ hybridization confirmed a significant up-regulation of Fezf2 in Tbr1-/- neocortex. However, analysis by immunostaining and immunoblotting revealed that SOX5 protein levels were relatively unaltered in late embryonic and neonatal Tbr1-/- cortex. This led us to the hypothesis that TBR1 regulates Fezf2 transcription via direct binding to regulatory sequences near Fezf2. To identify genome-wide TBR1 binding sites in an unbiased and hypothesis-independent manner, we analyzed TBR1-immu-noprecipitated chromatin using deep sequencing (ChIP-Seq). We tested several available anti-TBR1 antibodies and found that none was suitable for immunoprecipitating chromatin of sufficient quality for ChIP-Seq. Thus, we generated a V5-TBR1fusion construct and expressed it in N2A cells. V5-TBR1 was immunoprecipitated using an anti-V5 antibody. DNA-Seq was performed on the Illumina GAIIx platform.
Publication Title
TBR1 directly represses Fezf2 to control the laminar origin and development of the corticospinal tract.
Sample Metadata Fields
No sample metadata fields
View Samples