# _embedded.samples[].characteristics.description[].text
A small RNA library of stomach antrum tissue was sequenced using high-throughput SOLiD sequencing technology. The study aims to provide complementary information of the role of miRNAs in molecular regulation process in the healthy human stomach, in order to establish a reference for future comparisons of altered miRNA expression due to the gastric tract diseases.

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miR-181a1/b1, miR-181a2/b2, and miR-181c/d belong to a highly conserved family of microRNA clusters, yet their role in vivo is poorly understood. Here we show that the miR-181a1/b1 cluster is absolutely essential for NKT development and is a critical determinant of thymocyte proliferation, survival and T-cell receptor ?? locus rearrangement. Furthermore, while individual ablation of miR-181a2/b2 and miR-181c/d revealed no overt phenotypes, compound mutant mice lacking both miR-181a1/b1 and miR-181a2/b2 display decreased survival, reduced body weight, and abnormal B cell development. Mechanistically, we reveal that miR-181 regulates PTEN, a key tumor suppressor whose abundance determines key metabolic adaptations required to meet the biosynthetic demands of highly proliferative tissues. These results provide important insights into the physiological function of this family of microRNAs in vivo; moreover, it places miR-181 as a central regulator of the PI3K signaling pathway and cellular metabolism. Three sorted populations of double positive (DP) thymocytes from each of two conditions (WT and miR181a1/b1 -/- mice)

# _embedded.samples[].characteristics.submission title[].text
Mouse CD4+/CD8+ thymocytes from miR-181a1/b1 KO vs WT

# _embedded.samples[].characteristics.submission description[].text
Dicer is a central enzymatic player in RNA interference (RNAi) pathways that acts to regulate gene expression in nearly all eukaryotes. Although the cytoplasmic function of Dicer is well documented in mammals, there is little known about any possible nuclear function. Here we show that Dicer is present in both the nucleus and cytoplasm, but that its nuclear levels are tightly regulated. In its nuclear manifestation Dicer interacts with RNA polymerase II (Pol II) at actively-transcribed gene loci. Loss of Dicer causes the appearance of endogenous dsRNA, leading to induction of the interferon response pathway and consequent cell death. Our results suggest that Pol II-associated Dicer restricts endogenous dsRNA formation from overlapping non-coding RNA transcription units. Failure to do so has catastrophic effects on cell function. Taken together, we present here a micro (mi)RNA independent role for human nuclear Dicer. DICER ChIP-seq profile in wt 293 HEK cells, and dsRNA-seq profile in wt and DICER-depleted 293 HEK cells

# _embedded.samples[].characteristics.submission title[].text
Human nuclear Dicer restricts the deleterious accumulation of endogenous double strand RNA

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4 Lactococcus lactis subsp. lactis samples from ENA SRA

# _embedded.samples[].characteristics.submission title[].text
4 Lactococcus lactis subsp. lactis samples from ENA SRA

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Reduced representation bisulfite sequencing (RRBS) of hematopoeitic stem/progenitor cells and mature B-cells from wild-type mice and mice transiently expressing Bcl6 under control of the Sca1 promoter. CBAxC57BL/6J mice were engineered to transiently express a Bcl6 cDNA in hematopoeitic stem/progenitor cells under control of the Sca1 promoter and then delete the transgene by cre-mediated recombination upon expression of Cd79a (Sca1-BCL6??). Hematopoeitic stem/progentior cells (HSPC, Sca1+Lin-) from the bone marrow and mature B-cells (B220+) from the peripheral blood were isolated from these mice and wild-type CBAxC57BL/6J mice by fluorescence activated cell sorting. Cells from 6-9 mice were pooled, for a total of 4 experimental conditions. DNA was extracted for each condition and analyzed by reduced representation bisulfite sequencing.

# _embedded.samples[].characteristics.submission title[].text
Transient expression of Bcl6 is sufficient for oncogenic function and induction of mature B-cell lymphoma

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human miRNA expression profile from human U2OS cells which is treated by shDDX1 and control or DNA damage treated or nontreated Genome-wide miRNA expression profiling analyses were performed using microRNA Ready-to-Use PCR array (Human panel I+II, V2.M, Exiqon) according to the manufacturers??? instructions.

# _embedded.samples[].characteristics.submission title[].text
RNA binding protein DDX1 promotes subset of primary miRNA processing

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Jurkat T-cells were latently infected with a defective HIV provirus carrying a GFP reporer gene. The cells were superinfected with a lentiviral vector expressing shRNA to NELF-E. The impact of NELF-depletion on RNAP II distribution on cellular genes and the HIV provirus was measured by ChIP-Seq. Data sets contained between 45 and 56 million mapped reads Four samples were compared: Control shRNA, NELF-E shRNA, Control shRNA plus TNF-a, NELF-E shRNA plus TNF-a.

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It has been shown that DNA demethylation has a pivotal role in the generation of induced pluripotent stem (iPS) cells. However, the underlying mechanism is still unclear. Previous reports indicated that activation-induced cytidine deaminase (Aid) is involved in DNA demethylation in several developmental processes and cell fusion-mediated reprogramming. Based on the reports, we hypothesized that Aid may be involved in DNA demethylation during the iPS cell generation. In this study, we examined the function of Aid in iPS cell generation using Aid knockout (Aid-/-) mice expressing a GFP reporter under the control of a pluripotent stem cell marker, Nanog. By the introduction of Oct3/4, Sox2, Klf4 and c-Myc, Nanog-GFP positive iPS cells could be generated from the fibroblasts and primary B cells of Aid-/- mice. The Aid-/- iPS cells showed normal proliferation and gave rise to chimeras, indicating their capacity for self-renewal and pluripotency. The comprehensive DNA methylation analysis by MBD-sequening demonstrated that there were only a few differences between Aid+/+ and Aid-/- iPS cells. Aid+/+ and Aid-/- iPS colonies were generated from Aid+/+ and Aid-/- MEFs and picked up mechanically. The clones were passaged four times on feeder cells and two times on gelatin-coated dishes to exclude the contamination of feeder cells. Subsequently, the genome was isolated. Four Aid+/+ iPS cell clones and four Aid-/- iPS cell clones were compared. To confirm the validity of MBD-sequencing, four Aid+/+ iPS cell clones were compared with three ES cell clones or three Aid+/+ MEFs.

# _embedded.samples[].characteristics.submission title[].text
Effect of Aid deletion on the global DNA methylation status of iPS cells

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Center for iPS Cell Research and Application (CiRA)

# _embedded.samples[].organization[].Name
Center for iPS Cell Research and Application (CiRA)

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We report here that KSHV viral infection targets the NF-kB pathway which is crucial for cell survival. KSHV protein vFLIP K13 is known to directly interact with cellular protein NEMO of the NF-kB pathway. We used gene expression array to suggets that the interaction of K13 with NEMO is important to activate NF-kB pathway. We employed gene array analysis followed by bioinformatics analyses as well as biological pathways to determine the effect of K13 interaction with Nemo in Jurkat cell line system. Total RNA was isolated isolated using standard RNAeasy kit protocol (Qiagen). Their gene expression profiles were obtained using the Affymetrix Human Genome U133A 2.0 Array.

# _embedded.samples[].characteristics.submission title[].text
NF-kB essential modulator (NEMO) is essential for KSHV-encoded viral FLICE inhibitory protein (vFLIP) K13- induced gene expression and its N-terminal 251 resdidues are sufficent for this process

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We have created mice by performing gastric epithelium-specific knockout of common tumor suppressor genes. Mice with transgene were monitored for spontaneous gastric cancer. Gene expression profiles were obtained from fresh frozen mouse primary gastric cancer samples.

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We report a draft genome assembly of Elizabethkingia meningoseptica strain 502. The sample was isolated from the wound of a repatriated military serviceperson who suffered major trauma from an improvised explosive device (IED) resulting in wounds with extensive environmental contamination. E. meningoseptica was isolated from wounds in both legs. The genome encodes 26 putative beta-lactamases, indicating that the reservoir of these genes in the environment is large.

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1 Elizabethkingia meningoseptica 502 samples from ENA SRA

# _embedded.samples[].characteristics.submission title[].text
1 Elizabethkingia meningoseptica 502 samples from ENA SRA

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The unique cellular state of embryonic stem cells is maintained by pluripotency-associated transcription factors such as OCT4. The transcriptional regulatory circuitries between human and mouse pluripotent stem cells exhibit notable differences. Transposable elements have altered the pluripotency network by contributing new cis-regulatory elements to mammalian genomes. In our study, we found that the expression of HERVH is enriched in human embryonic stem cells (hESCs) and depletion of HERVH in hESCs induced differentiation. To confirm the differentiation phenotype and identify potential downstream target genes of HERVH, we conducted the microarray analysis on hESCs treated with control shRNA against Luciferase and shRNA against HERVH. Total RNA was extracted from cells treated with control shRNA or HERVH shRNA for 5 days. 3 replicates each.

# _embedded.samples[].characteristics.submission title[].text
Determination of genes affected by HERVH depletion

# _embedded.samples[].characteristics.submission description[].text
Innate immune cells control acute eosinophilic lung inflammation induced by cystein proteases. Here we characterize the dynamic change of gene expression profile in basophils, natural helper cells and eosinophils during lung inflammation via cystein protease Examination of mRNA levels in individual cell populations, basophils, natural helper cells and eosinophils of the lung from na??ve mice and papain treated mice.

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Expression profiling by high throughput sequencing

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Having found that LexA degradation was significantly higher under apoptotic like death (ALD) than under SOS conditions, we hypothesized that additional genes tightly regulated by LexA would be transcribed under ALD conditions. We used microarray analysis to test the transcription pattern of up-regulated genes in ALD. We added no NA (n.t.), 100 ??g/ml NA, or 10 ??g/ml NA to cultures of the WT MC4100relA+, or its ??mazEF or ??mazEFlexA3 derivatives.

# _embedded.samples[].characteristics.submission title[].text
Expression data from Escherichia coli after treatment with nalidixic acid (NA)

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The Hebrew University Hadassa Medical School

# _embedded.samples[].organization[].Name
The Hebrew University Hadassa Medical School

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Regulatory proteins can bind to different sets of genomic targets in various cell types or conditions. To reliably characterize such condition-specific regulatory binding we introduce MultiGPS, an integrated machine learning approach for the analysis of multiple related ChIP-seq experiments. MultiGPS is based on a generalized Expectation Maximization framework that shares information across multiple experiments for binding event discovery. We demonstrate that our framework enables the simultaneous modeling of sparse condition-specific binding changes, sequence dependence, and replicate-specific noise sources. MultiGPS encourages consistency in reported binding event locations across multiple-condition ChIP-seq datasets and provides accurate estimation of ChIP enrichment levels at each event. MultiGPS???s multi-experiment modeling approach thus provides a reliable platform for detecting differential binding enrichment across experimental conditions. We demonstrate the advantages of MultiGPS with an analysis of Cdx2 binding in three distinct developmental contexts. By accurately characterizing condition-specific Cdx2 binding, MultiGPS enables novel insight into the mechanistic basis of Cdx2 site selectivity. Specifically, the condition-specific Cdx2 sites characterized by MultiGPS are highly associated with pre-existing genomic context, suggesting that such sites are pre-determined by cell-specific regulatory architecture. However, MultiGPS-defined condition-independent sites are not predicted by pre-existing regulatory signals, suggesting that Cdx2 can bind to a subset of locations regardless of genomic environment. In this study, we characterize the binding of Cdx2 in embryonic stem cells, endodermal cells, and progenitor motor neurons using V5- or FLAG-tagged doxycycline inducible Cdx2 ESC lines (iCdx2). Endoderm and progenitor motor neurons are generated from the ES cells using directed differentiation approaches. The cells are then exposed to Dox to express the tagged Cdx2 construct. The genome-wide binding of the induced full-length Cdx2 transcription factor is profiled using ChIP-seq with an anti-V5 or anti-FLAG antibody. We also examine the binding behavior of a truncated version of the Cdx2 protein, where a protein interaction domain contained in the first 59 amino acids has been deleted. An appropriate pseudo-IP control experiment for these ChIP-seq experiments has been previously submitted under accession number GSM766062.

# _embedded.samples[].characteristics.submission title[].text
Induced Cdx2 binding in embryonic stem cells and endodermal cells

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The study investigated the changes in DNA-methylation and gene expression during granulopoiesis. To this end CMP, GMP, PMC and PMN cell populations were isolated by FACS from bone marrow from healthy donors and analysed by CAGE as well as expression and DNA microarrays. Bisulphite converted DNA from biological triplicate samples of CMP, GMP, PMC and PMN cell poplulations were hybridised to the Illumina Infinium 450k Human Methylation Beadchip.

# _embedded.samples[].characteristics.submission title[].text
Analysis of the DNA methylome and transcriptome in granulopoiesis reveal timed changes and dynamic enhancer methylation

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Transient leukemia (TL) is evident in 5-10% of all neonates with Down syndrome (DS) and associated with N-terminal truncating GATA1-mutations (GATA1s). Here we analyzed the effect of on gene expression upon ectopic expression of Gata1s or Gata1, while simultaneously knocking down endogenous GATA1, in wild-type CD34+-hematopoietic stem and progenitor cells during myeloid differentiation. Ectopic expression of Gata1s, but not Gata1, in wild-type CD34+-hematopoietic stem and progenitor cells induced hyperproliferation of eosinophil promyelocytes in vitro. While GATA1s retained the function of GATA1 to induce eosinophil genes by occupying their promoter regions, GATA1s was impaired in its ability to repress oncogenic MYC and the pro-proliferative E2F transcription network. We lentivirally transduced wild-type CD34+-hematopoietic stem and progenitor cells to ectopically express Gata1s or Gata1, while simultaneously knocking down endogenous GATA1, and cultured them in myeloid differentiation for 0, 4 and 14 days.

# _embedded.samples[].characteristics.submission title[].text
GATA1s induces hyperproliferation of eosinophil precursors in Down syndrome transient leukemia

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Use DNA microarray technology to discover transciprtional insights of HaCaT for continuous exposure to ELF-EMF We used a loop design in this study (details in the 'loop_design.tiff' supplementary file), cDNA microarray experiment consisted of ten RNA samples, including ELF-EMF exposed, UVB irradiated (positive control), and sham exposed samples.

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Study of extremely low frequency electromagnetic field (ELF-EMF) responses of human HaCaT keratinocytes: Control vs. ELF-EMF

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We performed RNA-Seq transcriptomics analyses of the Bordetella holmesii type strain ATCC 51541T under in vitro growth conditions that mimic exposure to the human bloodstream. We sequenced 3 biological replicates of each of the following conditions of exposure to heat-inactivated human serum: 5% serum, 0.5% serum, and a no serum control. RNA-Seq was performed on the Bordetella holmesii type strain ATCC 51541T grown under three conditions: 5% heat-inactivated human serum, 0.5% heat-inactivated human serum, and a no serum control.

# _embedded.samples[].characteristics.submission title[].text
Transcriptomics analysis of the Bordetella holmesii response to human serum exposure

# _embedded.samples[].organization[].Name
University of Maryland School of Medicine

# _embedded.samples[].organization[].Name
University of Maryland School of Medicine