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accession-icon SRP119486
Characterization of transcriptomics landscape in HUVEC cells exposed to oxidative stress (Small RNA)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The aim of the project was to characterize the transcriptional landscape of human HUVEC cells exposed to oxidative stress (oxstress). In order to do so cell cultures have been exposed to 200uM H2O2 for either 16 hours or 36 hours to induce oxstress. Total ribodepleted RNA obtained from both time points have been sequenced and small RNA for the 16 hours time point have been sequenced as well. Datasets have been characterized and overlapped. This entry contains the dataset of small RNA. Overall design: Two conditions are available: control untreated HUVEC cells and HUVEC cells exposed to 200uM H2O2 for 16 hours. Each condition is available in triplicate. All samples underwent two unpooled rounds of sequencing, for a total of 24 samples.

Publication Title

Central role of the p53 pathway in the noncoding-RNA response to oxidative stress.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE30442
Whole-exome sequencing identifies mutations of BCOR in acute myeloid leukemia with normal karyotype
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Among acute myeloid leukemias (AML) with normal karyotype (CN-AML), NPM1 and CEBPA mutations define WHO provisional entities accounting for ~60% of cases, but the remaining ~40% remains poorly characterized. By whole exome-sequencing (WES) of one CN-AML patient lacking mutations in NPM1, CEBPA, FLT3, MLL-PTD and IDH1, we newly identified a clonal somatic mutation in BCOR (BCL6 co-repressor), a gene located in chromosome X. Further analyses showed that BCOR mutations occurred in 11/262 (4.2%) CN-AML cases and represented a substantial fraction (14/82, 17.1%) of CN-AML patients showing the same genetic background as the index patient subjected to WES.

Publication Title

Whole-exome sequencing identifies somatic mutations of BCOR in acute myeloid leukemia with normal karyotype.

Sample Metadata Fields

Disease

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accession-icon SRP009246
High-resolution profiling and analysis of viral and host small RNAs during human cytomegalovirus infection
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Small RNA deep sequencing analysis was conducted on primary human fibroblasts infected with human cytomegalovirus (HCMV). HCMV-encoded miRNAs accumulated to ~20% of the total smRNA population at late stages of infection, and our analysis led to improvements in viral miRNA annotations and identification of novel HCMV miRNAs. Through crosslinking and immunoprecipitation of Argonaute-bound RNAs from infected cells, followed by high-throughput sequencing (Ago CLIP-seq), we obtained direct evidence for incorporation of all HCMV miRNAs into the endogenous host silencing machinery. Additionally, significant upregulation was observed during infection for a host miRNA cluster containing miR-96, miR-182 and miR-183. We also identified novel non-miRNA forms of virus-derived smRNAs, revealing greater complexity within the smRNA population during HCMV infection. Overall design: High-throughput profiling of smRNAs, Ago1-, and Ago2-associated miRNAs from HCMV-infected fibroblast cells. Wild-type HCMV Towne (Genbank FJ616285.1) was used for these studies.

Publication Title

High-resolution profiling and analysis of viral and host small RNAs during human cytomegalovirus infection.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE52108
Gene expression signature of EGR3 silencing in M12 human prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

EGR3 expression is upregulated in human prostate cancer compared to normal prostate tissue and is associated with absence of relapse, while low EGR3 expression in tumors is predicitive of disease relapse (Pio et al., PLOS One 2013; 8(1):e54096). However the function of EGR3 in prostate cancer is unknown. Human prostate cancer cells M12 containing high levels of EGR3 were used for shRNA-mediated silencing of EGR3. Gene expression analysis of EGR3 knockdown cells reveals a role in inflammation and the existence of a crosstalk with the NFkB pathway.

Publication Title

Early growth response 3 (Egr3) is highly over-expressed in non-relapsing prostate cancer but not in relapsing prostate cancer.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE45544
Ewing sarcoma compared to a normal body map
  • organism-icon Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Primary pediatric Ewing sarcoma (ES), one uncharacterized sarcoma as well as primary and well established ES cell lines were compared to probes of different normal tissues

Publication Title

Distinct transcriptional signature and immunoprofile of CIC-DUX4 fusion-positive round cell tumors compared to EWSR1-rearranged Ewing sarcomas: further evidence toward distinct pathologic entities.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP021476
Transcription-dependent positioning of Structural Maintenance of Chromosome complexes across the genome: RNA-Seq
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Structural Maintenance of Chromosomes (SMC) complexes regulate the chromosome structures essential for proper genome regulation and cell viability. In mammals, the coordinated actions of the SMC complexes condensin I, condensin II and cohesin regulate dynamic chromosome structures throughout the cell cycle, but it is not clear how these complexes are positioned across the genome. We report here that condensin I, condensin II and cohesin occupy active euchromatic regions of the embryonic stem cell genome, but not heterochromatic regions. Like cohesin, we find that condensin II is deposited at active genes by the SMC loading factor Nipbl. The recruitment of Condensin II to active genes is dependent on their transcriptional activation. Subsequent transcriptional elongation by RNA polymerase II distributes condensin II across gene bodies. During mitosis, condensin I occupies the same set of active genes occupied by condensin II during interphase. Thus, SMC complexes are positioned in the genome by transcription-dependent processes, indicating that condensin-dependent condensation mechanisms are preferentially utilized in euchromatic regions. Overall design: RNA-seq in mES cells after known-down of Smc1, CapH2 or Smc2.

Publication Title

Multiple structural maintenance of chromosome complexes at transcriptional regulatory elements.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE56015
Runx+ HSPC, kdrl+ endothelial, and negative cells sorted from DMSO- or Lycorine-treated 3 dpf zebrafish embryos
  • organism-icon Danio rerio
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Zebrafish Gene 1.0 ST Array (zebgene10st)

Description

The zebrafish is a powerful model for the study of hematopoietic stem and progenitor cells (HSPC). We have developed a novel HSPC-specific transgenic line (Runx1+23:GFP). We have used this line in time-lapse live imaging studies to track the migration of HSPC during development. We have also performed a chemical genetic screen to find small molecules that modulate HSPC numbers during development. Treating embryos from 2-3 days post fertilization (2-3 dpf) then fixing for in situ staining with HSPC probes cmyb and runx1, we found the compound lycorine increased HSPC numbers. Applying this compound during time-lapse live imaging showed increased accumulation of Runx+ HSPC in the caudal hematopoietic tissue (CHT). Treatment from 2-3 dpf, then washing off the compound, had a sustained effect on the size of the HSPC with Runx+ numbers higher at 5 and 7 dpf.

Publication Title

Hematopoietic stem cell arrival triggers dynamic remodeling of the perivascular niche.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP056896
Runx1 deficiency decreases ribosome biogenesis and confers stress resistance to hematopoietic stem and progenitor cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The transcription factor RUNX1 is frequently mutated in myelodysplastic syndrome and leukemia. RUNX1 mutations can be early events, creating pre-leukemic stem cells that expand in the bone marrow. Here we show that, counter-intuitively, Runx1 deficient hematopoietic stem and progenitor cells (HSPCs) have a slow growth, low biosynthetic, small cell phenotype and markedly reduced ribosome biogenesis (Ribi). The reduced Ribi involves decreased levels of rRNA and many mRNAs encoding ribosome proteins. Runx1 appears to directly regulate Ribi; Runx1 is enriched on the promoters of genes encoding ribosome proteins, and binds the ribosomal DNA repeats. Runx1 deficient HSPCs have lower p53 levels, reduced apoptosis, an attenuated unfolded protein response, and accordingly are resistant to genotoxic and endoplasmic reticulum stress. The low biosynthetic activity and corresponding stress resistance provides a selective advantage to Runx1 deficient HSPCs, allowing them to expand in the bone marrow and outcompete normal HSPCs. Overall design: Comparison of the phenotypic and molecular properties of normal (Runx1f/f, or WT) versus Runx1 deficient (Mut) hematopoietic stem cells.

Publication Title

Runx1 Deficiency Decreases Ribosome Biogenesis and Confers Stress Resistance to Hematopoietic Stem and Progenitor Cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE103367
Gene expression differences between leukemic cells from Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M mice by microarray
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Results showed that Chd7 deficiency delay Cbfb-MYH11 induced leukemia, to explore the mechanism, We also performed microarray analysis on c-Kit+ leukemic cells to determine gene expression differences between Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M leukemic cells.

Publication Title

<i>Chd7</i> deficiency delays leukemogenesis in mice induced by <i>Cbfb-MYH11</i>.

Sample Metadata Fields

Specimen part

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accession-icon GSE18433
Immortalized colonic epithelial progenitor cells express stem cell markers and differentiate in vitro
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Immortalized colonic epithelial progenitor cells derived from normal human colon biopsies express stem cell markers and differentiate in vitro

Publication Title

Immortalized epithelial cells derived from human colon biopsies express stem cell markers and differentiate in vitro.

Sample Metadata Fields

Sex, Age, Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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