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accession-icon SRP161185
HiSeq analysis of human gene expression profile following infection with highly pathogenic avian influenza A virus (H5N1; A/Chicken/Vietnam/0008/04)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Current prophylactic and therapeutic strategies targeting human influenza viruses include vaccines and antivirals. Given variable rates of vaccine efficacy and antiviral resistance, alternative strategies are urgently required to improve disease outcomes. Here we describe the use of HiSeq deep sequencing to analyze host gene expression in primary human alveolar epithelial type II (ATII) cells infected with highly pathogenic avian influenza H5N1 virus. We employed primary human ATII cells isolated from normal human lung tissue donated by patients that underwent lung resection. Human host gene expression following HPAI H5N1 virus (A/Chicken/Vietnam/0008/04) infection of primary ATII cells was analyzed using Illumina HiSeq deep sequencing. Overall design: Human non-tumor lung tissue samples were donated by three anonymous patients undergoing lung resection at Geelong Hospital, Barwon Health, Australia. The research protocols and human ethics were approved by the Human Ethics Committees of Deakin University, Barwon Health and the Commonwealth Scientific and Industrial Research Organisation (CSIRO). An informed consent was obtained from all tissue donors. All research were performed in accordance with the guidelines stated in the National Statement on Ethical Conduct in Human Research (2007). The sampling of normal lung tissue was confirmed by the Victorian Cancer Biobank, Australia.

Publication Title

Deep sequencing of primary human lung epithelial cells challenged with H5N1 influenza virus reveals a proviral role for CEACAM1.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP066204
Next generation sequencing to elucidate the novel function of RORC (RORgamma) in breast cancer
  • organism-icon Homo sapiens
  • sample-icon 141 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Exploring the novel role of RORC (RORgamma) in breast cancer, utilizing NEXTseq with genetic gain and loss of function and pharmacological treatment. Overall design: For loss of function, control-siRNA or RORC-siRNA was transfected for 48h in three cell lines (MCF-7, T-47D and MDA-MB-231). For gain of function, CMV-empty or CMV-RORC was transfected for 48h in MDA-MB-231 cells. Furthermore, the selective RORC antagonist, SR2211 was utilized. MCF-7 cells were treated either DMSO or SR2211 (5uM) for 24h. Total RNA was extracted with the RNeasy kit. NEXTseq was performed for transcriptome analysis.

Publication Title

The Nuclear Receptor, RORγ, Regulates Pathways Necessary for Breast Cancer Metastasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP142313
Paneth cells acquire multi-potency upon Notch activation after irradiation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

In murine models, we find that irradiation of Paneth cells caused a gain of a stem cell-like transcriptome and induced activation of the Notch signaling pathway. This study documents plasticity by Paneth cells, a fully committed cell population to participate in epithelial replenishment following stem cell loss. Overall design: Single-cell dissociation was carried out as previously described (Li et al., 2016; Sato et al., 2011). Cell pellets were washed with cold PBS and re-suspended in FACS buffer. Cells were stained with DAPI, PerCP/Cy5.5-conjugated EpCAM, BUV395-conjugated CD45, and APC/fire 750-conjugated CD24. Cell suspensions were subjected to sorting by BD Biosciences Aria II Flow Cytometer. Single viable intestinal epithelial cells were gated by forward scatter, side scatter, and by negative staining for DAPI and CD45, and positive staining for EpCAM. Subpopulations were further gated based on CD24 and tdTomato (using R-phycoerythrin/PE channel). Paneth cells (tdT+CD24+) and derivative (tdT+CD24-) cells were FACS-sorted from irradiated (5 days after radiation) and non-irradiated 8-14 week old Lyz1CreER; R26R-tdT mice with one dose of tamoxifen adminstration (10mg/mouse), and subjected to total RNA extraction using Qiagen RNeasy Plus Micro kit.

Publication Title

Paneth Cell Multipotency Induced by Notch Activation following Injury.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP017913
Extensive changes in DNA methylation are associated with expression of mutant huntingtin [mRNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

The earliest stages of Huntington’s disease are marked by changes in gene expression that are caused in an indirect and poorly understood manner by polyglutamine expansions in the huntingtin protein (HTT). To explore the hypothesis DNA methylation may be altered in cells expressing mutated HTT, we use reduced-representation bisulfite sequencing (RRBS) to map sites of DNA methylation in cells carrying either wild-type or mutant HTT. We find that a large fraction of the genes that change in expression in the presence of mutant huntingtin demonstrate significant changes in DNA methylation. Regions with low CpG content, which have previously been shown to undergo methylation changes in response to neuronal activity, are disproportionately affected. Based on the sequence of regions that change in methylation, we identify AP-1 and SOX2 as transcriptional regulators associated with DNA methylation changes, and we confirm these hypotheses using genome-wide chromatin immunoprecipitation (ChIP-Seq). Our findings suggest new mechanisms for the effects of polyglutamine-expanded HTT. These results also raise important questions about the potential effects of changes in DNA methylation on neurogenesis and at later stages, cognitive decline in Huntington’s patients. Overall design: mRNA-seq in STHdhQ7/Q7 and STHdhQ111/Q111 cells

Publication Title

Extensive changes in DNA methylation are associated with expression of mutant huntingtin.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE35877
Genome wide binding and expression profiling defines a Bapx1-Sox9 axis in vertebral column, Gut, Spleen and limbs in developing mouse embryo.
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchips

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.

Sample Metadata Fields

Specimen part

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accession-icon SRP010905
Comprehensive analysis of different in vitro insulin resistance models
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

Diet-induced obesity (DIO) predisposes individuals to insulin resistance, and adipose tissue has a major role in the disease. Insulin resistance can be induced in cultured adipocytes by a variety of treatments, but what aspects of the in vivo responses are captured by these models remains unknown. We use global RNA sequencing to investigate changes induced by TNF-a, hypoxia, dexamethasone, high insulin, and a combination of TNF-a and hypoxia, comparing the results to the changes in white adipose tissue from DIO mice. We found that different in vitro models capture distinct features of DIO adipose insulin resistance, and a combined treatment of TNF-a and hypoxia is most able to mimic the in vivo changes. Using genome-wide DNase I hypersensitivity followed by sequencing, we further examined the transcriptional regulation of TNF-a-induced insulin resistance, and we found that C/EPBß key regulator of adipose insulin resistance. Overall design: RNA-seq for 6 insulin resistance conditions and 2 control conditions, Dnase hypersensitivity-seq of 4 conditions and 1 control condition, ChIP-seq on p65 after TNFa treatment.

Publication Title

Analysis of in vitro insulin-resistance models and their physiological relevance to in vivo diet-induced adipose insulin resistance.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP046257
Dicer WT/KO MSC RNA-Seq [total RNA]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-Seq performed on Dicer KO and WT murine mesenchymal stem cells from total RNA MicroRNAs (miRNAs) are small non-coding RNAs that regulates development and disease but induce only moderate repression of directs mRNA targets, suggesting that they coordinate with other modes ofs cellular regulation to effect large changes in gene expression. Ins this work we decouple direct effects of global miRNA loss froms transcriptional changes downstream in a pair of isogenic murines fibroblast cell lines with and without Dicer expression. Wes demonstrate how effects on direct miRNA targets are amplified bys transcription machinery through the construction of a network models that identifies specific transcription factors that cause changes ins mRNA expression upon Dicer loss. Through transcription factors over-expression, we delineate miRNA-mediated transcriptional programss and identify miRNA-mediated coherent and incoherent feed-forwards loops, suggesting a functional role of the interaction between miRNAss and transcription factors. In total, our results indicate thats miRNAs tightly control transcription factors within a denses interconnected network to modulate gene expression. Overall design: Total RNA was analyzed from adult mesenchymal stem cells (immortalized monoclonal lines of murine MSCs) with and without Dicer (WT: Dicer f/f, KO: Dicer -/-), as well as from WT cells transfected with an empty vector or a vector containing Tead4, Sox9 or Pbx3 transcripts.

Publication Title

Elucidating MicroRNA Regulatory Networks Using Transcriptional, Post-transcriptional, and Histone Modification Measurements.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE31853
Expression data from oral squamous cell carcinoma (OSCC)-derived cell lines and normal oral keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Oral squamous cell carcinoma (OSCC) is a lethal disease and early death usually occurs as a result of local invasion and regional lymph node metastases. We used microarrays to identify down or upregulated genes in OSCCs compared with non-malignant controls.

Publication Title

Upregulation of Eps8 in oral squamous cell carcinoma promotes cell migration and invasion through integrin-dependent Rac1 activation.

Sample Metadata Fields

Disease, Disease stage, Cell line

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accession-icon GSE35898
Gene Expression profile of Sox9 sorted cells from Vertebral column of E12.5 wildtype (WT) and Homozygous (HOMO) mouse embryos
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchips

Description

This study aims to look at gene expresion profiles between wildtype and Sox9 knockout cells of the vertebral column in a E12.5 mouse embryo. Instead of looking at the whole vertebral column, only cells expressing Sox9 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.

Publication Title

In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.

Sample Metadata Fields

Specimen part

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accession-icon GSE35652
Gene Expression profiles of Bapx1 sorted cells from hindlimbs (HL) of wildtype (WT) and Bapx1 null (HOMO) E12.5 mouse embryos
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchips

Description

This study aims to look at gene expresion profiles between wildtype and Bapx1 knockout cells of the hindlimbs in a E12.5 mouse embryo. Instead of looking at the whole hindlimbs,only cells expressing Bapx1 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.

Publication Title

In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.

Sample Metadata Fields

Specimen part

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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