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accession-icon GSE11418
Passage dependent gene expression in normal human dermal fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human umbilical vein endothelial cells (HUVECs) formed capillary structures when co-cultured with normal human dermal fibroblasts (NHDFs). HUVEC competence and NHDF supportiveness of cord formation were found to be highly cell-passage dependent with the early passage cells forming more angiogenic cord structures. We thus profiled gene expression in NHDFs with different passages to understand the molecular mechanisms underlying the in vitro angiogenesis control.

Publication Title

Developing and applying a gene functional association network for anti-angiogenic kinase inhibitor activity assessment in an angiogenesis co-culture model.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE38719
Identify the downstream targets of Stat3 by using an engineered mouse ES cell line treated with GCSF and LIF plus PD0325901
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To identify downstream targets of Jak/Stat3 pathways without being distracted by differentiation signalings from MEK/ERK pathway, we exploited a engineered B6 cells, which stably stably expressing a chimeric receptor (GRgp-Y118F). The chimeric receptor can induce the phosphorylation of Stat3 by GCSF without activating the MEK/ERK pathway. To mimic the effect of GCSF, the chimeric B6 cells were also treated with LIF plus a selective MEK chemical inhibitor, PD0325901, to induce LIF/Jak/Stat3 but MEK/ERK pathways.

Publication Title

Gbx2, a LIF/Stat3 target, promotes reprogramming to and retention of the pluripotent ground state.

Sample Metadata Fields

Cell line

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accession-icon SRP052238
Gene expression profile for male SD Rats with and without traumatic brain injury (TBI) by RNA-Seq
  • organism-icon Rattus norvegicus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To investigate the effects of TBI on affecting the gene expressions in the hippocampus of male SD rats by RNA-Seq.. Overall design: Male Sprague–Dawley (SD) rats weighing between 200 and 240 g were housed in cages and maintained in environmentally-controlled rooms (22–24C) with a 12-h light/dark cycle. After acclimatization for 1 week on standard rat chow, the rats were subjected to TBI by fluid percussion injury (FPI) or sham surgery. At 1 week post-surgery the rats were tested for learning abilities, and then were sacrificed by decapitation. The fresh tissues including the hippocampus were dissected out, flash frozen, and stored at -70°C for later transcriptome and DNA methylome sequencing experiments. All experiments were performed in accordance with the United States National Institutes of Health Guide for the Care and Use of Laboratory Animals and were approved by the University of California at Los Angeles Chancellor’s Animal Research Committee.

Publication Title

Traumatic Brain Injury Induces Genome-Wide Transcriptomic, Methylomic, and Network Perturbations in Brain and Blood Predicting Neurological Disorders.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP048804
Identifying genes regulated by Kruppel-like factor-9 by RNA-seq in human glioblastoma stem cells.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation and neural development; however, the molecular basis for KLF9’s diverse contextual functions remains unclear. This study focuses on the functions of KLF9 in human glioblastoma stem-like cells. We establish for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stem-like cells, and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, shows that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation, and identify KLF9-regulated molecular targets applicable to cancer therapeutics. Overall design: Two cell lines were used as biological replicates. Each cell line has one KLF9 induction sample and one control sample.

Publication Title

Kruppel-like factor-9 (KLF9) inhibits glioblastoma stemness through global transcription repression and integrin α6 inhibition.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE30807
Expression data from human mesenchymal stem cell and osteosarcoma cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To determine whether enhanced self-renewal and tumorigenicity in UT2 cells (derived from the second humanmouse xenotransplantation of U2OS cell-formed osteosarcoma tissues) correlate with increased expression of stem/progenitor cell-associated genes, we measured global gene expression in MSC, U2OS and UT2 cells by microarray analysis.

Publication Title

Human osteosarcoma CD49f(-)CD133(+) cells: impaired in osteogenic fate while gain of tumorigenicity.

Sample Metadata Fields

Specimen part

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accession-icon SRP052846
Mus musculus breed:mix C57/bl6-129sv Transcriptome or Gene expression
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

CD19 positive B cells were sorted from spleens in wild type mice and conditional konckout PRMT7 mice. RNA-seq experiments were performed to identify the differential expressing genes.

Publication Title

Histone Arginine Methylation by PRMT7 Controls Germinal Center Formation via Regulating Bcl6 Transcription.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14328
Three non-invasive protein biomarkers for solid-organ transplant rejection found through integrative genomics
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We integrated three transplant rejection microarray studies examining gene expression in samples from pediatric renal, adult renal, and adult heart transplants. We performed one study ourselves and retrieved two others from the NCBI Gene Expression Omnibus (GEO)(GSE4470 and GSE1563). We identified 45 genes that were upregulated in common in acute rejection. Half were involved in one immune-related pathway. Among ten proteins we tested by serum ELISA, three successfully distinguished acute rejection from stable transplants. These were CXCL9, PECAM1, and CD44, with areas under the receiver operating characteristic curves of 0.844, 0.802, and 0.738, respectively. Immunohistochemistry showed that the PECAM1 protein was increased in acute rejection in renal, liver and heart transplants versus normal tissues. Our results show that integrating publicly-available gene expression data sets is a fast, powerful, and cost-effective way to identify serum-detectable diagnostic biomarkers.

Publication Title

Integrative urinary peptidomics in renal transplantation identifies biomarkers for acute rejection.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE64809
Gene Expressoin Profile in the Hypothalamus and Liver of Male Bgn_KO, FMOD_KO and WT Mice at 13 Weeks Old, With and Without DHA (omega-3) Treatment
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Biglycan gene connects metabolic dysfunction with brain disorder.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE38304
Gene Expression Profiles of MYC+ and MYC- mouse Germinal Center B cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Germinal centers (GC) arise within B cell follicles upon antigenic challenge. In the dark zones (DZ) of GCs, B cells proliferate and hypermutate their immunoglobulin genes, and mutants with increased affinity are positively selected in the light zone (LZ) to either differentiate into plasma and memory cells, or re-enter the DZ for further refinement. However, the molecular circuits governing GC positive selection are not known. Here, we show that the GC reaction requires the biphasic regulation of c-MYC expression, involving its transient induction during early GC commitment, its repression by BCL6 in DZ B cells, and its re-induction in a subpopulation of positively selected LZ B cells destined to DZ re-entry. Accordingly, acute disruption of MYC function in vivo leads to GC collapse, indicating an essential role in GC physiology. These results have implications for our understanding of GC selection and the role of MYC deregulation in B cell lymphomas.

Publication Title

The proto-oncogene MYC is required for selection in the germinal center and cyclic reentry.

Sample Metadata Fields

Specimen part

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accession-icon GSE64806
Gene Expressoin Profile in the Liver of Male WT and BGN_KO Mice at 13 Weeks Old
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

To investigate the effects of gene Bgn on affecting brain dysfunction and metabolic disorders by profiling the transcripome in the liver of male Bgn_KO and wild-type (WT, litter mate) mice at 13 weeks old.

Publication Title

Biglycan gene connects metabolic dysfunction with brain disorder.

Sample Metadata Fields

No sample metadata fields

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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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