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accession-icon GSE51980
CD44 is a negative cell surface marker for pluripotent stem cell identification during human fibroblast reprogramming
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of different iPSC clones in comparison to parental fibroblasts and Pluripotent ESC and iPSC lines

Publication Title

CD44 is a negative cell surface marker for pluripotent stem cell identification during human fibroblast reprogramming.

Sample Metadata Fields

Cell line

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accession-icon GSE55977
Gene expression anaylsis of tumor stimulated human NK cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Genome wide expression profiling of human NK cells stimulated with K562 erythroleukemic tumor cells after four hours of NK-tumor co-culture. Responding NK cells were compared to non-responding NK cells, delineated by display of CD107 on the NK cell surface following cytotoxic granule release. We hypothesized that tumor responses would initiate rapid changes in gene expression in the NK cell that would identify new features of the anti-tumor response of NK cells. Results identify NK cell activation responses and induction of TNF superfamily molecules with immunoregulatory activity.

Publication Title

Licensed human natural killer cells aid dendritic cell maturation via TNFSF14/LIGHT.

Sample Metadata Fields

Specimen part

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accession-icon GSE37967
MicroRNA-198 an inhibitor of keratinocyte migration
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This study identifies miR-198 as a potential inhibitor of keratinocyte migration in skin

Publication Title

'See-saw' expression of microRNA-198 and FSTL1 from a single transcript in wound healing.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE62079
CD73 as a therapeutic target of pancreatic neuroendocrine tumor stem cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Identification and purification of cancer stem cells (CSCs) lead to new therapeutic targets; however, there has been no study to identify and isolated pancreatic neuroendocrine tumor (pNET) CSC. Therefore the clinical significance and its target remain unknown. This study aimed to identify pNET CSCs and characterize therapeutic candidate for pNET CSCs. Methods: We isolated CSCs sorting by ALDH activity in pNET surgical section and cell lines. We verified whether these cells have the property of stemness in vivo and in vitro. Additionally in order to acquire CSC gene profile, genome-wide gene expression profiles were investigated using a microarray technique. Results: ALDHhigh cells, but not control bulk cells, formed spheres, proliferated in hypoxia as well as normoxia and promoted cell motility, which are features of CSCs. Injection of as few as 10 ALDHhigh cells led to subcutaneous tumor formation, and 105 ALDHhigh cells established metastases but not control bulk cells in mice. Comprehensive gene expression analysis revealed that genes associated with mesenchymal stem cell, including CD73, and epithelial-mesenchymal transition (EMT) were overexpressed in ALDHhigh cells. APCP, which is CD73 inhibitor, inhibited sphere formation and cell motility in ALDHhigh cells in vitro, and tumor growth inhibition were observed in ALDHhigh cells in vivo. Conclusions: We identified ALDHhigh cells of pNET and elucidated that they have stemness property. Furthermore we identified CD73 as a target of ALDHhigh cells. CD73 is a promising novel target of pNET CSCs.

Publication Title

CD73 as a therapeutic target for pancreatic neuroendocrine tumor stem cells.

Sample Metadata Fields

Cell line

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accession-icon GSE113925
Tripartite motif-containing 33 (Trim33) determines the pathogenic function of Th17 cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We report that Tripartite motif-containing 33 (Trim33), a protein that was previously associated with TGF-beta signaling, determines the pathogenic function of Th17 cells. Trim33 deficiency in T cells resulted in resistance to an autoimmune disease model. Lack of Trim33 did not impact TGF-beta signaling in mediating Foxp3 gene expression but greatly reduced TGF-beta induction of IL-17 production during Th17 cell differentiation. Importantly, we found TGF-beta not only increased IL-17 but also suppressed IL-10 expression; absence of Trim33 or Smad2 but not Smad4 in T cells enhanced IL-10 expression. In a Smad2-dependent manner, Trim33 was recruited to Il17 and Il10 gene loci and was crucial in appropriate histone modification accompanying Th17 differentiation.

Publication Title

Trim33 mediates the proinflammatory function of Th17 cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP051547
Enhancer-bound LDB1 Regulates a Corticotrope Promoter Pausing Repression Program [GRO-seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Substantial evidence supports the hypothesis that enhancers are critical regulators of cell type determination, orchestrating both positive and negative transcriptional programs; however, the basic mechanisms by which enhancers orchestrate interactions with cognate promoters during activation and repression events remain incompletely understood. Here we report the required actions of the LIM domain binding protein, LDB1/CLIM2/NLI, interacting with the enhancer binding protein, ASCL1, to mediate looping to target gene promoters and target gene regulation in corticotrope cells. LDB1-mediated enhancer:promoter looping appears to be required for both activation and repression of these target target gene promoter genes. While LDB1-dependend activated genes are regulated at the level of transcriptional initiation, the LDB1-dependent repressed transcription units appear to be regulated primarily at the level of promoter pausing, with LDB1 regulating recruitment of MTA2, a component of the NuRD complex, on these negative enhancers, required for the repressive enhancer function. These results indicate that LDB1-dependent looping events can deliver repressive cargo to cognate promoters to mediate promoter pausing events in a pituitary cell type. Overall design: Global Run On (GRO) assay followed by high throughput sequencing (GRO-seq)

Publication Title

Enhancer-bound LDB1 regulates a corticotrope promoter-pausing repression program.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40873
Low SLC22A7 expression in noncancerous liver promotes hepatocellular carcinoma occurrence - a prospective study
  • organism-icon Homo sapiens
  • sample-icon 49 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background & Aims: The recurrence determines the postoperative prognosis of patients with hepatocellular carcinoma (HCC). It is unknown whether de novo HCCs derive from the liver with disability of an organic anion transport. This study was designed to elucidate the link between such transporters and the multicentric occurrence (MO) after radical hepatectomy.

Publication Title

Mitochondrial metabolism in the noncancerous liver determine the occurrence of hepatocellular carcinoma: a prospective study.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE20562
Expression data in mouse liver exposed to low dose-rate radiation
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Expression profiles in mouse liver exposed to long-term gamma-irradiation were examined to assess in vivo effects of low dose-rate radiation. Three groups of male C57BL/6J mice were exposed to whole body irradiation at dose-rates of 17-20 mGy/day, 0.86-1.0 mGy/day or 0.042-0.050 mGy/day for 401-485 days (cumulative doses were approximately 8 Gy, 0.4 Gy or 0.02 Gy, respectively).

Publication Title

Gene expression profiles in mouse liver after long-term low-dose-rate irradiation with gamma rays.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE50836
Mepenzolate bromide displays beneficial effects in a mouse model of chronic obstructive pulmonary disease
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

For the clinical treatment of chronic obstructive pulmonary disease (COPD), it is important not only to improve the airflow limitation by bronchodilation but also to suppress emphysema by controlling inflammation. In this study, we have screened for compounds that prevent elastase-induced airspace enlargement in mice from medicines already used clinically. Mepenzolate bromide, a muscarinic antagonist used to treat gastrointestinal disorders was selected. Intratracheal administration or inhalation of mepenzolate bromide decreased the severity of elastase-induced airspace enlargement, alteration of lung mechanics and respiratory dysfunction. While mepenzolate bromide showed bronchodilatory activity, most of other muscarinic antagonists tested did not improve the elastase-induced pulmonary disorders. Mepenzolate bromide suppressed elastase-induced pulmonary inflammatory responses and production of superoxide anions, and reduced the level of cigarette smoke-induced airspace enlargement and alteration of lung mechanics. Based on these results, we propose that this drug is therapeutically effective for COPD as a consequence of both its anti-inflammatory and bronchodilatory activities.

Publication Title

Mepenzolate bromide displays beneficial effects in a mouse model of chronic obstructive pulmonary disease.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE93050
Tumor suppressor functions of DAXX through histone H3.3 deposition pathway in pancreatic neuroendocrine tumor
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Purpose: Pancreatic neuroendocrine tumors (PanNETs) have considerable malignant potential. Frequent somatic mutations and loss of DAXX protein expression have been frequently found in PanNETs. DAXX is known as a transcriptional repressor, however, molecular functions underlying loss of DAXX remain unclear in PanNETs.

Publication Title

Tumor suppressor functions of DAXX through histone H3.3/H3K9me3 pathway in pancreatic NETs.

Sample Metadata Fields

Treatment

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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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