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accession-icon GSE97172
Targets of Bmi1 in HCC pathogenesis
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE97170
Gene expression in the liver of Bmi1 knockout mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To explore the potential targets of Bmi1 in the liver development of hepatic carcinogenesis, we assayed the gene expression level in the liver of Bmi1 knockout mice. We isolated the liver tissue of Bmi1 WT and KO mice around 6-8 weeks. Then we extracted total RNA and run the microarray detection. Gene expression in Bmi1 KO mouse livers was compared with that in Bmi1 WT mouse livers to screen potential targets of Bmi1.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE97169
Gene expression in the Bmi1 knockout Huh7 and Hep3B cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Bmi1 plays a pivotal role in hepatic carcinoma (HCC), but its targets in HCC is unknown. To screen the potential targets, we transfected HCC cell line Huh7 and Hep3B with Bmi1 shRNA lenti-virus. After confirming the Bmi1 was knocked down using western blotting, we extracted total RNA and then run the microarray detection. Gene expression profiles in Bmi1 KO cells were compared with those in Bmi1 WT cells to screen potential targets of Bmi1.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE105763
MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-cell Acute Lymphoblastic Leukemia
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Little is known about the roles of methyl-CpG-binding domain protein 2 (MBD2), a reader of DNA methylation, in T-cell acute lymphoblastic leukemia (T-ALL). Here, we investigated the role of MBD2 in T-ALL by using an Mbd2 knockout mouse model. We found that MBD2 ablation impeded the progression and maintenance of Notch1-driven T-ALL.Our data reveals essential roles for MBD2 in lymphopoiesis and T-ALL and support an intriguing potential of MBD2 as a therapeutic target for T-ALL.

Publication Title

MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-ALL.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE87850
Expression data of siFAM210B and control A549 cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Our previous study screened a novel cancer progression suppressor gene, FAM210B, which encodes an outer mitochondrial membrane protein, by the suppression of mortality by antisense rescue technique (SMART). We demonstrated that FAM210B loss was significantly associated with cancer metastasis and decreased survival in a clinical setting.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE75543
miRNA and mRNA profiles in the genetic hypercalciuric stone-forming (GHS) rat compared to normal SD rat
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative microRNA-gene expression network analysis in genetic hypercalciuric stone-forming rat kidney.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE75542
Analysis of altered mRNA expression profiles in the genetic hypercalciuric stone-forming (GHS) rat compared to normal SD rat
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Urolithiasis is a common desease to human beings, and idiopathic hypercalciuria (IH) is an important risk factor of calcium urolithiasis, previous studies strongly suggested that the decreased tubular Ca2+ reabsorption played a key role of hypercalciuria. However,the molecular mechanism of IH-urolithiasis formation is still not completely elucidated. GHS rat is regarded as an ideal animal model of calcium urolithiasis, reveals many identical pathophysiologic characteristics with IH patients . We analyzed mRNA expression profiles of the kidney of GHS rat in order to find out the target genes and signaling pathways in the pathogenesis of IH.

Publication Title

Integrative microRNA-gene expression network analysis in genetic hypercalciuric stone-forming rat kidney.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE93695
Antidyskinetic effects of MEK inhibitor are associated with multiple neurochemical alterations in the striatum of hemiparkinsonian rats
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

L-DOPA-induced dyskinesia (LID) represents one of the major problems of the long-term therapy of patients with Parkinson's disease (PD). Although the pathophysiologic mechanisms underlying LID are not completely understood, activation of the extracellular signal regulated kinase (ERK) is recognized to play a key role. ERK is phosphorylated by mitogen-activated protein kinase kinase (MEK), and thus MEK inhibitor can prevent ERK activation. Here the effect of the MEK inhibitor PD98059 on LID and the associated molecular changes were examined. Rats with unilateral 6-OHDA lesions of the nigrostriatal pathway received daily L-DOPA treatment for three weeks, and abnormal involuntary movements (AIMs) were assessed every other day. PD98059 was injected in the lateral ventricle daily for 12 days starting from day 10 of L-DOPA treatment. Striatal molecular markers of LID were analyzed together with gene regulation using microarray. The administration of PD98059 significantly reduced AIMs. In addition, ERK activation and other associated molecular changes including FosB were reversed in rats treated with the MEK inhibitor. PD98059 induced significant up-regulation of 418 transcripts and down-regulation of 378 transcripts in the striatum. Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Analysis of protein levels showed that PD98059 reduced the striatal TH. These results support the association of p-ERK1/2, FosB, p-H3 to the regulation of TH and ARNT in the mechanisms of LID, and pinpoint other gene regulatory changes, thus providing clues for identifying new targets for LID therapy.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage

View Samples
accession-icon GSE71459
Different expression patterns in leukemia cells caused by decreased expression of TNF-
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To design an effective antibody therapy to improve clinical outcomes in leukemia, the identification of novel cell surface antigens is needed. Herein, we demonstrate a role for transmembrane tumor necrosis factor-in leukemia. To characterize tmTNF- expression in acute leukemia, normal hematopoietic cells, and non-hematopoietic tissues, we used a monoclonal antibody, termed C1, which specifically recognizes the tmTNF- domain. We found that tmTNF- was preferentially expressed by acute leukemia and leukemia stem cells. More abundant expression correlated with poor risk stratification, extramedullary infiltration, and adverse clinical parameters. Moreover, knockdown of tmTNF-+ expression rendered leukemia cells more sensitive to chemotherapy in vitro and delay regeneration of leukemia in NODSCID mice. Targeting tmTNF- by C1 resulted in leukemia cell killing via antibody-dependent cell-mediated and complement -dependent cytotoxicity in vitro, and inhibited leukemia cell growth in vivo while simultaneously sparing normal hematopoietic cells. Notably, C1 administration impaired the regeneration of leukemia in secondary serial transplantationin to NOD-SCID mice.

Publication Title

Transmembrane TNF-α preferentially expressed by leukemia stem cells and blasts is a potent target for antibody therapy.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE19882
Expression data from human lymphoma endothelium and reactive lymph node-derived endothelium
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Angiogenesis plays a key role in tumor metastasis. Many genes may act in this process including formation of vessels, immune evasion,etc. Different gene expression profiles between lymphoma endothelium cells and reactive lymph node-derived endothelium cells may uncover these genes. And intensive mechanism researches on such key genes may explain the mechanisim of tumor-specific angiogenesis and help to explore effective treatment strategies to prevent/reverse tumor metastasis.

Publication Title

Lymphoma endothelium preferentially expresses Tim-3 and facilitates the progression of lymphoma by mediating immune evasion.

Sample Metadata Fields

Specimen part

View Samples
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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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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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