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accession-icon GSE8772
KINK-1, a novel small-molecule inhibitor of IKKbeta, enhances susceptibility of melanoma cells to antitumoral treatment
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Interference with chemoresistance to enhance the efficacy of chemotherapeutics may be of great utility for cancer therapy. We have identified KINK-1 (Kinase Inhibitor of NF-kappaB-1), a highly selective small-molecule IKKkappa inhibitor, as a potent suppressor of both constitutive and induced NF-kappaB activity in melanoma cells. While KINK-1 profoundly diminished various NF-kappaB-dependent gene products regulating proliferation, cytokine production or anti-apoptotic responses, the compound by itself showed little antiproliferative or pro-apoptotic activity on the cellular level. However, its combination with some cytostatics markedly enhanced their antitumoral activities in vitro, and doxorubicin-induced NF-kappaB activation, a mechanism implicated in chemoresistance, was abrogated by KINK-1. In addition, when KINK-1 was combined with doxorubicin in an in vivo melanoma model, experimental metastasis was significantly diminished as compared to either treatment alone. Induction of chemoresistance by KINK-1 in vivo was not observed. Thus, KINK-1 or related substances might increase the susceptibility of tumors to chemotherapy.

Publication Title

KINK-1, a novel small-molecule inhibitor of IKKbeta, and the susceptibility of melanoma cells to antitumoral treatment.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE74297
MALT1 protease activity controls the expression of inflammatory genes in keratinocytes upon Zymosan stimulation
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

The protease activity of the paracaspase MALT1 plays an important role in antigen receptor-mediated lymphocyte activation by controlling the activity of the transcription factor NF-kB and is thus essential for the expression of inflammatory target genes.

Publication Title

MALT1 Protease Activity Controls the Expression of Inflammatory Genes in Keratinocytes upon Zymosan Stimulation.

Sample Metadata Fields

Treatment

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accession-icon GSE140882
Targeting chronic NFAT activation with calcineurin inhibitors in diffuse large B-cell lymphoma
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Diffuse large B-cell lymphoma (DLBCL) represents the most common form of lymphoma. We could show that in DLBCL cell lines the transcription factor NFAT is constitutively activated and drives the survival of a DLBCL subset. Aim of the analysis was to identify NFAT target genes in a NFAT-dependent (HBL-1) or -independent (HT) DLBCL cell line. To block NFAT activity, the DLBCL cells were treated with the calcineurin inhibitor cyclosporin A (CsA) up to 48 h. With this approach, we identified several survival-related NFAT target genes in HBL-1 cells that might explain the toxic effects of calcineurin inhibitors.

Publication Title

Targeting chronic NFAT activation with calcineurin inhibitors in diffuse large B-cell lymphoma.

Sample Metadata Fields

Treatment

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accession-icon SRP090989
Altered hepatic lipid metabolism in mice lacking both the melanocortin type 4 receptor and low density lipoprotein receptor
  • organism-icon Mus musculus
  • sample-icon 83 Downloadable Samples
  • Technology Badge IconIllumina HiScanSQ

Description

In this study we investigated the effect of normal chow (0 % cholesterol) or a semisynthetic diet (high sugar, 0.02 % cholesterol) fed to mice lacking either Mc4r, Ldlr or both and wildtype animals (total of 4 genotypes) by generating an expression profile of their livers after 6 months by RNA sequencing. Overall design: We investigated mice lacking either Mc4r, Ldlr or both and wildtype animals fed with normal chow or a semisynthetic diet with 10 replicates for each of the 8 resulting groups (4 genotypes * 2 diets).

Publication Title

Severe Atherosclerosis and Hypercholesterolemia in Mice Lacking Both the Melanocortin Type 4 Receptor and Low Density Lipoprotein Receptor.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE65058
Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients.

Sample Metadata Fields

Sex, Specimen part, Disease stage

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accession-icon GSE64998
Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients [transcriptome analysis]
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Type 2 diabetes is a complex disease associated with many underlying pathomechanisms. Epigenetic regulation of gene expression by DNA methylation has become increasingly recognized as an important component in the etiology of type 2 diabetes. We performed genome-wide methylome and transcriptome analysis in liver from severely obese patients with or without type 2 diabetes to discover aberrant pathways underlying the development of insulin resistance. We identified hypomethylation of five key genes involved in hepatic glycolysis, de novo lipogenesis and insulin resistance with concomitant increased mRNA expression and protein content. The CpG-site within the ATF-motif was hypomethylated in four of these genes in liver of non-diabetic and type 2 diabetic obese patients, suggesting epigenetic regulation of transcription by altered ATF-DNA binding. In conclusion, severely obese non-diabetic and type 2 diabetic patients have distinct alterations in the hepatic methylome and transcriptome and genes controlling glucose and lipid metabolism are hypomethylated at a regulatory site. Thus, obesity may epigenetically reprogram the liver towards increased lipid production and exacerbate the development of insulin resistance.

Publication Title

Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients.

Sample Metadata Fields

Sex, Specimen part, Disease stage

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accession-icon SRP057563
Investigating GPR34 expression regulation using whole transcriptome sequencing of spleens and dendritic cells from wildtype and GPR34 knockout mice
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiScanSQ, Illumina HiSeq 2500

Description

Naive spleens as well as naive and LPS-treated dendritic cells from wildtype and GPR34-/- mice were sequenced to integrate expression profiles with protein interaction networks and find functional modules that are affected by GPR34 Overall design: Expression profiles of dendritic cells and whole spleens were generated using Illumina HiSeq 2500/ Illumina HiScan

Publication Title

Dendritic Cells Regulate GPR34 through Mitogenic Signals and Undergo Apoptosis in Its Absence.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP186637
Circadian transcriptome in mouse skeletal muscle after exercise in the early rest versus active phase
  • organism-icon Mus musculus
  • sample-icon 116 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We performed the circadian transcriptome analysis using the skeletal muscle from sedentary and exercised mice either in the early rest phase (ZT3) or in the early active phase (ZT15). By the combination with circadian transcriptomic and metabolomic analysis, we revealed time-of-day-dependent remodeling of circadian muscular metabolic pathways involved in glucose and glycerol metabolism after exercise. We found that only exercise in the early active phase elevates the levels of genes encoding glycolytic enzymes followed by the activation of fatty acid oxidation, branched-chain amino acid catabolism and ketogenesis/ketosis. This study demonstrates that time-of-day is a critical factor to modulate the impact of exercise on metabolic pathways within skeletal muscle. Overall design: Skeletal muscles from sedentary (sham-exercise) mice and mice subjected to acute treadmill exercise either in the early rest phase (ZT3) or in the early active phase (ZT15) were harvested after 0, 4, 8, 12, 16, and 20 hours after exercise or sham-exercise treatment.

Publication Title

Time of Exercise Specifies the Impact on Muscle Metabolic Pathways and Systemic Energy Homeostasis.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE43854
Expression data from primary osteoblasts isolated from calvaria of Gnptab(c.3082insC) knock-in mice compared with osteoblasts isolated from wild-type littermates
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mucolipidosis type II (MLII) is a severe inherited multisystemic disorder caused by mutations in the GNPTAB gene. Skeletal abnormalities are a predominant feature of MLII. Here we investigate the gene expression in a knock-in mouse model for mucolipidosis type II, generated by the insertion of a cytosine in the murine Gnptab gene (c.3082insC) that is homologous to a homozygous mutation in an MLII patient.

Publication Title

Decreased bone formation and increased osteoclastogenesis cause bone loss in mucolipidosis II.

Sample Metadata Fields

Specimen part

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accession-icon GSE52220
Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Conditional ablation of Ezh2 in the neural crest lineage results in loss of the neural crest-derived mesenchymal derivatives. In this data sheet we determine gene expression analysis in Ezh2lox/lox and Wnt1Cre Ezh2lox/lox in E11.5 mouse BA1 cells.

Publication Title

Ezh2 is required for neural crest-derived cartilage and bone formation.

Sample Metadata Fields

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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