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accession-icon GSE23889
Transcriptome profiling and expression analyses of genes critical to wheat adaptation to low temperature
  • organism-icon Triticum aestivum
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

Understanding the mechanism of low temperature (LT) adaptation is crucial to the development of cold-tolerant crops. To identify the genes involved in the development of LT tolerance in the crown of hexaploid wheat we examined the global changes in genes expression during cold-treatment using the Affymetrix Wheat Genome Chip.

Publication Title

Genome-wide gene expression analysis supports a developmental model of low temperature tolerance gene regulation in wheat (Triticum aestivum L.).

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26980
Expression data from melanoma cells grown under neural crest cell culture conditions (spheroid cells) versus under classical adherent conditions (adherent cells) - 2 different specimens of melanoma tumors
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Summary: Melanoma spheroids grown under neural crest cell conditions are highly plastic migratory/invasive tumor cells endowed with immunomodulator function

Publication Title

Melanoma spheroids grown under neural crest cell conditions are highly plastic migratory/invasive tumor cells endowed with immunomodulator function.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE56548
PAX6 Regulates Melanogenesis in the Retinal Pigmented Epithelium through Feed-Forward Regulatory Interactions with MITF
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

During organogenesis, PAX6 is required for establishment of various progenitor subtypes within the central nervous system, eye and pancreas. PAX6 expression is maintained in a variety of cell types within each organ, although its role in each lineage and how it acquires cell-specific activity remain elusive. Herein, we aimed to determine the roles and the hierarchical organization of the PAX6-dependent gene regulatory network during the differentiation of the retinal pigmented epithelium (RPE). Somatic mutagenesis of Pax6 in the differentiating RPE revealed that PAX6 functions in a feed-forward regulatory loop with MITF during onset of melanogenesis. PAX6 both controls the expression of an RPE isoform of Mitf and synergizes with MITF to activate expression of genes involved in pigment biogenesis. This study exemplifies how one kernel gene pivotal in organ formation accomplishes a lineage-specific role during terminal differentiation of a single lineage.

Publication Title

PAX6 regulates melanogenesis in the retinal pigmented epithelium through feed-forward regulatory interactions with MITF.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE69524
NCI Sarcoma Cell Line Panel
  • organism-icon Homo sapiens
  • sample-icon 75 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2,coreR3,A20071112,EP.cdf (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sarcoma Cell Line Screen of Oncology Drugs and Investigational Agents Identifies Patterns Associated with Gene and microRNA Expression.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE68591
Exon expression for NCI Sarcoma cell line panel
  • organism-icon Homo sapiens
  • sample-icon 75 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2,coreR3,A20071112,EP.cdf (huex10st)

Description

Characterization of 68 cell lines derived from human sarcoma and 5 normal counterpart cells, including drug sensitivity testing, gene expression profiling and microRNA expression profiling have been completed. Data and tools for searching these data will be made publicly available through the NCI Developmental Therapeutics Program. The raw data (.cel files ) are provided through the GEO website. Sarcoma represents a variety of cancers at arise from cells of mesenchymal origin and have seen limited treatment advances in the last decade. Drug sensitivity data coupled with the transcription and microRNA profiles of a cohort of sarcoma cell lines may help define novel treatment paradigms.

Publication Title

Sarcoma Cell Line Screen of Oncology Drugs and Investigational Agents Identifies Patterns Associated with Gene and microRNA Expression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE66708
NALP3 inflammasome up-regulation and CASP1 cleavage of the glucocorticoid receptor causes glucocorticoid resistance in leukemia cells
  • organism-icon Homo sapiens
  • sample-icon 744 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene Expression Array (primeview), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NALP3 inflammasome upregulation and CASP1 cleavage of the glucocorticoid receptor cause glucocorticoid resistance in leukemia cells.

Sample Metadata Fields

Disease, Cell line, Treatment

View Samples
accession-icon GSE66702
NALP3 inflammasome up-regulation and CASP1 cleavage of the glucocorticoid receptor causes glucocorticoid resistance in leukemia cells [HG-U133A]
  • organism-icon Homo sapiens
  • sample-icon 253 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Glucocorticoids are universally used in the treatment of acute lymphoblastic leukemia (ALL), and glucocorticoid resistance in leukemia cells confers a poor prognosis. To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 newly diagnosed ALL patients and found significantly higher expression of caspase 1 (CASP1) and its activator NLRP3 in glucocorticoid resistant leukemia cells, due to significantly lower somatic methylation of CASP1 and NLRP3 promoters. Over-expression of CASP1 resulted in cleavage of the glucocorticoid receptor, diminished glucocorticoid-induced transcriptional response and increased glucocorticoid resistance. Knockdown or inhibition of CASP1 significantly increased glucocorticoid receptor levels and mitigated glucocorticoid resistance in CASP1 overexpressing ALL. Our findings establish a new mechanism by which the NLRP3/CASP1 inflammasome modulates cellular levels of the glucocorticoid receptor and diminishes cell sensitivity to glucocorticoids. The broad impact on glucocorticoid transcriptional response suggests this mechanism could also modify glucocorticoid effects in other diseases.

Publication Title

NALP3 inflammasome upregulation and CASP1 cleavage of the glucocorticoid receptor cause glucocorticoid resistance in leukemia cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE66705
NALP3 inflammasome up-regulation and CASP1 cleavage of the glucocorticoid receptor causes glucocorticoid resistance in leukemia cells [HG-U133_Plus_2]
  • organism-icon Homo sapiens
  • sample-icon 166 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Human Genome U133A Array (hgu133a)

Description

Glucocorticoids are universally used in the treatment of acute lymphoblastic leukemia (ALL), and glucocorticoid resistance in leukemia cells confers a poor prognosis. To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 newly diagnosed ALL patients and found significantly higher expression of caspase 1 (CASP1) and its activator NLRP3 in glucocorticoid resistant leukemia cells, due to significantly lower somatic methylation of CASP1 and NLRP3 promoters. Over-expression of CASP1 resulted in cleavage of the glucocorticoid receptor, diminished glucocorticoid-induced transcriptional response and increased glucocorticoid resistance. Knockdown or inhibition of CASP1 significantly increased glucocorticoid receptor levels and mitigated glucocorticoid resistance in CASP1 overexpressing ALL. Our findings establish a new mechanism by which the NLRP3/CASP1 inflammasome modulates cellular levels of the glucocorticoid receptor and diminishes cell sensitivity to glucocorticoids. The broad impact on glucocorticoid transcriptional response suggests this mechanism could also modify glucocorticoid effects in other diseases.

Publication Title

NALP3 inflammasome upregulation and CASP1 cleavage of the glucocorticoid receptor cause glucocorticoid resistance in leukemia cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE67045
NALP3 inflammasome up-regulation and CASP1 cleavage of the glucocorticoid receptor causes glucocorticoid resistance in leukemia cells [HG-U133A]
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Glucocorticoids are universally used in the treatment of acute lymphoblastic leukemia (ALL), and glucocorticoid resistance in leukemia cells confers a poor prognosis. To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 newly diagnosed ALL patients and found significantly higher expression of caspase 1 (CASP1) and its activator NLRP3 in glucocorticoid resistant leukemia cells, due to significantly lower somatic methylation of CASP1 and NLRP3 promoters. Over-expression of CASP1 resulted in cleavage of the glucocorticoid receptor, diminished glucocorticoid-induced transcriptional response and increased glucocorticoid resistance. Knockdown or inhibition of CASP1 significantly increased glucocorticoid receptor levels and mitigated glucocorticoid resistance in CASP1 overexpressing ALL. Our findings establish a new mechanism by which the NLRP3/CASP1 inflammasome modulates cellular levels of the glucocorticoid receptor and diminishes cell sensitivity to glucocorticoids. The broad impact on glucocorticoid transcriptional response suggests this mechanism could also modify glucocorticoid effects in other diseases.

Publication Title

NALP3 inflammasome upregulation and CASP1 cleavage of the glucocorticoid receptor cause glucocorticoid resistance in leukemia cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE73162
NCI small cell lung cancer cell line panel
  • organism-icon Homo sapiens
  • sample-icon 76 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [HuEx-1_0-st-v2,coreR3,A20071112,EP.cdf (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Small Cell Lung Cancer Screen of Oncology Drugs, Investigational Agents, and Gene and microRNA Expression.

Sample Metadata Fields

Specimen part, Cell line

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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