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accession-icon GSE29323
Effects of KLF5 overexpression on renal collecting duct epithelial cell line (mIMCD-3)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Analysis of expression changes in renal collecting duct epithelial cells by adenoviral mediated Krppel like transcription factor 5 (KLF5) overexpression. KLF5 is a key regulator of static and inflammatory stage in renal collecting duct epithelial cells. We thought these results provide insights into downstream genes of KLF5 in renal collecting duct epithelial cells.

Publication Title

Renal collecting duct epithelial cells regulate inflammation in tubulointerstitial damage in mice.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP042124
Genome wide analysis of gene expression in LPS stimulated splenic B cell.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Analysis of class switch recombination, maturation or differenciation of B cells at gene expression levels. The hypothesis tested in the present study was that TLR signaling in B cells plays an pivotal role for class switch, maturation and differenciation. Overall design: Total RNA obtained from cultured splenic B cells. Gene expression compared between control and cKO B cells.

Publication Title

Control of Toll-like receptor-mediated T cell-independent type 1 antibody responses by the inducible nuclear protein IκB-ζ.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE45005
Expression data from renal cortex of ICR-derived Glomerulonephritis (ICGN) mice and ICR mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

ICR-derived glomerulonephritis (ICGN) mice is a novel inbred strain of mice with a hereditary nephrotic syndrome. Deletion mutation of tensin 2 (Tns2), a focal adhesion molecule, has been suggested to be responsible for nephrotic syndrome in ICGN mice, however, existence of other associative factors has been suggested. To identify additional associative factors and to better understand onset mechanism of nephrotic syndrome in ICGN mice, comprehensive gene expression analysis using DNA microarray was conducted. Immune-related pathways were markedly altered in ICGN mice kidney as compared with ICR mice. Furthermore, gene expression level of complement component 1, s subcomponent (C1s), whose human homologue has been reported to associate with lupus nephritis, was markedly low in ICGN mice kidney.

Publication Title

Gene expression analysis detected a low expression level of C1s gene in ICR-derived glomerulonephritis (ICGN) mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE49429
Genome-wide approaches reveal functional VEGF-inducible NFATc1 binding to the angiogenesis-related genes in endothelium
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide approaches reveal functional vascular endothelial growth factor (VEGF)-inducible nuclear factor of activated T cells (NFAT) c1 binding to angiogenesis-related genes in the endothelium.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE49426
Global analysis of NFATc1 targets in human vascular endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns.

Publication Title

Genome-wide approaches reveal functional vascular endothelial growth factor (VEGF)-inducible nuclear factor of activated T cells (NFAT) c1 binding to angiogenesis-related genes in the endothelium.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE65020
Gene expression profiles in E3.0 WT and Klf5 KO embryos
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Klf5 has essential functions during early embryogenesis and in the derivation of ES cells from inner-cell mass of blastocyst. Among Kruppel-like factor (Klf) family members, only Klf5 shows peri-implantation lethal phenotype, but the precise mechanisms still remain unknown. To understand and identify molecular mechanisms, we performed microarray analysis by using E3.0 WT and Klf5 KO embryos when first phenotype of Klf5 deficiency appears.

Publication Title

<i>Klf5</i> maintains the balance of primitive endoderm versus epiblast specification during mouse embryonic development by suppression of <i>Fgf4</i>.

Sample Metadata Fields

Specimen part

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accession-icon GSE78153
Expression data from peritoneal macrophages stimulated with lipid A
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Setdb1 is one of the H3K9 methyltransferases and represses gene expression by H3K9 methylation. In an attempt to elucidate the role of Setdb1 in the TLR4-mediated inflammatory responses, we performed DNA microarray analysis using lipid A (the active component of LPS)-stimulated peritoneal macrophages from macrophage specific Setdb1 KO (KO) and WT mice.

Publication Title

The H3K9 methyltransferase Setdb1 regulates TLR4-mediated inflammatory responses in macrophages.

Sample Metadata Fields

Specimen part

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accession-icon GSE52338
Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Macrophage-inducible C-type lectin (Mincle, Clec4e) is a pathogen sensor that recognizes pathogenic fungi and Mycobactrium tuberculosis. We perfomed microarray analysis using peritoneal macrophages stimulated with TDM, a mycobacterial cell wall glycolipid that is known to be a Mincle ligand.

Publication Title

Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE8646
The Hay Wells Syndrome-Derived TAp63alphaQ540L Mutant Has Impaired Transcriptional and Cell Growth Regulatory Activity
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

p63 mutations have been associated with several human hereditary disorders characterized by ectodermal dysplasia such as EEC syndrome, ADULT syndrome and AEC syndrome . The location and functional effects of the mutations that underlie these syndromes reveal a striking genotype-phenotype correlation. Unlike EEC and ADULT that result from missense mutations in the DNA-binding domain of p63, AEC is solely caused by missense mutations in the SAM domain of p63. We report a study on the TAp63a isoform, the first to be expressed during development of the embryonic epithelia, and on its naturally occurring Q540L mutant derived from an AEC patient. To assess the effects of the Q540L mutation, we generated stable cell lines expressing TAp63a wt, DeltaNp63 alpha or the TAp63 alpha-Q540L mutant protein and used them to systematically compare the cell growth regulatory activity of the mutant and wt p63 proteins and to generate, by microarray analysis, a comprehensive profile of differential gene expression. We found that the Q540L substitution impairs the transcriptional activity of TAp63a and causes misregulation of genes involved in the control of cell growth and epidermal differentiation.

Publication Title

The Hay Wells syndrome-derived TAp63alphaQ540L mutant has impaired transcriptional and cell growth regulatory activity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE52640
Transcript profiling of transgenic rice lines where the OsMADS26 gene is over-expressed or down growing cultivated in standard or osmotic stress condition
  • organism-icon Oryza sativa
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Functional analyses of MADS-box transcription factors in plants have unraveled their role in major developmental programs (e.g; flowering and floral organ identity), in stress-related developmental processes such as abscission, fruit ripening and senescence and the role of some of them in stress response regulation was reported. The aim of this study was to decipher the genes that are under the control of the OsMADS26 transcription factor in rice in standard or osmotic stress condition.

Publication Title

OsMADS26 Negatively Regulates Resistance to Pathogens and Drought Tolerance in Rice.

Sample Metadata Fields

Age, 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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