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accession-icon GSE67714
DLX3-dependent p53 signaling network controls keratinocyte cell cycle and squamous tumor growth
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP057020
DLX3 alters transcriptomic profile of adhesion, cell cycle, and cell death in Squamous Cell Carcinoma Cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Reinstatement of DLX3 into SCC13 cells upregulates genes involved with cell cycle exit, signaling, and adhesion whiles downregulates genes involved with cell death, proliferation, and movement. Overall design: We used RNA-sequencing data analysis to assess gene expression in SCC13 cells infected with Adeno-GFP or Adeno-DLX3 in order to understand the effects of DLX3 in a Squamous Cell Carcinoma Cell Line. We identified a specific subset of genes involved in regulation of cell cycle arrest and inhibition of apoptosis.

Publication Title

The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE63049
Role of DLX3 in primary human keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

DLX3 is expressed by differentiated cells in human skin and it has a functional role in epidermal maturation.

Publication Title

The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth.

Sample Metadata Fields

Specimen part

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accession-icon GSE16837
Gene expression data from S. aureus-exposed neutrophils
  • organism-icon Homo sapiens
  • sample-icon 112 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Neutrophil lysis after phagocytosis is a process potentially important in the pathogenesis of community-associated methicillin-resistant S. aureus (CA-MRSA) infection. The mechanism for this process is not currently known. Therefore, to better understand CA-MRSA virulence we used human oligonucleotide microarrays to investigate the mechanism underlying enhanced PMN lysis that occurs after phagocytosis of CA-MRSA.

Publication Title

Rapid neutrophil destruction following phagocytosis of Staphylococcus aureus.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE9308
The ACME and SCCmec Linkage of Virulence with Resistance in the Community Methicillin Resistant S. aureus USA300 Clone
  • organism-icon Staphylococcus aureus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix S. aureus Genome Array (saureus)

Description

The epidemic character of community-associated methicillin resistant Staphylococcus aureus (CA-MRSA), especially the geographically widespread clone USA300, is poorly understood. USA300 isolates carry a type IV staphylococcal chromosomal cassette mec (SCCmec) element conferring -lactam antibiotic class resistance and a putative pathogenicity island, ACME (arginine catabolic mobile element).

Publication Title

The arginine catabolic mobile element and staphylococcal chromosomal cassette mec linkage: convergence of virulence and resistance in the USA300 clone of methicillin-resistant Staphylococcus aureus.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE78227
The maleless gene mitigates global aneuploid effect and evolutionary shift from X to autosomes
  • organism-icon Drosophila melanogaster
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

During sexual dimorphism, the loss of one entire X chromosome in Drosophila males is achieved largely via a broad genome-wide aneuploid effect. Exploring how MSL proteins and two large non coding RNAs (roX1 and roX2) modulate trans-acting aneuploid effect for equality to females, we employ a system biology approach (microarray) to investigate the global aneuploid effect of maleless(mle) mutation by disrupting MSL binding. A large number of the genes (144) that encode a broad spectrum of cellular transport proteins and transcription factors are located in the autosomes of Drosophila melanogaster.

Publication Title

Drosophila maleless gene counteracts X global aneuploid effects in males.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE80489
Transcript expression analysis of the NETotic neutrphils
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Neutrophils are short-lived innate immune cells. Upon encountering appropriate stimuli, neutrophils generate and release neutrophil extracellular traps (NETs), primarily via NADPH oxidase (Nox)-dependent (~2 hours) or Nox-independent NETosis (~15-60 minutes). Ironically, DNA transcription in dying neutrophils remains an enigma. We hypothesized that transcriptional activation, regulated by NETosis-specific kinases, is important to drive the chromatin decondensation necessary for NETosis. For the first time, we show here that (i) the degree of NETosis corresponds to the degree of genome-wide transcription; (ii) kinase-specific transcriptional activation reflects transcriptional firing during different types of NETosis; and (iii) Transcriptomics suggests that NETosis could differentially regulate inflammation. Therefore, we propose that the initial steps of transcriptional firing, but neither transcription per se help to drive NETosis.

Publication Title

Transcriptional firing helps to drive NETosis.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon GSE44073
Liver X Receptors play an antitumoral role in the intestine
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Liver X receptors inhibit proliferation of human colorectal cancer cells and growth of intestinal tumors in mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE44071
Genome-wide analysis of gene expression profile of Intestinal (ILEUM) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Changes in gene expression profile of intestinal (ILEUM) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16. The hypothesis tested in the present study was that LXRa overexpression influence cancer growth modulating lipid metabolism in cancer cells. Results provide the information that LXRa induces genes encoding proteins able to regulate cholesterol efflux.

Publication Title

Liver X receptors inhibit proliferation of human colorectal cancer cells and growth of intestinal tumors in mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE17301
The effect of IFN on human CD8 T cells_with other concomitant signals
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

IFN alpha mediated gene expression pattern. The effect of IFN alpha on human CD8 T cells responding to antigen (signal 1) and costimulatory signals (signal 2) provided by beads coated with anti-CD3 and anti-CD28 mAbs.

Publication Title

Effects of IFN-α as a signal-3 cytokine on human naïve and antigen-experienced CD8(+) T cells.

Sample Metadata Fields

Specimen part, Subject, Time

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)

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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