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accession-icon GSE58033
Interleukin-32 is progressively expressed in Mycosis Fungoides independent of helper T-cell 2 and helper T-cell 9 polarization
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mycosis Fungoides (MF) is typically characterized by a mature CD4+ memory T-cell phenotype, and regarded as a helper T-cell (Th)2-skewed disease. Here, using skin samples from MF (n=21), healthy volunteers (n=17), atopic dermatitis (n=17), and psoriasis (n=9), we performed RT-PCR to show highest interleukin (IL)-32 mRNA expression in MF compared to benign inflammatory diseases, and its increasing expression with disease progression. By immunohistochemistry and immunofluorescence, we confirmed IL-32 protein expression by numerous CD3+CD4+ T-cells and some epidermotropic T-cells in MF lesions. IL-32 is expressed by MyLa cells (MF cell line) and promoted their proliferation and viability in a dose-dependent fashion. IL-32-treated MyLa and HH cells (CTCL cell line) showed upregulation of cell proliferation and survival genes. Of major 'polar' T-cell cytokines, only IFN- mRNA increases with MF progression and positively correlates with IL-32 mRNA expression levels. Th2 cytokines do not show consistent increases with MF progression nor positive correlation with IL-32 mRNA expression levels. Furthermore, by flow cytometry, IL-32 production by circulating activated T-cells in healthy individulas was found in IFN-+ and IFN-- cells but not in IL-4+ or IL-13+ cells. In conclusion, we identified IL-32+ cells as likely tumor cells in MF, and clearly showed that IL-32 mRNA expression levels increase with MF progression. We found that IL-32 mRNA expression levels in MF are significantly higher than those in other skin diseases, and that some IL-32+ T-cells are independent from defined Th subsets. Thus IL-32 may play a unique role in MF progression as an autocrine cytokine.

Publication Title

IL32 is progressively expressed in mycosis fungoides independent of helper T-cell 2 and helper T-cell 9 polarization.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE59307
Aurora kinase A is upregulated in cutaneous T-cell lymphoma and represents a potential therapeutic target
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cutaneous T-cell lymphomas form a heterogeneous group of non-Hodgkin lymphomas characterized by only poor prognosis in advanced stage. Despite significant progress made in the identification of novel genes and pathways involved in the pathogenesis of cutaneous lymphoma, the therapeutic value of these findings has still to be proven. Here, we demonstrate by gene expression arrays that aurora kinase A is one of highly overexpressed genes of the serine/threonine kinase in CTCL. The finding was confirmed by qualitative RT-PCR, Western blotting and immunohistochemistry in CTCL cell lines and primary patient samples. Moreover, treatment with a specific aurora kinase A inhibitor blocks cell proliferation by inducing cell cycle arrest in G2 phase as well as apoptosis in CTCL cell lines. These new data provide a promising rationale for using aurora kinase A inhibition as a therapeutic modality of CTCL.

Publication Title

Aurora Kinase A Is Upregulated in Cutaneous T-Cell Lymphoma and Represents a Potential Therapeutic Target.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE53223
Discrimination of dysplastic nevi from common melanocytic nevi by cellular and molecular criteria
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cellular and molecular differences between DNs and CMNs are not completely understood. Using cDNA microarray, quantitative RT-PCR, and immunohistochemistry, we molecularly characterized DNs and analyzed the difference between DNs and CMNs.

Publication Title

Discrimination of Dysplastic Nevi from Common Melanocytic Nevi by Cellular and Molecular Criteria.

Sample Metadata Fields

Specimen part

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accession-icon GSE24169
Finding direct target genes of VND7
  • organism-icon Arabidopsis thaliana
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The Arabidopsis thaliana NAC domain transcription factor, VASCULAR-RELATED NAC-DOMAIN7 (VND7), acts as a key regulator of xylem vessel differentiation. In order to identify direct target genes of VND7, we performed global transcriptome analysis using Arabidopsis transgenic lines in which VND7 activity could be induced post-translationally. This analysis identified 63 putative direct target genes of VND7, which encode a broad range of proteins, such as transcription factors, IRREGULAR XYLEM proteins and proteolytic enzymes, known to be closely associated with xylem vessel formation. Recombinant VND7 protein binds to several promoter sequences present in candidate direct target genes: specifically, in the promoter of XYLEM CYSTEINE PEPTIDASE1, two distinct regions were demonstrated to be responsible for VND7 binding. We also found that expression of VND7 restores secondary cell wall formation in the fiber cells of inflorescence stems of nst1nst3 double mutants, as well as expression of NAC SECONDARY WALL THICKENING PROMOTING FACTOR3 (NST3, however, the vessel-type secondary wall deposition was observed only as a result of VND7 expression. These findings indicated that VND7 upregulates, directly and/or indirectly, many genes involved in a wide range of processes in xylem vessel differentiation, and that its target genes are partially different from those of NSTs.

Publication Title

VASCULAR-RELATED NAC-DOMAIN7 directly regulates the expression of a broad range of genes for xylem vessel formation.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon SRP032275
Changes in the expression of miR-381 and miR-495 are inversely associated with the expression of the MDR1 gene and development of multi-drug resistance
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Multidrug resistance (MDR) frequently develops in cancer patients exposed to chemotherapeutic agents and is usually brought about by over-expression of P-glycoprotein (P-gp) which acts as a drug efflux pump. MiRNAome profiling using next-generation sequencing identified differentially expressed microRNAs (miRs) between parental K562 cells and MDR K562 cells (K562/ADM) induced by chronic adriamycin treatment. Overall design: MiRNAome profiling in untreated K562 cells and K562 cells exposed to long-term adriamycin treatment

Publication Title

Changes in the expression of miR-381 and miR-495 are inversely associated with the expression of the MDR1 gene and development of multi-drug resistance.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8051
Gene expression in a resistance artery in 2 models of hypertension in the rat
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively.

Publication Title

Vascular microarray profiling in two models of hypertension identifies caveolin-1, Rgs2 and Rgs5 as antihypertensive targets.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE80026
Comparison between WT and apl in a novel in vitro tissue culture system, VISUAL
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

We established a novel in vitro tissue culture system (named VISUAL), in which xylem and phloem differentiation can be induced with Arabidopsis thaliana cotyledons

Publication Title

Vascular Cell Induction Culture System Using Arabidopsis Leaves (VISUAL) Reveals the Sequential Differentiation of Sieve Element-Like Cells.

Sample Metadata Fields

Age, Specimen part, Time

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accession-icon GSE80027
Cell-sorting analysis with SEOR1pro::SEOR1-YFP in a novel in vitro tissue culture system, VISUAL
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Arabidopsis Gene 1.0 ST Array (aragene10st)

Description

We established a novel in vitro tissue culture system (named VISUAL), in which xylem and phloem differentiation can be induced with Arabidopsis thaliana cotyledons

Publication Title

Vascular Cell Induction Culture System Using Arabidopsis Leaves (VISUAL) Reveals the Sequential Differentiation of Sieve Element-Like Cells.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE28183
Expression data in double knockout of HsfA1d and HsfA1e Arabidopsis mutants (KO-HsfA1d/A1e) at 30 min under high-light stress
  • organism-icon Arabidopsis thaliana
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The transcript levels of 560 genes were decreased (less than two-fold), while those of 312 genes were increased (more than two-fold) in the KO-HsfA1d/A1e plants compared with the wild-type plants. The transcript levels of HsfA2, HsfA7a, HsfA7b, HsfB1, and HsfB2a were down-regulated in the KO-HsfA1d/A1e

Publication Title

HsfA1d and HsfA1e involved in the transcriptional regulation of HsfA2 function as key regulators for the Hsf signaling network in response to environmental stress.

Sample Metadata Fields

Specimen part

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accession-icon SRP049458
The RNA editing enzyme ADAR1 is a key regulatory of innate immune responses to RNA
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The ADAR RNA editing enzymes deaminate adenosine bases to inosines in cellular RNAs, recoding open reading frames. Human ADAR1 mutations cause Aicardi-Goutieres Syndrome (AGS) and Adar1 mutant mice showing an aberrant interferon response and death by embryonic day E12.5 model the human disease. Searches have not identified key ADAR1 RNA editing sites recoding immune/haematopoietic proteins but editing is widespread in Alu sequences. We show that Adar1 embryonic lethality is rescued in Adar1; Mavs double mutant mice in which general antiviral responses to cytoplasmic dsRNA are prevented. We propose that inosine bases are epigenetic marks identifying cellular RNA as innate immune ÒselfÓ. Consistent with this idea we show that an editing-active cytoplasmic ADAR is required to prevent aberrant immune responses in Adar1 mutant mouse embryo fibroblasts. No dramatic increase in repetitive transcripts is observed. AGS mutations in ADAR1 affect editing by the interferon-inducible cytoplasmic ADAR1 isoform. Overall design: RNA-seq expression profiling in Adar1 and Adar1/Mavs knockout mice embryos.

Publication Title

The RNA-editing enzyme ADAR1 controls innate immune responses to RNA.

Sample Metadata Fields

No sample metadata fields

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)

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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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