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accession-icon GSE12748
Weighted Gene Coexpression Network Analysis Identifies Biomarkers in Glycerol Kinase Deficient Mice
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Symptomatic glycerol kinase deficiency (GKD) is associated with episodic metabolic and central nervous system deterioration. We report here the first application of Weighted Gene Co-Expression Network Analysis (WGCNA) to investigate a knockout (KO) murine model of a human genetic disease. WGCNA identified networks and key hub transcripts from liver mRNA of glycerol kinase (Gyk) KO and wild type (WT) mice. Day of life 1 (dol1) samples from KO mice contained a network module enriched for organic acid metabolism before Gyk KO mice develop organic acidemia and die on dol3-4 and the module containing Gyk was enriched with apoptotic genes. Roles for the highly connected Acot, Psat and Plk3 transcripts were confirmed in cell cultures and subsequently validated by causality testing. We provide evidence that GK may have an apoptotic moonlighting role that is lost in GKD. This systems biology strategy has improved our understanding of GKD pathogenesis and suggests possible treatments.

Publication Title

Weighted gene co-expression network analysis identifies biomarkers in glycerol kinase deficient mice.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE18736
Differential Expression of NF-kB target genes in MALT lymphoma with and without chromosome translocation: insights into molecular mechanism
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

MALT lymphoma is characterized by t(11;18)(q21;q21)/API2-MALT1, t(1;14)(p22;q32)/BCL10-IGH and t(14;18)(q32;q21)/IGH-MALT1, which commonly activate the NF-B pathway. Gastric MALT lymphomas harboring such translocation do not respond to H. pylori eradication, while those without translocation can be cured by antibiotics. To understand the molecular mechanism of these different MALT lymphoma subgroups, we performed gene expression profiling analysis of 24 MALT lymphomas (15 translocation-positive, 9 translocation-negative). Gene set enrichment analysis (GSEA) of the NF-B target genes and 4394 additional gene sets covering various cellular pathways, biological processes and molecular functions showed that translocation-positive MALT lymphomas are characterized by an enhanced expression of NF-B target genes, particularly TLR6, CCR2, CD69 and BCL2, while translocation-negative cases were featured by active inflammatory and immune responses, such as IL8, CD86, CD28 and ICOS. Separate analyses of the genes differentially expressed between translocation-positive and negative cases and measurement of gene ontology term in these differentially expressed genes by hypergeometric test reinforced the above findings by GSEA. Finally, expression of TLR6, in the presence of TLR2, enhanced both API2-MALT1 and BCL10 mediated NF-B activation in vitro. Our findings provide novel insights into the molecular mechanism of MALT lymphomas with and without translocation, potentially explaining their different clinical behaviors.

Publication Title

Differential expression of NF-kappaB target genes in MALT lymphoma with and without chromosome translocation: insights into molecular mechanism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8906
Comparative gene expression profiles of T-dependent and T-independent germinal centre B cells in mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Selection of B cells subjected to hypermutation in germinal centres (GC) during T-dependent (TD) antibody responses yields memory cells and long-lived plasma cells that produce high affinity antibodies biased to foreign antigens rather than self-antigens. GC also form in T-independent (TI) responses to polysaccharide antigens but failed selection results in GC involution and memory cells are not generated. To date there are no markers that allow phenotypic distinction of T-dependent and T-independent germinal centre B cells. We have now compared the global gene expression of GC B cells purified from mice immunized with either TD or TI antigens and identified eighty genes that are differentially expressed in TD GC.

Publication Title

Axon growth and guidance genes identify T-dependent germinal centre B cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6787
Expression data from wildtype and Rb-/- fetal liver at e12.5
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Rb null embryos exhibit defective fetal liver erythropoiesis. We used microarrays to compare Wt and Rb null fetal livers and to analyse gene expression differences which accompany and may underlie Rb null fetal liver degeneration, erythroid failure, and erythropoietic island dissolution.

Publication Title

Hypoxic stress underlies defects in erythroblast islands in the Rb-null mouse.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6206
Expression data of untreated or cisplatin-treated wildtype or Rb-/- MEFs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The absence of the Rb tumor suppressor gene changes levels/activities of transcription factors (e.g., E2F and p53) which alter gene expression patterns, related to cell cycle control and cellular response to DNA damage. Cisplatin is a genotoxic chemotherapeutic agent and wildtype or Rb null cells have different sensitivities to cisplatin-induced cytotoxicity.

Publication Title

Elevated poly-(ADP-ribose)-polymerase activity sensitizes retinoblastoma-deficient cells to DNA damage-induced necrosis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE110064
Downregulation of Endothelin Receptor B Contributes to Defective B Cell Lymphopoiesis in Trisomy 21 Pluripotent Cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Individuals with Trisomy 21 (T21) exhibit numerous hematological abnormalities, including reductions in numbers of circulating B and T lymphocytes. To elucidate molecular mechanisms underlying these phenotypes, we differentiated human isogenic disomic and trisomic pluripotent cells, and observed that trisomic cells showed defects in B cell, but not T, cell differentiation. Global gene expression of differentiated, trisomic B cells revealed reduced expression of genes encoding endothelin signaling components, namely the Endothelin Receptor B (Ednrb), and its ligand Endothelin1 (Edn1).. Depletion of Ednrb mRNA in cord blood CD34+ cells led to defective B cell differentiation, supporting an hypothesis that low expression of Ednrb in T21 contributes to intrinsic lymphoid defects. Further evidence for the role of the Ednrb pathway in B cell differentiation was obtained through CRISPR/Cas9 gene targeting in disomic and trisomic iPS cells. Knockout of Ednrb in both cell backgrounds reduced the capacity for B cell differentiation. Collectively, this work identifies downregulation of Ednrb as a causative factor for impaired B lymphocyte generation in trisomic cells, which may contribute to defects in immune function associated with T21. Furthermore, a novel role for endothelin signaling in regulation of B cell development has been identified.

Publication Title

Downregulation of Endothelin Receptor B Contributes to Defective B Cell Lymphopoiesis in Trisomy 21 Pluripotent Stem Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE17479
Effect of auxin signaling on flg22 response
  • organism-icon Arabidopsis thaliana
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Expression data after flg22 treatment on leaf discs in Col-0, 35S:AFB1 and 35S:miR393

Publication Title

The microRNA miR393 re-directs secondary metabolite biosynthesis away from camalexin and towards glucosinolates.

Sample Metadata Fields

Specimen part

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accession-icon GSE17500
Effect of auxin signaling on Pseudomonas syinrgae pv tomato DC3000 response
  • organism-icon Arabidopsis thaliana
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Expression data 24hrs after PstDC3000 inoculation in Col-0, 35S:AFB1 and 35S:miR393.

Publication Title

The microRNA miR393 re-directs secondary metabolite biosynthesis away from camalexin and towards glucosinolates.

Sample Metadata Fields

Specimen part

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accession-icon GSE9201
Identification of genes responding to the activity of the Arabidopsis cytochrome P450 KLUH/CYP78A5
  • organism-icon Arabidopsis thaliana
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The Arabidopsis cytochrome P450 KLUH (KLU)/CYP78A5 promotes organ growth in a non-cell autonomous manner. To identify genes regulated by KLU activity, homozygous klu-2 mutants carrying constructs for EtOH-inducible overexpression of wild-type KLU (35S::AlcR-AlcA::KLU) or of enzymatically inactive KLU protein (35S::AlcR-AlcA::KLUmut) were induced with EtOH and sampled at 90 min and 240 min after induction for gene expression changes.

Publication Title

Control of plant organ size by KLUH/CYP78A5-dependent intercellular signaling.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17049
Parasite strain-specific pathogenesis in murine infections with Trypanosoma brucei
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Different strains of T. brucei induce different degrees of pathology in infected animals, and TREU927-infected mice display greater splenomegaly and anaemia than 247-infected mice. The analysis of differential host gene expression in infected spleens has allowed the identification of which pathways or processes are crucial in determining the progression of disease, for example IL10, LXR/RXR activation and alternative macrophage activation.

Publication Title

Role for parasite genetic diversity in differential host responses to Trypanosoma brucei infection.

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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