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accession-icon GSE38754
Temporal changes of gene expression in mouse heart, kidney and lung during juvenile growth
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon

Description

Temporal changes of gene expression from 1-wk- to 4-wk and 8-wk-old mouse in heart, kidney and lung. Mammalian somatic growth is rapid in early postnatal life but then slows and eventually ceases in multiple tissues. We hypothesized that there exists a postnatal gene expression program that is common to multiple tissues and is responsible for this coordinate growth deceleration. Consistent with this hypothesis, microarray analysis identified >1600 genes that were regulated with age coordinately in kidney, lung, and heart of juvenile mice, including many genes that regulate proliferation. As examples, we focused on three growth-promoting genes, Igf2, Mest, and Peg3, that were markedly downregulated with age. We conclude that there exists an extensive genetic program occurring during postnatal life. Many of the involved genes are regulated coordinately in multiple organs, including many genes that regulate cell proliferation. At least some of these are themselves apparently regulated by growth, suggesting that, in the embryo, a gene expression pattern is established that allows for rapid somatic growth of multiple tissues but then, during postnatal life, this growth leads to negative-feedback changes in gene expression that in turn slow and eventually halt somatic growth, thus imposing a fundamental limit on adult body size.

Publication Title

An extensive genetic program occurring during postnatal growth in multiple tissues.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE24873
IL-17-induced NF-kB activation via CIKS/Act1: Physiologic significance and signaling mechanisms
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon

Description

Interleukin-17 (IL-17) is essential in host defense against extracellular bacteria and fungi, especially at mucosal sites, but it also contributes significantly to inflammatory and autoimmune disease pathologies. Binding of IL-17 to its receptor leads to recruitment of the adaptor protein CIKS/Act1 via heterotypic association of their respective SEFIR domains and to activation of the transcription factor NF-kB; it is not known whether CIKS and/or NF-kB are required for all gene induction events. Here we report that CIKS is essential for all IL-17 induced immediate-early genes in primary mouse embryo fibroblasts, while NF-kB is profoundly involved. We also identify a novel sub-domain in the N-terminus of CIKS that is essential for IL-17-mediated NF-kB activation. This domain is both necessary and sufficient for the interaction between CIKS and TRAF6, an adaptor required for NF-kB activation. The ability of decoy peptides to block this interaction may provide a new therapeutic strategy for intervention in IL-17-driven autoimmune and inflammatory diseases.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE41789
Senescence gene signature of radiation fibrosis
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon

Description

Radiation lung injury is characterized by early inflammation and late fibrosis. The causes underlying the chronic, progressive nature of radiation injury are poorly understood. Here, we report that the gene expression of irradiated lung tissue correlates with that observed in the lungs in aged animals. We demonstrate that NOX4 expression and superoxide elaboration is increased in irradiated lungs and pneumocytes in a dose dependent fashion.

Publication Title

Role of type II pneumocyte senescence in radiation-induced lung fibrosis.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, Time

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accession-icon GSE10263
Mutant huntingtin's effects on striatal gene expression in mice
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE63627
Global gene expression profiling of primary tumors and lung metastases using a mouse model of spontaneous metastatic mammary carcinoma
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon

Description

In this study, we explored the molecular basis of site-specific metastasis of breast cancer to the lungs in a clinically relevant model based on the JygMC(A) cell line. In this dataset, we include expression data from JygMC(A) primary mammary tumors, lung metastases, normal mammary glands and normal lung parenchyma.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE9857
Striatal gene expression data from 12 weeks-old R6/2 mice and control mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14561
Expression data of murine GPI-deficient bone marrow cells in a mouse model of targeted Pig-a deletion
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon

Description

Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE16564
Expression data from AtT20 mouse pituitary gland cells following overexpression or down regulation of NSBP1
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

Chromatin architectural protein NSBP1/HMGN5 belongs to the family of HMGN proteins which specifically interact with nucleosomes via Nucleosome Binding Domain, unfold chromatin and affect transcription. Mouse NSBP1 is a new and uncharacterized member of HMGN protein family. NSBP1 is a nuclear protein which is localized to euchromatin, binds to linker histone H1 and unfolds chromatin.

Publication Title

The interaction of NSBP1/HMGN5 with nucleosomes in euchromatin counteracts linker histone-mediated chromatin compaction and modulates transcription.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE35332
Stem cell factor programs the mast cell activation phenotype
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Mast cells, activated by antigen via the high affinity receptor for IgE (FcRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders.

Publication Title

Stem cell factor programs the mast cell activation phenotype.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE20371
PPARd target genes in MEFs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

The PPAR (Peroxisome proliferator-activated receptor) family of nuclear receptors has three members: PPARg, PPARa and PPARd. Although they share similar structures, their biological functions are distinct. PPARg controls lipid storage and adipogenesis, while PPARd is associated with fat burning. The highly specific synthetic ligand for PPARd, GW501516, is a promising drug candidate for obesity and diabetes. Here we use Affymetrix microarray to analyze gene expression profile in mouse embryo fibroblasts treated with 100 nM GW501516 for 0, 2, 8 and 24 hours. These data may provide new clues into the molecular mechanism by which GW501516 ameliorates obesity and diabetes.

Publication Title

No associated publication

Sample Metadata Fields

Cell line, 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)

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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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