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accession-icon GSE60761
Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the non-selective S1P receptor agonist FTY720 causes increased bone formation in wildtype, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo, and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts.

Publication Title

Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE4324
Sex Differences in Response to Plasmodium chabaudi Infection: Involvement of Gonadal Steroids
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The goal of this study was to examine whether immune responses to Plasmodium chabaudi infection differ between the sexes and are altered by the presence of gonadal steroids. Gonadally-intact males were more likely than intact females to die following P. chabaudi infection, exhibit slower recovery from infection-associated weight loss, hypothermia, and anemia, have reduced IFN-associated gene expression and IFN production during peak parasitemia, and produce less antibody during the recovery phase of infection. Gonadectomy of male and female mice altered these sex-associated differences, suggesting that sex steroid hormone, in particular androgens and estrogens, may modulate immune responses to infection.

Publication Title

Involvement of gonadal steroids and gamma interferon in sex differences in response to blood-stage malaria infection.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49629
Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization
  • organism-icon Homo sapiens
  • sample-icon 9 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

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE49628
Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization [Expression Array]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To determine what DNA methylation and gene expression changes occur following EBV transformation. B-cells were isolated from 3 donors. Resting, CD40 activated and EBV transfromed cells from each donor was analyzed. Each sample was assayed using Affymetrix expression arrays and whole genome bisulfite sequenicng. Additional time points during transformation and activation were sequenced as well, but not assayed for expression.

Publication Title

Large-scale hypomethylated blocks associated with Epstein-Barr virus-induced B-cell immortalization.

Sample Metadata Fields

Specimen part

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accession-icon GSE14051
Expression signatures and cytogenetic aberrations in HPV16 E6, E7 and E6/E7-positive immortalized human epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Identification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes

Publication Title

Complementation of non-tumorigenicity of HPV18-positive cervical carcinoma cells involves differential mRNA expression of cellular genes including potential tumor suppressor genes on chromosome 11q13.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14052
Differentially expressed cellular genes in non-tumorigenic and tumorigenic HPV18 positive HeLa x fibroblast hybrid cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Identification of genes differentially expressed in tumorigenic compared to non-tumorigenic, HPV18 positive cells

Publication Title

Complementation of non-tumorigenicity of HPV18-positive cervical carcinoma cells involves differential mRNA expression of cellular genes including potential tumor suppressor genes on chromosome 11q13.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13878
Widespread regulation of gene expression by the histone acetyltransferase dTip60
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

We used microarrays to detail the global gene expression changes following RNAi knock-down of dTip60 in Drosophila SL2 cells

Publication Title

Widespread regulation of gene expression in the Drosophila genome by the histone acetyltransferase dTip60.

Sample Metadata Fields

Cell line

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accession-icon GSE55448
Carbon monoxide metabolism is essential for circadian transcription and dynamics
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Circadian clocks are cell-autonomous oscillators regulating daily rhythms in a wide range of physiological, metabolic and behavioral processes. Conversely, metabolic signals such as redox state, NAD+/NADH and AMP/ADP ratios or heme feed back to and modulate circadian mechanisms to optimize energy utilization across the 24-hour cycle. We show that the signaling molecule carbon monoxide (CO) generated by rhythmic heme degradation is required for normal circadian rhythms as well as circadian metabolic outputs.

Publication Title

Reciprocal regulation of carbon monoxide metabolism and the circadian clock.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE23751
In Vitro Transcriptome Analysis of Porcine Plexus Epithelial Cells in Response to Streptococcus suis: Functions of the Choroid Plexus in Antimicrobial Defense
  • organism-icon Sus scrofa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Porcine Genome Array (porcine)

Description

We used microarrays to detail the global gene expression changes following apical infection of porcine choroid plexus epithelial cells (PCPEC) with Streptococcus suis (S. suis)

Publication Title

In vitro transcriptome analysis of porcine choroid plexus epithelial cells in response to Streptococcus suis: release of pro-inflammatory cytokines and chemokines.

Sample Metadata Fields

Specimen part

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accession-icon GSE9302
A perturbation in the system leads to period doubling
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Perturbation of the gated-synchrony system in yeast with phenelzine, an antidepressant drug used in the treatment of affective disorders in humans, leads to a rapid lengthening in the period of the genome-wide transcriptional oscillation. The effect is a concerted, genome-scale change in expression that is first seen in genes maximally expressed in the late-reductive phase of the cycle, doubling the length of the reductive phase within two cycles after treatment. Clustering of genes based on their temporal patterns of expression yielded just three super clusters whose trajectories through time could then be mapped into a simple 3D figure. In contrast to transcripts in the late-reductive phase, most transcripts do not show transients in expression relative to others in their temporal cluster but change their period in a concerted fashion. Mapping the trajectories of the transcripts into low-dimensional surfaces that can be represented by simple systems of differential equations provides a readily testable model of the dynamic architecture of phenotype. In this system, period doubling may be a preferred pathway for phenotypic change. As a practical matter, low-amplitude, genome-wide oscillations, a ubiquitous but often unrecognized attribute of phenotype, could be a source of seemingly intractable biological noise in microarray studies.

Publication Title

A rapid genome-scale response of the transcriptional oscillator to perturbation reveals a period-doubling path to phenotypic change.

Sample Metadata Fields

No sample metadata fields

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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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