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accession-icon GSE70401
TLR4 Signaling Is a Major Mediator of the Female Tract Response to Seminal Fluid in Mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

To examine the effect of seminal fluid on the whole genome expression profile of endometrial tissue following mating, RNA was extracted from endometrial tissue collected 8 h after CBAF1 females were mated with intact Balb/c males and compared to RNA from endometrial tissue of females mated with seminal fluid deficient SVX/VAS Balb/c males. This comparison controlled for ovarian hormone status, exposure to the male and mating activity, and the neuroendocrine response to cervical and vaginal stimulus at mating, so that changes in endometrial gene expression could be attributed specifically to contact with seminal fluid. The endometrial RNA from n=16 individual females was pooled into four independent biological replicates per treatment group (n=4 endometrial samples per replicate) and expression profiles were analyzed by Affymetrix microarray. Seminal fluid exposure induced a clear difference in the profile of genes expressed in the endometrium with a total of 335 genes were differentially regulated with a fold-change greater than 1.5 and p<0.05. Of these, 190 genes were upregulated and 145 genes were downregulated following contact with seminal fluid. Bioinformatics analysis revealed TLR4 signaling as a strongly predicted upstream regulator activated by the differentially expressed genes.Additional experiments confirmed the role of TLR4 with the absence of TLR4 in TLR4 null mice resulting in a failure for seminal fluid to induce endometrial Csf3, Cxcl2, Il6 and Tnf expression. This study provides evidence that TLR4 contributes to seminal fluid modulation of the periconception immune environment. Activation of TLR4 signaling by microbial or endogenous components of seminal fluid is thus implicated as a key element of the female tract response to seminal fluid at the outset of pregnancy in mice.

Publication Title

TLR4 Signaling Is a Major Mediator of the Female Tract Response to Seminal Fluid in Mice.

Sample Metadata Fields

Sex, Specimen part, Time

View Samples
accession-icon GSE14523
A Regenerative Trait in Mice with a Point Mutation in TGFBR1
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Regeneration of differentiated tissue in mammals is rare. In an effort to identify genes that affect the healing process, we screened G3 mice containing germline point mutations for closure of an ear punch wound. One particular line was identified with a heritable hole closure phenotype containing differentiated tissue. Mapping and sequencing efforts revealed that the mutant mice harbor a R244Q point mutation coded by the TGFBR1 gene which leads to enhanced signaling activity in a reporter gene assay. Although there was no obvious effect on the immune system, bone marrow stromal cells from the mutant mice revealed accelerated chondrogenesis, mimicking the in vivo development of cartilage islands in the regenerated ears. This genetically well-defined mouse model should help to further dissect the role of TGF-beta signaling in vertebrate healing and regeneration.

Publication Title

Regenerative phenotype in mice with a point mutation in transforming growth factor beta type I receptor (TGFBR1).

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE63252
Induction of ER stress in HCT116 colon cancer cells
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours.

Publication Title

A close connection between the PERK and IRE arms of the UPR and the transcriptional regulation of autophagy.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon E-TABM-163
Transcription profiling of murine presomitic mesoderms of 17 samples at various time points to identify cyclic genes of the mouse segmentation clock
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2), Affymetrix Mouse Expression 430A Array (moe430a)

Description

A microarray time series was generated to identify cyclic genes of the segmentation clock in the mouse. The right posterior half presomitic mesoderms (PSM) from 17 mouse embryos were dissected while the contralateral side of the embryo containing the left PSM was immediately fixed to be analyzed by in situ hybridization using a Lfng probe to order the samples along the segmentation clock oscillation cycle. Probes were produced from RNA extracted from the 17 dissected posterior half PSMs using a two-step amplification protocol and were hybridized to Affymetrix GeneChip MOE430A. The reproducibility of the amplification procedure was initially assessed by comparing array data generated from the right and the left posterior PSM from the same embryo. Because of the symmetry of the paraxial mesoderm along the left-right axis, left and right samples are expected to show overtly similar gene expression. RNA was amplified from three such sample pairs (1, a and b; 2, a and b; 3, a and b) and hybridized on Murine Genome U74Av2 array (MG-U74Av2)

Publication Title

A complex oscillating network of signaling genes underlies the mouse segmentation clock.

Sample Metadata Fields

Age, Specimen part, Subject, Time

View Samples
accession-icon GSE10167
Microarray Analysis of Treacher Collins Syndrome
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The object of this study was to identify genes transcriptionally upregulated and downregulated in response to Tcof1 haploin-sufficiency during mouse embryogensis

Publication Title

Prevention of the neurocristopathy Treacher Collins syndrome through inhibition of p53 function.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE5606
Expression data from Normal (control) and Diabetic animals LV heart tissue (At 16wks)
  • organism-icon Rattus norvegicus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Analysis of gene expression changes in the LV of a rodent heart that occur with uncontrolled diabetes

Publication Title

Transcriptomic analysis of the cardiac left ventricle in a rodent model of diabetic cardiomyopathy: molecular snapshot of a severe myocardial disease.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP058066
Human beta cell proliferation induced by inhibition of Dyrk1a and GSK3b
  • organism-icon Rattus norvegicus
  • sample-icon 170 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

Purpose: Single-cell whole transcriptome sequencing was used to better understand the mechanism of action of our Dyrk1a inhibitor''s proliferation of pancreatic islets. Methods: primary pancreatic islets were isolated, cultured, and stimulated with either 0.1% DMSO or 3 µM GNF4877. Single cells were captured and cDNA isolated on a Fluidigm C1 instrument. Sequencing libraries were made with Nextera XT reagents (Illumina) and single-end 50 bp reads were generated on an Illumina HiSeq 1000. Reads were mapped to the rat transcriptome. Results: Consistent with GNF4877 eliciting beta cell proliferation, we observed an increase in the number of beta cells co-expressing insulin 1 and genes involved in cell cycle including the M phase marker Cyclin B1. Comparison of Cyclin B1 expressing cells from GNF4877-treated islets to beta cells from DMSO-treated islets further revealed a significant increase expression of genes associated with full cell cycle progression and enrichment of Gene Ontology (GO) categories for proliferation. Conclusions: Since only a small subset of islet cells proliferate when stimulated with GNF4877, single-cell transcriptome sequencing allowed us to examine expression of genes co-regulated with known proliferation markers and will hopefully allow us to characterize beta cell subsets which are responsive to proliferation-associated therapies. Overall design: 84 GNF4877-treated and 86 DMSO-treated rat islet cells containing greater than 100,000 mapped sequencing reads per cell and having a single verified cell per port were compared

Publication Title

Inhibition of DYRK1A and GSK3B induces human β-cell proliferation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE12038
XBP1 links ER stress to intestinal inflammation
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

XBP1 is the transcriptino factor that is activated by the ER stress. XBP1 is known to induce the ER dexpansion and increase the expression of the ER chaperone genes to prtect the cell from the ER stress. We generated a mouse strain that lacked XBP1 specifically in the mouse intestine by breeding the XBP1flox mice with Villin-cre mice. Here we examined genes that are differentially expressed between WT and XBP1 KO mouse intestine to identify genes that are downstream of XBP1.

Publication Title

XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE68138
An Immune and Inflammation Signature in Prostate Tumors of Smokers
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 52 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An Immune-Inflammation Gene Expression Signature in Prostate Tumors of Smokers.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE68135
An Immune and Inflammation Signature in Prostate Tumors of Smokers (part 1)
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Current smokers develop metastatic prostate cancer more frequently than nonsmokers, suggesting that a tobacco-derived factor induces metastasis. To identify smoking-induced alterations in human prostate tumors, we analyzed gene and protein expression of tumors from current, past, and never smokers and observed distinct molecular alterations in current smokers. Specifically, an immune and inflammation signature was identified in prostate tumors of current smokers that was either attenuated or absent in past and never smokers. Key characteristics of this signature included augmented immunoglobulin expression by tumor-infiltrating B cells, NF-kB activation, and increased interleukin-8 in tumor and blood. In an alternate approach to characterize smoking-induced oncogenic alterations, we explored the effects of nicotine in prostate cancer cells and prostate cancer-prone TRAMP mice. These experiments showed that nicotine increases both invasiveness of human prostate cancer cells and metastasis in tumor-bearing TRAMP mice, indicating that nicotine can induce a phenotype that resembles the epidemiology of smoking-associated prostate cancer progression. In summary, we describe distinct oncogenic alterations in prostate tumors from current smokers and show that nicotine can enhance prostate cancer metastasis.

Publication Title

An Immune-Inflammation Gene Expression Signature in Prostate Tumors of Smokers.

Sample Metadata Fields

Specimen part

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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