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accession-icon GSE65048
Copy number variation in Y chromosome multicopy genes is linked to a paternal parent-of-origin effect on CNS autoimmune disease in female offspring
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Copy number variation in Y chromosome multicopy genes is linked to a paternal parent-of-origin effect on CNS autoimmune disease in female offspring.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE65038
Lymph node CD4+ T cell expression data from nave female offspring of C57BL/6J and C57BL/6J-ChrY^SJL
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS.

Publication Title

Copy number variation in Y chromosome multicopy genes is linked to a paternal parent-of-origin effect on CNS autoimmune disease in female offspring.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP068959
RNA-seq of Drosophila unfertilized eggs
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the identification of stable intronic sequence RNAs (sisRNAs) in Drosophila. Overall design: RNA was obtained from unfertilized eggs and subjected to deep sequencing.

Publication Title

Generation of Drosophila sisRNAs by Independent Transcription from Cognate Introns.

Sample Metadata Fields

Subject

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accession-icon SRP058703
RNA-seq of Drosophila 0-2 hr embryos
  • organism-icon Drosophila melanogaster
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the identification of stable intronic sequence RNAs (sisRNAs) in Drosophila. Overall design: RNA was obtained from 0-2 hr embryos and subjected to deep sequencing.

Publication Title

Stable intronic sequence RNAs have possible regulatory roles in Drosophila melanogaster.

Sample Metadata Fields

Subject

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accession-icon GSE101937
GABP-dependent gene regulation in T cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Ets transcription factor GABP controls T cell homeostasis and immunity.

Sample Metadata Fields

Specimen part

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accession-icon GSE101935
Gene expression in GABP-sufficient and -deficient T cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Ets family transcription factor GA-binding protein (GABP) regulates gene expression in CD4 and CD8 T cells.

Publication Title

Ets transcription factor GABP controls T cell homeostasis and immunity.

Sample Metadata Fields

Specimen part

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accession-icon SRP076879
JQ1 +/- Vemurafenib in BRAF mutant melanoma (A375)
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The combination of JQ1 and Vemurafenib acted synergistically in BRAF-mutant cell lines, resulting in marked apoptosis in vitro, with up-regulation of pro-apoptotic proteins. In vivo, combination treatment suppressed tumor growth and significantly improved survival compared to either drug alone. RNA sequencing of tumor tissues revealed almost four thousand genes that were uniquely modulated by the combination, with several anti-apoptotic genes significantly down-regulated. Overall design: 16 samples analyzed from 8 mice (each mouse was bearing two tumors, one on each flank) in 4 treatment groups (control, vemurafenib alone, JQ1 alone, JQ1+vemurafenib)

Publication Title

BET and BRAF inhibitors act synergistically against BRAF-mutant melanoma.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP108762
RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

G protein coupled receptor (GPCR) signalling covers three major mechanisms. GPCR agonist engagement allows for the G proteins to bind to the receptor leading to a classical downstream signalling cascade. The second mechanism is via the utilization of the ß-arrestin signalling molecule and thirdly via transactivation dependent signalling. GPCRs can transactivate protein tyrosine kinase receptors (PTKR) to activate respective downstream signalling intermediates. In the past decade GPCR transactivation dependent signalling was expanded to show transactivation of serine/threonine kinase receptors (S/TKR). Kinase receptor transactivation enormously broadens the GPCR signalling paradigm. This work utilizes next generation RNA-sequencing to study the contribution of transactivation dependent signalling to total protease activated receptor (PAR)-1 signalling. Transactivation, assessed as gene expression, accounted for 50 percent of the total genes regulated by thrombin acting through PAR-1 in human coronary artery smooth muscle cells. GPCR transactivation of PTKRs is approximately equally important as the transactivation of the S/TKR with 209 and 177 genes regulated respectively, via either signalling pathway. This work shows that genome wide studies can provide powerful insights into GPCR mediated signalling pathways Overall design: Human CASMCS cells were subject to various treatments: basal, thrombin, thrombin + SB, thrombin + AG and thrombin + SB + AG. Gene expression was studies after 30 minutes to assess genes that are differentially expressed by treat emnt with agonists and antagonists. The agonoists and antagonists are associated with transactivation of GPCRs and the gene expression results will help identify relevant genes.

Publication Title

RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE90548
Expression data from U2OS-ER-alpha cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Understanding the mechanism of SRC-1 dependent and independent E2 signaling in bone will provide a better understanding of the biology underlying osteoporosis.

Publication Title

Steroid receptor coactivator-1 can regulate osteoblastogenesis independently of estrogen.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE19234
Immune profile and mitotic index of metastatic melanoma lesions enhance clinical staging in predicting patient survival.
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Although remission rates for metastatic melanoma are generally very poor, some patients can survive for prolonged periods following metastasis. We used gene expression profiling, mitotic index (MI), and quantification of tumor infiltrating leukocytes (TILs) and CD3+ cells in metastatic lesions to search for a molecular basis for this observation and to develop improved methods for predicting patient survival. We identified a group of 266 genes associated with postrecurrence survival. Genes positively associated with survival were predominantly immune response related (e.g., ICOS, CD3d, ZAP70, TRAT1, TARP, GZMK, LCK, CD2, CXCL13, CCL19, CCR7, VCAM1) while genes negatively associated with survival were cell proliferation related (e.g., PDE4D, CDK2, GREF1, NUSAP1, SPC24).

Publication Title

Immune profile and mitotic index of metastatic melanoma lesions enhance clinical staging in predicting patient survival.

Sample Metadata Fields

Sex, Age

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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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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