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accession-icon GSE141650
Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

We demonstrated that, four weeks after the pulmonary artery banding (PAB) operation, rats could be divided into two groups: an F+ group in which the fibrotic area occupied more than 6.5% of the whole area of the heart tissues, and an F- group in which the fibrotic area occupied less than 6.5% of this area.

Publication Title

Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP172692
RNA-seq data from VavCre;Jak2+/+; Cdk6+/+, VavCre;Jak2V617F; Cdk6+/+, VavCre;Jak2V617F; Cdk6-/-, VavCre; Jak2+/+; Cdk6-/- murine bone marrow LSK cells and VavCre; Jak2V617F; Cdk6+/+ Palbociclib treated murine bone marrow LSK cells
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We describe a critical role for Cdk6 in JAK2V617F+ MPN evolution. The absence of Cdk6 ameliorates clinical symptoms and prolongs survival of JAK2V617F fl/+ vav-Cre mice. The Cdk6 protein interferes with three hallmarks of disease: besides regulating malignant stem cell quiescence, it promotes NFkB signaling and contributes to cytokine production while inhibiting apoptosis. The treatment with palbociclib did not mirror these effects, showing that the functions of Cdk6 in MPN pathogenesis are largely kinase-independent. Overall design: LSK-sorted (FACS) bone marrow cells from 8-week-old VavCre;Jak2+/+; Cdk6+/+, VavCre;Jak2V617F; Cdk6+/+, VavCre;Jak2V617F; Cdk6-/-, VavCre; Jak2+/+; Cdk6-/- mice, and the same cell type from palbociclib-treated (38mg/kg, 3x in one week) VavCre;Jak2V617F; Cdk6+/+ mice, n=3 for all genotypes

Publication Title

CDK6 coordinates <i>JAK2</i> <sup><i>V617F</i></sup> mutant MPN via NF-κB and apoptotic networks.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE82225
Androgen-induced lncRNA SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE82224
Effects of SOCS2-AS1 inhibition in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified a novel androgen-regulated long non-coding (lnc) RNA, SOCS2-AS1.

Publication Title

Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE49814
Genome-wide cheater screen reveals safeguards for cell cooperation during embryogenesis
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Ensuring cooperation among formerly autonomous cells has been a central challenge in the evolution of multicellular organisms. One solution is monoclonality, but this option does not eliminate genetic and epigenetic variability, leaving room for exploitative behavior. We therefore hypothesized that embryonic development must be protected by robust regulatory mechanisms that prevent aberrant clones from superseding wild-type cells. Using a genome-wide screen in murine induced pluripotent stem cells, we identified a network of genes (centered on p53, topoisomerase 1, and olfactory receptors) whose downregulation caused the cells to replace wild-type cells, both in vitro and in the mouse embryowithout perturbing normal development. These genes thus appear to fulfill an unexpected role in fostering cell cooperation.

Publication Title

Safeguards for cell cooperation in mouse embryogenesis shown by genome-wide cheater screen.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE50883
Expression data from mouse bone marrow-derived macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a danger signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a calm down signal.

Publication Title

Immunosuppression via adenosine receptor activation by adenosine monophosphate released from apoptotic cells.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE46211
Gene expression profiling of anterior and posterior palatal tissue from Tgfbr2 mutant mouse models
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The overall goal of this project is to investigate the role of TGF-beta signaling in epithelial cells as it pertains to the orientation of muscle fibers in the soft palate during embryogenesis. Here, we first conducted gene expression profiling of the anterior and posterior portions of the palate from wild-type mice. In addition, we also conducted gene expression profiling of the posterior palate in mutant mice with an epithelium-specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of submucosal cleft palate, which is a congenital birth defect commonly observed in many syndromic conditions.

Publication Title

TGFβ regulates epithelial-mesenchymal interactions through WNT signaling activity to control muscle development in the soft palate.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE58309
The role of AR-associated factors in androgen signaling
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified androgen-regulated genes, CTBP2, FOXP1 and RUNX1. These factors interact with AR ligand dependently.

Publication Title

CtBP2 modulates the androgen receptor to promote prostate cancer progression.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE60401
Pregnane X receptor knockout mice display aging-dependent wearing of articular cartilage
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Steroid and xenobiotic receptor (SXR) and its murine ortholog pregnane X receptor (PXR) are nuclear receptors that are expressed mainly in the liver and the intestine. They function as xenobiotic sensors by inducing genes involved in detoxification and drug excretion. Recent evidence showed that SXR and PXR are also expressed in bone tissue where they mediate bone metabolism. Here we report that systemic deletion of PXR results in aging-dependent wearing of articular cartilage of knee joints. Histomorphometrical analysis showed remarkable reduction of width and an enlarged gap between femoral and tibial articular cartilage in PXR knockout mice. We hypothesized that genes induced by SXR in chondrocytes have a protective effect on articular cartilage and identified Fam20a (family with sequence similarity 20a) as an SXR-dependent gene induced by the known SXR ligands, rifampicin and vitamin K2. Lastly, we demonstrated the biological significance of Fam20a expression in chondrocytes by evaluating osteoarthritis-related gene expression of primary articular chondrocytes. Consistent with epidemiological findings, our findings indicate that SXR/PXR protects against aging-dependent wearing of articular cartilage and that ligands for SXR/PXR have potential role in preventing osteoarthritis caused by aging.

Publication Title

Pregnane X receptor knockout mice display aging-dependent wearing of articular cartilage.

Sample Metadata Fields

Cell line

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accession-icon GSE8712
The effects of Yariv-reagent on barley aleurone GA signaling
  • organism-icon Hordeum vulgare
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

Microarray analysis was performed to know how many gibberellin (GA)-responsive genes are inhibited by beta-Yariv reagent, a specific binder of plant arabinogalactan-proteins. cRNAs were prepared from mRNAs isolated from aleurone protoplasts that were treated with GA, GA plus beta-Yariv reagent, or mock (DMSO)-treated for 24 hours, and were subjected to microarray analysis. The analysis was performed twice using target cRNAs prepared independently.

Publication Title

Defense-related signaling by interaction of arabinogalactan proteins and beta-glucosyl Yariv reagent inhibits gibberellin signaling in barley aleurone cells.

Sample Metadata Fields

No sample metadata fields

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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