refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 200 results
Sort by

Filters

Technology

Platform

accession-icon GSE80431
Identification of a novel PPAR/ / miR-21-3p axis in UV-induced skin inflammation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 22 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

Identification of a novel PPARβ/δ/miR-21-3p axis in UV-induced skin inflammation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE80427
Identification of a novel PPAR/ / miR-21-3p axis in UV-induced skin inflammation [mouse mRNA]
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPAR/ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPAR/-dependent molecular cascade involving TGF-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.

Publication Title

Identification of a novel PPARβ/δ/miR-21-3p axis in UV-induced skin inflammation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE80429
Identification of a novel PPAR/ / miR-21-3p axis in UV-induced skin inflammation [human mRNA]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPAR/ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPAR/-dependent molecular cascade involving TGF-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.

Publication Title

Identification of a novel PPARβ/δ/miR-21-3p axis in UV-induced skin inflammation.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE15287
Transcriptomic computational analysis of mastic oil-treated Lewis lung carcinomas
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina Mouse Ref-6 V1

Description

Mastic oil from Pistacia lentiscus variation chia, a blend of bioactive terpenes with recognized medicinal properties, has been recently shown to exert anti-tumor activity. Lewis lung carcinoma (LLC) cells are mastic oil-susceptible cells and were used in this work to study the effects of mastic oil at the transcriptomic level.

Publication Title

A transcriptomic computational analysis of mastic oil-treated Lewis lung carcinomas reveals molecular mechanisms targeting tumor cell growth and survival.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP159271
Innate mesenchymal TLR4/MyD88 signals promote spontaneous intestinal tumorigenesis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

This study shows that the TLR4/MyD88 pathway in intestinal mesenchymal cells promotes intestinal carcinogenesis in the APCmin mouse model. Overall design: 3' RNA-Seq (QuantSeq) profiling of ColVIcre+ wt and MyD88 knockout primary mouse intestinal mesenchymal cells before and after treatment with LPS for 6 hours. 3 replicates per group.

Publication Title

Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon GSE75588
Transcriptomic analysis of Human Umbilical Vein Endothelial Cells (HUVEC) in response to compound treatment
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Human Umbilical Vein Endothelial Cells were treated with three newly synthesized compounds and DMSO as vehicle. Total RNA was isolated 6 and 24h after treatment and gene expression analysis was performed. Three independent experiments were performed, corresponding to rep1, rep2 and rep3. Experiment 1 (rep1) contained all substances at both time points tested. Experiment 2 (rep2) contained two of the compounds and control DMSO at both time points. Experiment 3 (rep3) contained the third compound and control DMSO at both time points.

Publication Title

Novel pyrazolopyridine derivatives as potential angiogenesis inhibitors: Synthesis, biological evaluation and transcriptome-based mechanistic analysis.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon E-MEXP-958
Transcription profiling of human wild type and deltaTOR-containing hepatocyte-like cells to compare total RNA and polysome-bound RNA populations upon hepatocytic differentiation
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Comparison of Total RNA and Polysome-bound RNA populations in deltaTOR containing cells and control cells upon hepatocyitc differentiation.

Publication Title

Mammalian target of rapamycin activation impairs hepatocytic differentiation and targets genes moderating lipid homeostasis and hepatocellular growth.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE31245
Unique gene expression profile based upon pathologic response in epithelial ovarian cancer
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

PURPOSE:

Publication Title

Unique gene expression profile based on pathologic response in epithelial ovarian cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE43334
hCAF1/CNOT7 regulates interferon signaling by targeting STAT1
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Stringent regulation of the interferon signaling pathway is essential for maintaining the immune response to pathogens and tumors. The transcription factor STAT1 is a crucial mediator of this response. Here we show that hCAF1/CNOT7 regulates class I and II interferon pathways at different crucial steps. In resting cells hCAF1 can control STAT1 trafficking by interacting with the latent form of STAT1 in the cytoplasm. IFN treatment induces STAT1 release, suggesting that hCAF1 may shield cytoplasmic STAT1 from undesirable stimulation. Consistent, hCAF1 silencing enhances STAT1 basal promoter occupancy associated with increased expression of a subset of STAT1-regulated genes. Consequently, hCAF1 knockdown cells exhibit an increased protection against viral infection and reduced viral replication. Furthermore, hCAF1 participates in the extinction of the IFN signal, through its deadenylase activity, by speeding up the degradation of some STAT1-regulated mRNAs. Since abnormal and unbalanced JAK/STAT activation is associated with immune disorders and cancer, hCAF1 could play a major role in innate immunity and oncogenesis, contributing to tumor escape.

Publication Title

hCAF1/CNOT7 regulates interferon signalling by targeting STAT1.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE87433
Hyperglycemic Memory New insights into a thought to be known topic
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Hyperglycemic memory is part of the pathogenesis of diabetic retinopathy. We established a novel mouse model of intermediate-term hyperglycemic memory and demonstrated that changes in gene expression and microvascular damage in the neurovascular unit of the diabetic retina persist after euglycemic reentry, indicating memory.

Publication Title

Hyperglycaemic memory affects the neurovascular unit of the retina in a diabetic mouse model.

Sample Metadata Fields

Specimen part, Disease

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

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact