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accession-icon SRP140471
A Zebrafish Acromegaly Model Elevates DNA Damage and Impairs DNA Repair Pathways
  • organism-icon Danio rerio
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Acromegaly is a pathological condition due to excess growth hormone (GH) secretion. Acromegaly patients exhibit a deterioration of health and many associated complications, such as cardiovascular issues, arthritis, kidney diseases, muscular weakness, and colon cancer. Since these complications are generalized throughout the body, we investigated the effect of GH excess on cellular integrity. Here, we established stable acromegaly model zebrafish lines that overexpress tilapia GH and the red fluorescence protein (RFP) reporter gene for tracking GH gene expression throughout generations, and performed RNA-Seq data analysis from different organs. Intriguingly, heatmap and Expression2Kinases (X2K) analysis revealed the enrichment of DNA damage markers in various organs. Moreover, H2A.X immunostaining analysis in acromegaly zebrafish larvae and the adult acromegaly model brain and muscle showed a robust increase in the number of DNA-damaged cells. Using Gene Set Enrichment Analysis (GSEA), we found that the acromegaly zebrafish model had impaired DNA repair pathways in the liver, such as double-strand break (DSB), homologous recombination repair (HRR), non-homologous end joining (NHEJ), nucleotide excision repair (NER), and translesion synthesis (TLS). Interestingly, the impairment of DNA repair was even more prominent in acromegaly model than in aged zebrafish (three years old). Thus, our study demonstrates that affection of cellular integrity is characteristic of acromegaly Overall design: Total mRNA obtained from 1-years old acromegaly zebrafish model muscle, brain, kidney, liver and 3-day old larvae compared to wild-type (WT) zebrafish were generated by deep sequencing using Illumina.

Publication Title

An Acromegaly Disease Zebrafish Model Reveals Decline in Body Stem Cell Number along with Signs of Premature Aging.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE44116
Cytosolic Fe-S cluster assembly-deficient mutant, nar1 and nbp35 mutant seedling
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Expression profiling of two-weeks-old wild type, nar1-4/- and nbp35-3/- mutant seedlings. The cytosolic Fe -S cluster assembly pathway is involved in cytosolic and nucleus Fe-S protein maturation.

Publication Title

The role of Arabidopsis thaliana NAR1, a cytosolic iron-sulfur cluster assembly component, in gametophytic gene expression and oxidative stress responses in vegetative tissue.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE11119
SOL2 mutation affect gene expresstion at root apex
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Analysis of sol2 mutant. SOL2 protein is a receptor-like kinase

Publication Title

The receptor-like kinase SOL2 mediates CLE signaling in Arabidopsis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE140855
Microarray of HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Transcriptome analysis of total RNA samples from HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells. To check whether KO of UBE2J1 upregulates genes of GPI biosthesis pathway, we used microarrays to analyze gene expression change by KO of UBE2J1 and comfirmed that known GPI pathway genes are not changed by ERAD-deficiency.

Publication Title

Cross-talks of glycosylphosphatidylinositol biosynthesis with glycosphingolipid biosynthesis and ER-associated degradation.

Sample Metadata Fields

Cell line

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accession-icon GSE16494
Expression profiling MOLT-4 treated with MABL
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Analysis of MOLT-4 cells at various time points up to 6 hours following treatment with mouse anti-CD47 antibody (MABL) and goat anti-mouse IgG (GAM) as the crosslinker of MABL. MABL induces apoptosis in CD47-positive MOLT-4 cells. Cell death signals via CD47 ligation were analyzed by using Affymetrix Human Genome U133A microarray.

Publication Title

A new disulfide-linked dimer of a single-chain antibody fragment against human CD47 induces apoptosis in lymphoid malignant cells via the hypoxia inducible factor-1α pathway.

Sample Metadata Fields

Cell line, Time

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accession-icon GSE67823
Master transcription factors in corneal epithelial cells
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconAgilent-028004 SurePrint G3 Human GE 8x60K Microarray (Probe Name Version), Affymetrix Human Gene 2.0 ST Array (hugene20st), Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

OVOL2 Maintains the Transcriptional Program of Human Corneal Epithelium by Suppressing Epithelial-to-Mesenchymal Transition.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE67820
Master transcription factors in corneal epithelial cells [6TFs transduced experimental samples]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconAgilent-028004 SurePrint G3 Human GE 8x60K Microarray (Probe Name Version), Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

In development, embryonic ectoderm differentiates into several lineages including neuroectoderm and surface ectoderm, through the mechanism largely unclear. Here we report that OVOL2 is required for the transcriptional program of corneal epithelium cell(CEC)s, a derivative of surface ectoderm, and it might regulates the differential transcriptional programs between the two lineages. By a functional screening, we identified transcription factors (TFs) maintaining human CECs. OVOL2 was necessary to maintain the transcriptional program in CECs, particularly through repressing expression of mesenchymal genes. OVOL2 combined with several TFs were able to activate the transcriptional program of CECs in fibroblasts, accompanied by induction of chromatin landscape. Moreover, our analysis revealed that neuroectoderm derivatives express some of mesenchymal genes. In fact, OVOL2 alone was able to induce the transcriptional program of CECs in neural progenitor cells (NPCs) through repression of mesenchymal genes as well as activation of epithelial genes. Our data suggest that the difference between the transcriptional programs of surface ectoderm-derivatives and neuroectoderm-derivatives is regulated in part by the reciprocally-repressive mechanism between epithelial and mesenchymal genes that is seen in epithelial-to-mesenchymal transition.

Publication Title

OVOL2 Maintains the Transcriptional Program of Human Corneal Epithelium by Suppressing Epithelial-to-Mesenchymal Transition.

Sample Metadata Fields

Specimen part

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accession-icon SRP072256
Bach2 keeps homeostasis in lung by regulating inflammatory response and maintaining function of alveolar macrophage.
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Alveolar macrophages (AMs) of Bach2 KO mice show multiple alternations in their functions including lipid metabolism. We aimed to clarify the mechanism whereby deficiency of Bach2 impairs the function of AMs and ruins the homeostasis of lungs. Now we report that some cytokines produced from Bach2-deficient T cells alter the character of AMs and expression of Bach2 is necessary for AMs to maintain the function of lipid metabolism. Overall design: mRNA profiling of AMs from 16-week old control mice, Bach2-floxed CD4cre mice, WT mice and Bach2 germline KO mice were examined by deep sequencing using HiSeq2500. Please note that two macrophage populations observed in Bach2-floxed/CD4-cre cKO mice were analyzed; One with normal surface marker phenotype that was the same as control mice (normal). The other with aberrant surface marker phenotype compared with control mice (abnormal).

Publication Title

Inflammatory responses induce an identity crisis of alveolar macrophages, leading to pulmonary alveolar proteinosis.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE61510
Expression data from neural crest cells and neural crest cell-derived MSCs from human pluripotent stem cells of FOP patients and controls
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

NCCs and NCC-derived MSCs were induced from FOP-iPSCs and control iPSCs, and their expresion profiles were compared.

Publication Title

Derivation of mesenchymal stromal cells from pluripotent stem cells through a neural crest lineage using small molecule compounds with defined media.

Sample Metadata Fields

Specimen part

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accession-icon GSE60313
Expression data from neural crest cells and neural crest cell-derived MSCs from human pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We developed simple, robust, efficient, and serum-free/feeder-free induction protocol for neural crest cells from human pluripotent stem cells. To characterize the hNCCs and hNCC-derived MSCs, we performed gene expression profiling experiments.

Publication Title

Derivation of mesenchymal stromal cells from pluripotent stem cells through a neural crest lineage using small molecule compounds with defined media.

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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