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accession-icon SRP064356
Comparative analysis of Rtf1- and PAF1C-regulated genes
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIonTorrentProton

Description

Paf1 and Ski8 were selected as representative subunits of the Paf1 complex (PAF1C), and RNA-seq analysis was performed in triplicate to compare the genes affected by Paf1, Ski8, and Rtf1 knockdown in HeLa cells. Overall design: Total RNA was harvested from control HeLa and Ski8 knockdown cells at day 4 and from Rtf1 or Paf1 knockdown cells at day 7 and was subjected to RNA-seq in triplicates.

Publication Title

Correction for Cao et al., Characterization of the Human Transcription Elongation Factor Rtf1: Evidence for Nonoverlapping Functions of Rtf1 and the Paf1 Complex.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP100217
Identification of PKA-dependent signaling network using CRISPR-Cas9 coupled with quantitative transcriptomics, proteomics and phosphoproteomics
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 3000

Description

Purpose: PKA plays a crucial role in vasopressin signaling of renal collecting duct cells. To understand regulation of mRNA expression mediated by vasopressin/PKA signaling, mRNA expression was profiled by RNA-Seq in double knockout cells (both PKA catalytic genes) generated from mouse cortical collecting duct mpkCCD cell line versus control lines with intact PKA expression. Methods: PKA double knockout (dKO) cell lines were generated from mouse cortical collecting duct mpkCCDc11 cells by CRISPR/Cas-9 genome editing method. For mRNA profiling using RNA-Seq analysis, three biological replicates of control (not mutated in PKA two catalytic subunits) cell lines and PKA double knockout cell lines were used. The reads uniquely mapped on GENCODE mouse gene set were analyzed with HOMER (v4.8) and edgeR (v3.10.5). Results and conclusion: About 40-50 million sequence reads per sample were sucessfully mapped in the mouse genome (GENCODE, GPCm38.p5). Among total transcripts of the mouse genome, 10,190 transcripts (cutoff: Counts Per Million > 4 by edgeR) were considered as genes expressed in the cell lines. In differential expression analysis by standard edgeR analysis, 354 transcripts were differentially expressed between control cell lines and PKA dKO cell lines (FDR < 0.05). We also identified nine genes that were markedly decreased in PKA dKO cell lines (log2 PKA dKO/Control < -2, FDR < 0.05) including aquaporin-2 (Aqp2) and two genes that were markedly increased in PKA dKO cell lines (log2 PKA dKO/Control > 2, FDR < 0.05). These results suggest PKA signaling is important for regulation of expression of a very limited number of genes in vasopressin-responsive renal collecting duct cells. Overall design: Total mRNA profiling of three control cell lines and three PKA double knockout cell lines generated from mpkCCDc11 cell line were carried out by standard RNA-Seq protocols with deep sequencing on an Illumina HiSeq 3000.

Publication Title

Systems-level identification of PKA-dependent signaling in epithelial cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP119207
Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of human U2OS cells under mild replication stress by low dose aphidicolin (APH)
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To detect transcripts before and after APH treatment, we subjected total RNA isolated from U2OS cells expressing human FANCD2-3xFLAG to next generation sequencing. Overall design: U2OS cells expressing human FANCD2-3xFLAG were treated with 0.4 micro M APH, or left antreated for 24 hrs.

Publication Title

Replication stress induces accumulation of FANCD2 at central region of large fragile genes.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE49117
Expression analysis of 32Dcl3 cells expressing ASXL-MT in the presence of IL-3 or G-CSF
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Recurrent mutations in ASXL1 are found in various hematological malignancies and are associated with poor prognosis. In particular, ASXL1 mutations are frequently found in patients with hematological malignancies associated with myelodysplasia including myelodysplastic syndromes (MDS), and chronic myelomonocytic leukemia. Although loss-of-function ASXL1 mutations promote myeloid transformation, a large subset of ASXL1 mutations is thought to result in stable truncation of ASXL1. Here we demonstrate that C-terminal truncating ASXL1 mutations (ASXL1-MT) inhibit myeloid differentiation and induce MDS-like disease in mice, displaying all the features of human MDS including multi-lineage myelodysplasia, pancytopenia and occasional progression to overt leukemia. Concerning the molecular mechanisms, ASXL1-MT derepressed expression of Hoxa9 and miR-125a through inhibiting PRC2-mediated methylation of H3K27. miR-125a targeted expression of a surface receptor Clec5a, which was found to supports for myeloid differentiation. In addition, HOXA9 expression was high in MDS patients with ASXL1 mutations while Clec5a expression was generally low in MDS patients. Thus, ASXL1-MT induced MDS-like disease in mice via derepression of Hoxa9 and miR-125a, and Clec5a downregulation. Our data provide evidence for a novel axis of MDS pathogenesis (ASXL1 mutations-upregulation of HoxA9 and miR-125a-downregulation of Clec5a) and implicate both ASXL1 mutants and miR-125a as therapeutic targets in MDS.

Publication Title

Myelodysplastic syndromes are induced by histone methylation–altering ASXL1 mutations.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE49118
Expression analysis of BM cells of ASXL-MT induced MDS mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Recurrent mutations in ASXL1 are found in various hematological malignancies and are associated with poor prognosis. In particular, ASXL1 mutations are frequently found in patients with hematological malignancies associated with myelodysplasia including myelodysplastic syndromes (MDS), and chronic myelomonocytic leukemia. Although loss-of-function ASXL1 mutations promote myeloid transformation, a large subset of ASXL1 mutations is thought to result in stable truncation of ASXL1. Here we demonstrate that C-terminal truncating ASXL1 mutations (ASXL1-MT) inhibit myeloid differentiation and induce MDS-like disease in mice, displaying all the features of human MDS including multi-lineage myelodysplasia, pancytopenia and occasional progression to overt leukemia. Concerning the molecular mechanisms, ASXL1-MT derepressed expression of Hoxa9 and miR-125a through inhibiting PRC2-mediated methylation of H3K27. miR-125a targeted expression of a surface receptor Clec5a, which was found to supports for myeloid differentiation. In addition, HOXA9 expression was high in MDS patients with ASXL1 mutations while Clec5a expression was generally low in MDS patients. Thus, ASXL1-MT induced MDS-like disease in mice via derepression of Hoxa9 and miR-125a, and Clec5a downregulation. Our data provide evidence for a novel axis of MDS pathogenesis (ASXL1 mutations-upregulation of HoxA9 and miR-125a-downregulation of Clec5a) and implicate both ASXL1 mutants and miR-125a as therapeutic targets in MDS.

Publication Title

Myelodysplastic syndromes are induced by histone methylation–altering ASXL1 mutations.

Sample Metadata Fields

Specimen part

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accession-icon GSE148777
Expression data from isorhamnetin (Iso)-treated human amnion epithelial cells (hAECs)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Gene expression profiling reveals a potential role of Iso towards hepatic differentiation of hAECs.

Publication Title

Global Gene Expression Profiling Reveals Isorhamnetin Induces Hepatic-Lineage Specific Differentiation in Human Amniotic Epithelial Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE153391
Expression data from adipocyte differentiation from diabetic adipose-derived stem cells (dADSC) treated with squalene (Sq) and its derivative (HH-Sq)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Gene expression profiling reveals functional difference between Sq and HH-Sq on differentiation, metabolism, and lipid droplot formation of dADSC

Publication Title

New Amphiphilic Squalene Derivative Improves Metabolism of Adipocytes Differentiated From Diabetic Adipose-Derived Stem Cells and Prevents Excessive Lipogenesis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE153617
Expression data from TCQA-treated hAECs
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Gene expression profiling reveals a potential role of TCQA in neuronal and pigment cell differentiation of hAECs.

Publication Title

Regulating cell fate of human amnion epithelial cells using natural compounds: an example of enhanced neural and pigment differentiation by 3,4,5-tri-O-caffeoylquinic acid.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE148776
Expression data from Cyanidine (Cyanidine 3-glucoside)-treated human amnion epithelial cells (hAECs)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Gene expression profiling of the effect of Cyanidine 3 glucoside treatment in hAECs.

Publication Title

Human Amniotic Epithelial Cells as a Tool to Investigate the Effects of Cyanidin 3-<i>O</i>-Glucoside on Cell Differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE66387
Microarray analysis of differentially expressed genes in ovarian and fallopian tube epithelium from risk-reducing salpingo-oophorectomies
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Mutations in BRCA1 and BRCA2 genes confer an increased lifetime risk for breast and ovarian cancer. Ovarian cancer risk can be decreased by risk-reducing salpingo-oophorectomy (RRSO). Studies on RRSO material have altered the paradigm of serous ovarian cancer pathogenesis.

Publication Title

Microarray analysis of differentially expressed genes in ovarian and fallopian tube epithelium from risk-reducing salpingo-oophorectomies.

Sample Metadata Fields

Specimen part, Subject

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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