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accession-icon SRP126786
RNA sequence on the fed and fasted state of kidneys in mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We studied whether the accumulation of lipids in the fasted kidney are derived from lipoproteins or (non-esterified fatty acids) NEFAs. With overnight fasting, kidneys accumulated triglyceride, but had reduced levels of ceramide and glycosphingolipid species. Fasting led to a nearly 5-fold increase in kidney uptake of plasma [14C]oleic acid. Increasing circulating NEFAs using a ß adrenergic receptor agonist caused a 15-fold greater accumulation of lipid in the kidney, while mice with reduced NEFAs due to adipose tissue deficiency of adipose triglyceride lipase had reduced triglycerides. Cluster of differentiation (Cd)36 mRNA increased 2-fold, and angiopoietin-like 4 (Angptl4), an LPL inhibitor, increased 10-fold. Fasting-induced kidney lipid accumulation was not affected by inhibition of LPL with poloxamer 407 or by use of mice with induced genetic LPL deletion. Despite the increase in CD36 expression with fasting, genetic loss of CD36 did not alter fatty acid uptake or triglyceride accumulation. Our data demonstrate that fasting-induced triglyceride accumulation in the kidney correlates with the plasma concentrations of NEFAs, but is not due to uptake of lipoprotein lipids and does not involve the fatty acid transporter, CD36. Overall design: Mice (n=4-5/group) were either fasted for 16 hours or fed ad libitum. Kidneys were removed and snap frozen. RNA was extracted for sequencing.

Publication Title

Kidney triglyceride accumulation in the fasted mouse is dependent upon serum free fatty acids.

Sample Metadata Fields

Sex, Cell line, Treatment, Subject

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accession-icon GSE22109
Expression data for wt/wt and KLF1 p.K288X/wt human erythroid progenitors
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hereditary Persistence of Fetal Hemoglobin (HPFH) is characterized by persistent high levels of fetal hemoglobin (HbF) in adults. Several contributory factors, both genetic and environmental, have been identified, but others remain elusive. Ten of twenty-seven members from a Maltese family presented with HPFH. A genome-wide SNP scan followed by linkage analysis revealed a candidate region on chromosome 19p13.12-13. Sequencing identified a nonsense mutation in the KLF1 gene, p.K288X, ablating the DNA binding domain of this key erythroid transcriptional regulator. Only HPFH family members were heterozygote carriers of this mutation. Expression profiling on primary erythroid progenitors revealed down-regulation of KLF1 target genes in HPFH samples. Functional assays demonstrated that, in addition to its established role in adult globin expression, KLF1 is a critical activator of the BCL11A gene, encoding a suppressor of HbF expression. These observations provide a rationale for the effects of KLF1 haploinsufficiency on HbF levels. To identify differentially expressed genes, RNA was isolated from erythroid progenitors (HEPs) cultured from peripheral blood of four HPFH (KLF1 p.K288X/wt) and four non-HPFH family members (wt/wt) and used for genome-wide expression analysis.

Publication Title

Haploinsufficiency for the erythroid transcription factor KLF1 causes hereditary persistence of fetal hemoglobin.

Sample Metadata Fields

Specimen part

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accession-icon SRP056838
Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

These data include RNA Seq data generated from Ring1b wild type and Ring1b KO Ring1a-/- Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa. Overall design: Total RNA extracted from Ring1b wild type and Ring1b KO Ring1a-/- Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa.

Publication Title

Maintenance of leukemic cell identity by the activity of the Polycomb complex PRC1 in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP081101
Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq_2)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

These data include RNA Seq data generated from wild type and Ring1a Ring1b dKO Cdkn2a-/- MLL-AF9 Leukemic cells Overall design: mRNA library preparation from Ring1a-/-;Ring1bf/f Cdkn2a-/- MLL-AF9 leukemic cells treated with OHT or EtOH

Publication Title

Maintenance of leukemic cell identity by the activity of the Polycomb complex PRC1 in mice.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE74120
Gene profile analysis of sorted Sca1+/cKit- BMCs obtained from young and aged mice bearing tumor or not
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Sca1+/cKit hematopoietic BMCs of hosts bearing primary tumors promote the growth of distant tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from old mice bearing primary tumors lack this ability

Publication Title

Hematopoietic Age at Onset of Triple-Negative Breast Cancer Dictates Disease Aggressiveness and Progression.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE75333
Aging reduces the pro-tumorigenic potential of bone marrow cells and influences triple-negative breast cancer progression
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To examine the effects of recombinant granulin on human mammary stromal fibroblasts, we cultured immortalized GFP+ normal human mammary fibroblasts in the presence of recombinant human granulin (1ug/ml) or PBS every 24h for 6 days. To generate GRN-independent CAFs, we injected immortalized GFP+ human mammary fibroblasts, MCF7Ras human breast carcinoma cells, and 20% Matrigel subcutaneously into nude mice. Tumors were allowed to form for a period of 45 days. GFP+ fibroblasts were isolated from tumors by mincing the tumors, dissociating, and culturing in the presence of 1 ug/ml puromycin for ~3-4 weeks. CAF purity was confirmed by ensuring that 100% of the population was GFP-positive.

Publication Title

Hematopoietic Age at Onset of Triple-Negative Breast Cancer Dictates Disease Aggressiveness and Progression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39323
Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells
  • organism-icon Mus musculus
  • sample-icon 4 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

Tet proteins connect the O-linked N-acetylglucosamine transferase Ogt to chromatin in embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE39321
Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells [expression array]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

O-linked N-acetylglucosamine (O-GlcNAc ) transferase (OGT) activity is essential for embryonic stem (ES) cell viability and mouse development. OGT is present in both cytoplasm and nucleus of different cell types and mediates serine or threonine glycosylation. The Ogt gene locus resides on the X-chromosome and its activity is required for the viability of male ES cells. Using Ogt conditional knock out (KO) ES cells it was shown the failure of establishing stable KO ES clones further suggesting that Ogt activity is required for ES cell self-renewal and pluripotency. For understanding these changes, we performed global gene expression upon silencing of Ogt mediated by esiRNA in mouse Embryonic Stem Cells.

Publication Title

Tet proteins connect the O-linked N-acetylglucosamine transferase Ogt to chromatin in embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE48520
Polycomb proteins link Proliferation with DNA Replication
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Polycomb proteins control proliferation and cellular transformation regulating DNA replication independently of cell cycle checkpoints

Publication Title

Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication.

Sample Metadata Fields

Specimen part

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accession-icon SRP090129
Fam60a defines a variant Sin3a-Hdac complex in embryonic stem cells required for self-renewal
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-Sequencing (RNA-seq). The aim of this RNA-seq experiment was to monitor the genome-wide transcriptional changes in mouse embryonic stem cells depleted of either Fam60a or Sin3a. Overall design: RNA-Seq of mRNA level of mESCs depleted for Sin3a and Fam60a.

Publication Title

Fam60a defines a variant Sin3a-Hdac complex in embryonic stem cells required for self-renewal.

Sample Metadata Fields

Specimen part, Subject

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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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