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accession-icon SRP044651
mRNA expression in human DAOY cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We generate ZNF423 knockdown and control DAOY cells with lentivirus that co-expressed the fluorescent protein mCherry. We performed whole genome RNA sequencing (RNA-seq) of three batched of cultured ZNF423 KD or control KD cells. The sequence reads were analyzed by Homer followed by edgeR. The analyzed RNA-seq results showed differential expression profile including 12 known cilia genes, and 3 of these were validated with qRT-PCR on mouse granule cell precursors. This study proved data how ZNF423 linked to cilia complexes. Overall design: RNA-seq in three batched of control and ZNF423 KD cells(generated by lentivirus delivered shRNA targeting ZNF423 sequence).

Publication Title

Zfp423 Regulates Sonic Hedgehog Signaling via Primary Cilium Function.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP104440
Changes in gene expression due to alpha-crystallin mutations cryaa-R49C and cryab-R120G in mutant knock-in mouse lenses
  • organism-icon Mus musculus
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To investigate the relationship between histones, chaperone function, and cataracts, we performed RNA-seq, isothermal titration calorimetry (ITC), size-exclusion chromatography, and gel electrophoresis of histones. The RNA-seq of postnatal lenses from 2-day-old cryaa -R49C  mice revealed increased histone gene expression, suggesting that a a-crystallin mutation regulates histones via a transcriptional mechanism . Overall design: RNA-seq studies on lenses of 2-day-old wild-type and 2-day-old cryaa-R49C heterozygous mutant and cryaa-R49C homozygous mutant knock-in mice; and 14-day old wild-type and 14-day-old cryab-R120G heterozygous mutant and cryab-R120G homozygous mutant knock-in mice

Publication Title

Probing the changes in gene expression due to α-crystallin mutations in mouse models of hereditary human cataract.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE44651
Laser Capture Microdissection isolation of preovulatory granulosa cells from WT and bERKO ovaries
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Determining the spatial and temporal expression of genes involved in the ovulatory pathway is critical for the understanding of the role of each estrogen receptor in the modulation of folliculogenesis and ovulation. Estrogen receptor (ER) is highly expressed in ovarian granulosa cells and mice lacking ER (ERKO) are subfertile due to inefficient ovulation. Previous work has focused on isolated granulosa cells or cultured follicles and while informative, provides confounding results due to the heterogeneous cell types present including granulosa, theca and oocytes and exposure to in vitro conditions. Herein, we isolated preovulatory granulosa cells from WT and ER-null mice using laser capture microdissection to examine the genomic transcriptional response downstream of PMSG (mimicking FSH) and PMSG/hCG (mimicking LH) stimulation. This allows for a direct comparison of in vivo granulosa cells at the same stage of development from both WT and ER-null ovaries. ER-null granulosa cells showed altered expression of genes known to be regulated by FSH (Akap12 and Runx2) as well as not previously reported (Arnt2 and Pou5f1) in WT granulosa cells. Our analysis also identified 304 genes not previously associated with ER in granulosa cells. LH responsive genes including Abcb1b and Fam110c show reduced expression in ER-null granulosa cells; however novel genes including Rassf2 and Megf10 were also identified as being downstream of LH signaling in granulosa cells. Collectively, our data suggests that granulosa cells from ER-null ovaries may not be appropriately differentiated and are unable to respond properly to gonadotropin stimulation

Publication Title

The absence of ER-β results in altered gene expression in ovarian granulosa cells isolated from in vivo preovulatory follicles.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE9630
Expression data from mouse liver
  • organism-icon Mus musculus
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.

Publication Title

Laboratory diet profoundly alters gene expression and confounds genomic analysis in mouse liver and lung.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11056
Expression data from mouse lung
  • organism-icon Mus musculus
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.

Publication Title

Chronic exposure to arsenic in the drinking water alters the expression of immune response genes in mouse lung.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13428
Gene Expression Profiling of Rat Hippocampus Following Exposure to the Acetylcholinesterase Inhibitor Soman
  • organism-icon Rattus norvegicus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Soman (O-Pinacolyl methylphosphonofluoridate) is a potent neurotoxicant. Acute exposure to soman causes profound inhibition of the critical enzyme acetylcholinesterase, resulting in excessive levels of the neurotransmitter acetylcholine. Excessive acetylcholine levels cause convulsions, seizures, and respiratory distress. The initial cholinergic crisis can be overcome by rapid anti-cholinergic therapeutic intervention, resulting in increased survival. However, conventional treatments do not protect the brain from seizure-related damage, and thus neurodegeneration of soman-sensitive areas of the brain is a potential post-exposure outcome. We performed gene expression profiling of rat hippocampus following soman exposure to gain greater insight into the molecular pathogenesis of soman-induced neurodegeneration.

Publication Title

Gene expression profiling of rat hippocampus following exposure to the acetylcholinesterase inhibitor soman.

Sample Metadata Fields

Sex

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accession-icon GSE6364
Gene Profiling of Endometrium Reveals Progesterone Resistance and Candidate Genetic Loci in Women with Endometriosis
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transition of regularly cycling endometrium from the proliferative or Estrogen-dominant phase of the menstrual cycle to the Progesterone-dominant Early and Mid Secretory phases requires wide-spread changes in gene expression that shift the endometrium from a proliferative capacity to a differentiated 'decidual' phenotype in preparation for implantation. This process appears delayed in women with severe endometriosis, suggestive of a progesterone resistant endometrium in this disease.

Publication Title

Gene expression analysis of endometrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE58911
Gene expression in normal and tumor samples from patients with HNSCC
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Tissue samples were collected from patients diagnosed with HNSCC (oropharynx, hypopharynx, larynx). Samples were taken from the tumor site (tumor samples) and from a site distant to the tumor (normal samples) prior to therapy.

Publication Title

Prognostic biomarkers for HNSCC using quantitative real-time PCR and microarray analysis: β-tubulin isotypes and the p53 interactome.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE50379
Expression data from striatum of a mouse model of Huntingtons disease (HD) (HdhQ111/Q111) crossed with mGluR5 knockout mice (mGluR5-/-) and their respective controls (HdhQ20/Q20 and mGluR5+/+).
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To try to investigate the mechanism behind the adaptive phenotypes observed in a mice model model of HD crossed with mGluR5 knockout, we analyzed whether mutated huntingtin (Htt) expression in a mGluR5 null background could be altering the expression of genes that might be involved in the pattern of Htt aggregation and HD-related locomotor alterations.

Publication Title

Metabotropic glutamate receptor 5 knockout promotes motor and biochemical alterations in a mouse model of Huntington's disease.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE45553
Transcriptional profiling of ovarian cancer spheroids reveals genes and related biological pathways associated with cisplatin resistance
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Characterization of differential gene expression due to cisplatin resistance in human ovarian cancer spheroids by microarray analysis.

Publication Title

Cisplatin Resistant Spheroids Model Clinically Relevant Survival Mechanisms in Ovarian Tumors.

Sample Metadata Fields

Specimen part, Cell line

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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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