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accession-icon SRP150459
Transcriptional profiling by 4SU-seq in mouse ESCs and ESC-derived neural progenitor cells.
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

Nascent RNA was metabolically labelled with 4SU in undifferentiated and ESC-derived neural progenitor cells (NPCs). 4SU incorporated RNA was isolated and deep-sequenced at day 0 (ESCs), 3, 5 and 7 of differentiation. NPC differentiation was monitored through expression of a GFP reporter insereted into the Sox1 locus (46C reporter ESC line; PMID: 12524553). The aim was to monitor changes in transcription as ESCs differentiate into NPCs and relate this to enhancer activity. Overall design: For each of the 4 differentiation time points, two independent biological replicates were prepared and sequenced. For each assayed time point, both merged and individual replicate 4SU-seq profiles were generated.

Publication Title

Decreased Enhancer-Promoter Proximity Accompanying Enhancer Activation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE18678
Expression data from ependymal layer of wild type and FoxJ1 null postnatal male mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

FoxJ1 dependent gene expression is required for establishment of ependymal cells in the postnatal brain. This data set compares gene expression profiles of wildtype and FoxJ1 null microdissected dissected tissues at multiple postnatal time points.

Publication Title

FoxJ1-dependent gene expression is required for differentiation of radial glia into ependymal cells and a subset of astrocytes in the postnatal brain.

Sample Metadata Fields

Specimen part

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accession-icon GSE53590
Dietary fat disturbance of of gut microbial diurnal patterns uncouples host metabolic networks.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Diet-induced obesity (DIO) is rapidly becoming a global health problem, particularly as Westernization of emerging nations continues. Currently, one third of adult Americans are considered obese and, if current trends continue, >90% of US citizens are predicted to be affected by 2050. However, efforts to fight this epidemic have not yet produced sound solutions for prevention or treatment. Our studies reveal a balanced and chronobiological relationship between food consumption, daily variation in gut microbial evenness and function, basomedial hypothalamic circadian clock (CC) gene expression, and key hepatic metabolic regulatory networks , including CC and nuclear receptors (NR), that is are essential for metabolic homeostasis. Western diets high in saturated fats dramatically alter diurnal variation in microbial composition and function, which in turn lead to uncoupling of the hepatic CC and NR networks from central CC control in ways that offset the timing and types of regulatory factors directing metabolic function. These signals include microbial metabolites such as short chain fatty acids (SCFAs) and hydrogen sulfide (H2S) that can directly regulate or disrupt metabolic networks of the hepatocyte. Our study therefore provides insights into the complex and dynamic relationships between diet, gut microbes, and the host that are critical for maintenance of health. Perturbations of this constellation of processes, in this case by diet-induced dysbiosis and its metabolomic signaling, can potentially promote metabolic imbalances and disease. This knowledge opens up many possibilities for novel therapeutic and interventional strategies to treat and prevent DIO, ranging from the manipulation of gut microbial function to pharmacological targeting of host pathways to restore metabolic balance.

Publication Title

Effects of diurnal variation of gut microbes and high-fat feeding on host circadian clock function and metabolism.

Sample Metadata Fields

Specimen part

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accession-icon SRP125932
RNA-seq for U937 cells with or without 3 day differentiation with PMA and recovery
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

Sequencing data related to our manuscript "Systematic identification of general and context-specific regulators of phagocytosis using magnetic genome-wide CRISPR screens" Overall design: Two groups of U937 cells were sequenced before and after PMA differentiation. One group carried Streptococcus pyogenes Cas9 and a safe-harbor control sgRNA, and the second group was a clonally expanded U937 line expressing GFP. Each group was separated into eight separate wells at d0, and half of the wells were treated with 50 nM PMA. At day 3, undifferentiated cells were split to prevent overcrowding, and differentiated cells were trypsinized and replated. Cells were allowed to recover for 2 additional days before cells were lysed for RNA harvest and sequencing.

Publication Title

Identification of phagocytosis regulators using magnetic genome-wide CRISPR screens.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE104922
Molecular subtype classification of urothelial carcinoma in Lynch syndrome
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We aimed to provide a molecular description of Lynch syndrome-associated urothelial cancer in relation to molecular subtypes of sporadic bladder cancer. Whole genome mRNA expression profiles of 41 tumors and immunohistochemical stainings against FGFR3, KRT5, CCNB1, RB1, and CDKN2A (p16) of 37 tumors from Lynch syndrome patients were generated. Pathological data, microsatellite instability, anatomic location, and overall survival data was analyzed and compared with data from sporadic bladder cancer.

Publication Title

Molecular subtype classification of urothelial carcinoma in Lynch syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP099137
Global transcriptional profiling using RNA sequencing and DNA methylation patterns in highly enriched mesenchymal cells from young versus elderly women.
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Identification of relevant genetic pathways that are altered with aging knowing that the precursors for bone-forming osteoblasts reside in the mesenchymal cell population of bone marrow. Method: harvested and characterized, without in vitro culture, mesenchymal cells form human bone marrow capable of osteogenic differentiation Results: Identification of differentially regulated genes with aging in a highly enriched human bone marrow mesenchymal cell population. Conclusions: we have for the first time identified age-related differential gene expression and DNA methylation patterns in a highly enriched human bone marrow mesenchymal cell populationprofiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions. Overall design: Examination of gene expression and DNA methylation patterns from a highly enriched bone marrow mesenchymal cell population from young (mean age, 28.7 years) versus old (mean age, 73.3 years) women

Publication Title

Global transcriptional profiling using RNA sequencing and DNA methylation patterns in highly enriched mesenchymal cells from young versus elderly women.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP071232
Modeling the Neuropathology of Tuberous Sclerosis with Human Stem Cells Reveals a Role for Inflammation and Angiogenic Growth Factors [Cell Model]
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Tuberous sclerosis complex (TSC) is a rare genetic disease characterized by mTOR hyperfunction induced benign tumor growths in multiple organs and neurological symptoms. Because the molecular pathology is highly complex and the etiology poorly understood we employed a defined human neuronal model with a single mTOR activating mutation to dissect the disease-relevant molecular responses driving the neuropathology. TSC2 deficient neural stem cells showed severely reduced neuronal functional maturation and characteristics of astrogliosis instead. Accordingly, transcriptome analysis uncovered an inflammatory response and increased metabolic activity, while ribosome profiling revealed excessive translation of ribosomal transcripts and higher synthesis rates of angiogenic growth factors. Treatment with mTOR inhibitors corrected translational alterations but not transcriptional dysfunction. These results extend our understanding of the molecular pathophysiology of TSC brain lesions, and suggest phenotype-tailored pharmacological treatment strategies. Overall design: Two TSC+/- cell lines and two TSC-/- cell lines were independently generated from wild-type human embryonic stem cells by genome editting with zinc finger nucleases. Two cell lines were handled in the same way but without any known human gene editted and they are used as negative controls. Two independent biological replicates of each of the six cell lines are profiled with ribosome profiling technique.

Publication Title

Genomic analysis of the molecular neuropathology of tuberous sclerosis using a human stem cell model.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12275
MEF FAN TNF
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

FAN (Factor associated with neutral sphingomyelinase activation) is an adaptor protein that constitutively binds to TNF-R1. Microarray analysis was performed in fibroblasts derived from wild-type or FAN knockout mouse embryos to evaluate the role of FAN in TNF-induced gene expression.

Publication Title

FAN stimulates TNF(alpha)-induced gene expression, leukocyte recruitment, and humoral response.

Sample Metadata Fields

Treatment

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accession-icon GSE22083
Expression data from human skin exposed to solar-simulated radiation with or without sunscreen
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Despite widespread use of sunscreens that minimize erythema by blocking ultraviolet B (UVB) radiation, incidence rates of melanoma continue to rise. In considering this disparity between intervention and disease prevalence, we investigated the in vivo transcriptome of human skin treated with sunscreen and solar-simulated radiation (ssR). A focal skin area of healthy participants was exposed to ssR at 1 minimal erythema dose (MED), 0.1 MED or 100 J/m2 with or without prior application of sunscreen, or to non-UVB-spectrum of ssR (solar-simulated UVA/visible/infrared radiation: ssA). Skin biopsies were analyzed using expression microarrays.

Publication Title

Transcriptional signatures of full-spectrum and non-UVB-spectrum solar irradiation in human skin.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP148514
Disruption of GRIN2B impairs differentiation in human neurons
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Mutations in GRIN2B are associated with intellectual disability in humans. We generated iPSC derived mature cortical neurons with mutations in GRIN2B and compared them to isogenic control cells. We found that both loss of function (LOF) and reduced dosage (RD) mutations in GRIN2B lead to reduced expression of NMDAR genes and increased expression of marker of immaturity, including KI67 and MET. Overall design: Examination of transcriptome in iPSC-derved mature neurons with and without the presence of mutations in GRIN2B

Publication Title

Disruption of GRIN2B Impairs Differentiation in Human Neurons.

Sample Metadata Fields

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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