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accession-icon SRP007885
CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons. Overall design: CTCF ChIP-seq was performed in BJAB and BL41 B cell lines and normalized relative to Rabbit Ig control IP-seq reads. RNA-seq was performed in BJAB and BL41 cells transduced with shRNA against CTCF or RFP as a control, and in untransduced cells as well.

Publication Title

CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE69501
FGF18 Signaling for Hair Cycle Resting Phase Determines Radioresistance of Hair Follicles by the Arrest of Hair Cycling
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Telogen (resting phase) hair follicles are more radioresistant than anagen (growth phase) ones. Irradiation of BALB/c mice in the anagen phase with -rays at 6 Gy induced hair follicle dystrophy, whereas irradiation in the telogen phase induced the arrest of hair follicle elongation without any dystrophy after post-irradiation depilation. In contrast, FGF18 was highly expressed in the telogen hair follicles to maintain the telogen phase and also the quiescence of hair follicle stem cells. Therefore, the inhibition of FGF receptor signaling at telogen induced the dystrophy after post-irradiation depilation. In addition, the administration of recombinant FGF18 suppressed cell proliferation in the hair follicles and enhanced the repair of radiation-induced DNA damage, so FGF18 protected the anagen hair follicles against radiation damage to enhance hair regeneration. Moreover, FGF18 reduced the expression of cyclin B1 and cdc2 in the skin and FGF18 signaling induced G2/M arrest in the keratinocyte cell line HaCaT, although no obvious change of the expression of DNA repair genes was detected by DNA microarray analysis. These findings suggest that FGF18 signaling for the hair cycle resting phase causes radioresistance in telogen hair follicles by arresting the proliferation of hair follicle cells.

Publication Title

FGF18 signaling in the hair cycle resting phase determines radioresistance of hair follicles by arresting hair cycling.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE44786
Rat mammary cancer (spontaneous, radiation, MNU, PhIP, radiation + MNU, radiation + PhIP) (high corn oil diet)
  • organism-icon Rattus norvegicus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Although various mechanisms have been inferred for combinatorial actions of multiple carcinogens, these mechanisms have not been well demonstrated in experimental carcinogenesis models. We evaluated mammary carcinogenesis initiated by combined exposure to various doses of radiation and chemical carcinogens. Female rats at 7 weeks of age were -irradiated (0.22 Gy) and/or exposed to 1-methyl-1-nitrosourea (20 or 40 mg/kg, single intraperitoneal injection) or 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (40 mg/kg/day by gavage for 10 days) and were observed until 50 weeks of age. The incidence of mammary carcinoma increased steadily as a function of radiation dose in the absence of chemicals; mathematical analysis supported an additive increase when radiation was combined with a chemical carcinogen, irrespective of the chemical species and its dose. Hras mutations were characteristic of carcinomas that developed after chemical carcinogen treatments and were overrepresented in carcinomas induced by the combination of radiation and MNU (but not PhIP), indicating an interaction of radiation and MNU at the level of initiation. The expression profiles of seven classifier genes, previously shown to distinguish two classes of rat mammary carcinomas, categorized almost all examined carcinomas that developed after individual or combined treatments with radiation (1 Gy) and chemicals as belonging to a single class; more comprehensive screening using microarrays and a separate test sample set failed to identify differences in gene expression profiles among these carcinomas. These results suggest that a complex, multilevel interaction underlies the combinatorial action of radiation and chemical carcinogens in the experimental model.

Publication Title

Molecular characterization of cancer reveals interactions between ionizing radiation and chemicals on rat mammary carcinogenesis.

Sample Metadata Fields

Specimen part

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accession-icon SRP132239
Transcriptomic analysis of multiple myeloma cell lines
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

We found that a small molecule inhibitor of PRMT4 inhibited cell growth of a subset of multiple myeloma cell lines. To identify biomarkers that predict the sensitivity of myeloma cells to PRMT4 inhibition, we performed transcriptomic analysis of multiple myeloma cell lines. Overall design: Amplicon sequencing of thirteen multiple myeloma cell lines was performed on the Ion Torrent platform. Steady-state gene expression profile of sensitive cells were compaired with that of insensitive cells.

Publication Title

TP-064, a potent and selective small molecule inhibitor of PRMT4 for multiple myeloma.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP151069
Fibroblasts in cholesteatoma activate osteoclasts.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Cholesteatoma arises from a tympanic membrane and expands in the middle ear. It erodes the surrounding bone and leads to hearing loss or brain abscess which is lethal complication. Currently, the only effective treatment is the complete surgical removal of cholesteatoma. However, possibility of recurrence is not satisfactory, other clinical treatment is desired. A mechanism of bone erosion in rheumatoid arthritis, which is one of the bone destructive disease, is progressing to be clarified. Receptor activator of NF-?B ligand (RANKL) secreted by synovial fibroblasts, T cells, and B cells lead to differentiation and activation of osteoclast precursor in rheumatoid arthritis. In contrast it has been still unclear why cholesteatoma erodes bone. In the current study we studied that osteoclasts statistically increased in cholesteatoma, and that fibroblasts in the prematrix of cholesteatoma express RANKL. In this study we studied that osteoclasts statistically increased in cholesteatoma, and that fibroblasts in the prematrix of cholesteatoma express RANKL. We investigated upstream of RANKL from RNA sequence results by Ingenuity Pathways Analysis, which is data base of abundance information about molecular biology. Overall design: To generate the transcriptome profiles of the permatrix of cholesteatoma and dermis cut by laser micro dissection from cholesteatoma, three pairs of both sample from the same patients were adapted to RNA sequencing.

Publication Title

Osteoclasts Modulate Bone Erosion in Cholesteatoma via RANKL Signaling.

Sample Metadata Fields

Disease, Subject

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accession-icon GSE45155
The effect of YAP/TAZ knockdown on the intestinal epithelium
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The Hippo pathway plays a crucial in organ size control during development and tissue homeostasis in adult life. To examine a role for Hippo signaling in the intestinal epithelium, we analyzed gene expression patterns in the mouse intestinal epithelilum transfected with siRNAs or expression plasmids for shRNAs targeting the Hippo pathway effectors, YAP and TAZ.

Publication Title

Dual role of YAP and TAZ in renewal of the intestinal epithelium.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE56936
Expression data from NEAT1 regulated genes with or without polyI:C
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Although thousands of long non-coding RNAs (lncRNAs) are localized in the nucleus, only a few dozen have been functionally characterized.

Publication Title

Long noncoding RNA NEAT1-dependent SFPQ relocation from promoter region to paraspeckle mediates IL8 expression upon immune stimuli.

Sample Metadata Fields

Cell line

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accession-icon SRP061101
RNA sequencing of olfactory bulb projection neurons in neurotensin-GFP (NTS-GFP) mice at different developing time points
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Characterize the spatiotemporal dynamics of gene expression in neurons in developing olfactory bulb Overall design: Comparison of transcriptome profiles of GFP+ and GFP- cells derived from olfactory bulb of NTS-GFP at different developmetal time points (E13, E15, E17 and P0).

Publication Title

RNA-seq analysis of developing olfactory bulb projection neurons.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE74862
HOXA5 counteracts stem cell traits by inhibiting Wnt signaling
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Here we identify HOXA5 as an important repressor of intestinal stem cell fate in vivo and identify a reciprocal feedback between HOXA5 and Wnt signaling. HOXA5 is suppressed by the Wnt pathway to maintain stemness and becomes active only outside the intestinal crypt where it inhibits Wnt signaling to enforce differentiation. In colon cancer, HOXA5 is down-regulated and its re-expression induces loss of the cancer stem cell phenotype preventing tumor progression and metastasis. Tumor regression by HOXA5 induction can be triggered by retinoids, which represents a tangible means to treat colon cancer by eliminating cancer stem cells.

Publication Title

HOXA5 Counteracts Stem Cell Traits by Inhibiting Wnt Signaling in Colorectal Cancer.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE52259
Expression data from the Schizosaccharomyces pombe opi10- strain.
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Opi10 is the S. pombe homolog of human Hikeshi, which imports Hsp70s into the nucei during the heat shock.

Publication Title

The Schizosaccharomyces pombe Hikeshi/Opi10 protein has similar biochemical functions to its human homolog but acts in different physiological contexts.

Sample Metadata Fields

No sample metadata fields

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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Developed by the Childhood Cancer Data Lab

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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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