refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 12 results
Sort by

Filters

Technology

Platform

accession-icon SRP105407
Nudix-type RNA pyrophosphohydrolase regulates pathogenesis-associated factors in Pseudomonas aeruginosa
  • organism-icon Pseudomonas aeruginosa
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

The PA0336 protein from Pseudomonas aeruginosa belongs to the family of widely distributed Nudix pyrophosphohydrolases which catalyze the hydrolysis of pyrophosphate bonds in a variety of nucleoside diphosphate derivatives. The amino acid sequence of the PA0336 protein is highly similar to that of the RppH Nudix RNA pyrophosphohydrolase from E. coli which removes pyrophosphate from 5'-end of triphosphorylated RNA transcripts. Trans-complementation experiments showed that the P. aeruginosa enzyme can functionally substitute for RppH in E. coli cells indicating that, similarly to RppH, the Pseudomonas hydrolase mediates RNA turnover in vivo. In order to elucidate the biological significance of the PA0336 protein in Pseudomonas cells, a PA0336 mutant strain was constructed. The mutated strain considerably increased level of the virulence factor pyocyanin compared to wild type, suggesting that PA0336 could be involved in down-regulation of P. aeruginosa pathogenicity. This phenotype was reversed by complementation with the wild type, but not catalytically inactive PA0336, indicating that the catalytic activity was indispensable for its biological function. To study the role of PA0336 further, transcriptomes of the PA0336 mutant and the wild type strain were compared using RNA sequencing. The cellular level of a number of transcripts was affected by the lack of PA0336. We focused our attention on pathogenesis-related genes. Up-regulated in the PA0336 mutant were transcripts coding for, i. a., proteins involved in the regulation and/or production of pyocyanin, biofim-associated alginates and exotoxins. The results from the global analysis were verified by determining the cellular level of chosen transcripts by quantitative RT-PCR method. Pathogenesis tests in Caenorhabditis elegans showed that the PA0336 mutant of P. aeruginosa was significantly more virulent than the parental strain, confirming further that the P. aeruginosa RNA pyrophosphohydrolase PA0336 modulates bacterial pathogenesis by down-regulating production of virulence factors. Overall design: Study comparing RNA expression of P. aeruginosa PA0336 mutant strain with wild type reference, both in biological triplicates, by RNA-seq performed on Ion Torrent Proton platform

Publication Title

Nudix-type RNA pyrophosphohydrolase provides homeostasis of virulence factor pyocyanin and functions as a global regulator in Pseudomonas aeruginosa.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE17620
Expression data from motor nerve-stimulated and the contralateral control tabialis anterior muscles in mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Exercise induces skeletal muscle adaptation, and the p38 mitogen-activated protein kinase signaling pathway is thought to play an important role in the adaptive processes. We have obtained new evidence that the gamma isoform of p38 is required for exercise-induced metabolic adaptation in skeletal muscle; however, the neuromuscular activity-dependent target genes of p38gamma remain to be defined.

Publication Title

p38gamma mitogen-activated protein kinase is a key regulator in skeletal muscle metabolic adaptation in mice.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE85682
Expression data from intestinal dendritic cells and macrophages of VDTR mice at 4 hours post diphtheria toxin administration
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Recognition and removal of apoptotic cells by professional phagocytes, including dendritic cells and macrophages, preserve self-tolerance and prevent chronic inflammation and autoimmune pathologies. However the diverse array of phagocytes residing within different tissues combined with the necessarily prompt nature of apoptotic cell clearance has made it difficult to study this process in situ. Thus, the full spectrum of functions executed by tissue resident phagocytes in response to homeostatic apoptosis remains unclear.

Publication Title

Different tissue phagocytes sample apoptotic cells to direct distinct homeostasis programs.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE27692
Molecular profiles for GTL16 cell lines
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression and copy number variation arrays for parental GTL16 and GTL16 clones resistant to c-Met inhibitor.

Publication Title

A novel SND1-BRAF fusion confers resistance to c-Met inhibitor PF-04217903 in GTL16 cells through [corrected] MAPK activation.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP056033
SF3B1 Degron knockdown RNA-seq
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Overall design: Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

Publication Title

A chemical genetics approach for the functional assessment of novel cancer genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE47736
Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE47734
Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice [BeadArray]
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

The preferential localization of some neoplasms, such as serrated polyps, in specific areas of the intestine suggests that non-genetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine, but develop serrated polyps only in the cecum.

Publication Title

Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE77942
Human alveolar epithelial cells (A549) exposed to cigarette smoke extract
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Human alveolar epithelial cells were exposed to cigarette smoke extract (CSE) for 1, 3 and 5 weeks at 1%, 5% and 10%, and gene expression was evaluated by complete transcriptome microarrays.

Publication Title

Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells.

Sample Metadata Fields

Cell line, Time

View Samples
accession-icon GSE9237
Endothelial Cell Line Expression Patterns
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sphingosine 1-phosphate (S1P) influences T cell migration into and out of secondary lymphoid organs; however, its mechanism of action remains uncertain. Our previous research shows that agonism of the S1P receptor S1P1 inhibits the egress of T lymphocytes from the peripheral tissues into afferent lymphatics. To better define the mechanism of inhibition, we developed an in vitro model to characterize T cell transendothelial migration across lymphatics. Two commercially available endothelial cell lines (MS-1 and SVEC4-10) were characterized by flow cytometry, real time RT-PCR, and Affymetrix Gene Array. These cell lines were grown to confluent monolayers in transwell systems, on either the upper or lower surface of the transwell insert. T cells were isolated from the spleens of (C57BL/6 x C3H/HeJ)F1, S1P1 KO, or S1P1 KO littermate controls, and either treated with the S1P receptor modulator FTY720 or left untreated. Cells were migrated to chemokines (CCL19 or CCL21) for 4 hours, and migration quantified. Flow cytometry, RT-PCR, and array results identified MS-1 as a blood vascular endothelial cell line, expressing high levels of CD31, CD34, and ICAM-1 as well as other endothelial cell markers; while SVEC4-10 closely resemble a lymphatic phenotype, expressing LYVE-1, VEGFR-3, and podoplanin. T cells efficiently migrate across MS-1, whether grown on the upper or lower surface; whereas migration across SVEC4-10 only occurs when cells are grown on the lower surface of the transwell (iSVEC), recapitulating basal (abluminal) to apical (luminal) migration that occurs in vivo. FTY720 inhibits T cell migration across iSVEC, but not across MS-1. Inhibition is due to drug effects only on T cells but not endothelial cells. S1P1 KO T cells treated with FTY720 are not inhibited in their migration across the iSVEC line, showing that S1P1 stimulation is required for migration inhibition. The in vitro model developed here is the first to use endothelial cell lines to analyze the regulation of T cell migration across lymphatic endothelium. The results show there is directional control of T cell migration across lymphatic cells, such that T cells only migrate from a basal to apical direction. Agonism of S1P1 specifically inhibits migration, while absence of the receptor does not. These findings have important implications for the use of S1P1 agonists in transplantation, as inhibition of cell entry into afferent lymphatics and lymph nodes could impede the development of graft rejection.

Publication Title

The sphingosine 1-phosphate receptor 1 causes tissue retention by inhibiting the entry of peripheral tissue T lymphocytes into afferent lymphatics.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE101466
Type I IFN and not TNF, is essential for cyclic di-nucleotide-elicited CTL by a cytosolic cross-presentation pathway
  • organism-icon Mus musculus
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dendritic cells are the initiators of the adaptive immune response, therefore its gene expression allow us to predict the responses to vaccination. We used bone marrow derived dendritic cells (BMDC) to analyze the gene expression that result from the exposure to adjuvants. We use model antigen OVA and cyclic di-AMP (CDA) as an adjuvant in order to characterize the genes involved in the activation of dendritic cells by CDA alone or when the antigen is present.

Publication Title

Type I IFN and not TNF, is Essential for Cyclic Di-nucleotide-elicited CTL by a Cytosolic Cross-presentation Pathway.

Sample Metadata Fields

Treatment, Time

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact