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accession-icon GSE50675
Global transcriptome analysis of Staphylococcus aureus biofilms in response to innate immune cells
  • organism-icon Staphylococcus aureus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix S. aureus Genome Array (saureus)

Description

S. aureus biofilms are associated with the organism's ability to cause disease. Biofilm associated bacteria must cope with the host's innate immune system.

Publication Title

Global transcriptome analysis of Staphylococcus aureus biofilms in response to innate immune cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6810
Response of murine splenocytes to infection with wild type or virB mutant Brucella strains
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The virB operon, encoding a Type IV secretion system (T4SS), is essential for intracellular survival and persistent infection of Brucella spp. To better understand the role of the T4SS in evading host defense mechanisms and establishing chronic infection, we compared transcriptional profiles of the host response to infection with wild type Brucella strains and strains that fail to express the virB genes. Analysis of host gene expression profiles three days after inoculation with wild type Brucella strains revealed an inflammatory response dominated by interferon-induced genes. This analysis found that not only the type II but also type I interferon pathway was elicited by Brucella infection. Real time RT-PCR showed that a group of genes from these pathways was induced by day 3 post-infection and declined to baseline levels by day 7. In contrast, neither of the two virB mutant strains elicited expression of interferon-induced genes, demonstrating that the T4SS was required to trigger an inflammatory response early during infection.

Publication Title

Brucella requires a functional Type IV secretion system to elicit innate immune responses in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21373
Staphylococcus aureus nonribosomal peptide secondary metabolites regulate virulence
  • organism-icon Staphylococcus aureus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix S. aureus Genome Array (saureus)

Description

Staphylococcus aureus is a major human pathogen and resistant to numerous clinically used antibiotics. The first antibiotic developed for S. aureus infections was the nonribosomal petide secondary metabolite penicillin. We discovered cryptic nonribosomal peptide secondary metabolites, the aureusimines, made by S. aureus itself that are not antibiotics, but function as small molecule regulators of virulence factor expression. Using established rules and codes for nonribosomal peptide assembly we predicted these nonribosomal peptides, and used these predictions to identify them from S. aureus culture broths. Functional studies using global microarray and mouse bacteremia models established that the aureusimines control virulence factor expression and are necessary for productive infections. This is the first report of the aureusimines and has important implications for the treatment of drug resistant S. aureus. Targeting aureusimine synthesis may provide novel anti-infectives.

Publication Title

Staphylococcus aureus nonribosomal peptide secondary metabolites regulate virulence.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP065219
Transcriptome response to 4h IL-1b stimulation of primary chondrocytes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Using RNA sequencing (Illumina Hi-Seq 2000 sequencer) we report the transcriptome profile of primary human chondrocytes isolated from patients with hip osteoarthritis (OA), and the transcriptome response of these cells to 4h stimulation with IL-1ß (1ng/ml). In total, 983 long non-coding RNAs (lncRNAs) were identified, which included 642 intergenic lncRNAs (lincRNAs), 124 antisense and pseudogenes. Less than 4% of the identified lncRNAs overlapped with putative eRNAs regions, and visual inspection showed that they were uni-directional and multi-exonic. Upon IL-1ß stimulation 499 protein-coding genes were differentially expressed, and 158 lncRNAs were differentially expressed, including 92 lincRNAs, 13 antisense and 18 psudogenes. This study demonstrates that IL-1ß induces a rapid and widespread change in the transcriptome of the primary human OA chondrocyte. Overall design: RNA sequencing analysis of primary human chondrocytes isolated from n=3 patients with hip osteoarthritis, with and without 4h IL-1b (1ng/ml) stimulation

Publication Title

Long Intergenic Noncoding RNAs Mediate the Human Chondrocyte Inflammatory Response and Are Differentially Expressed in Osteoarthritis Cartilage.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP068773
EPCR Expression Defines the Most Primitive Subset of Human HSPC and Is Required for Their In Vivo Activity
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Cell purification technology combined with whole transcriptome sequencing and small molecule agonist of hematopoietic stem cell self-renewal has allowed us to identify the endothelial protein c receptor protein (EPCR) as a surface maker that defines a rare subpopulation of human cells which is highly enriched for stem cell activity in vivo. EPCR-positive cells exhibit a robust multi-lineage differentiation potential and serial reconstitution in immunocompromised mice. In culture, most if not all of the HSC activity is detected in the EPCR+ subset, arguing for the stability of this marker on the surface of cultured cells, a feature not found with more recently described markers such as CD49f. Functionally EPCR is essential for human HSC activity in vivo. Cells engineered to express low EPCR expression proliferate normally in culture but lack the ability to confer long-term reconstitution. EPCR is thus a stable marker for human HSC. Its exploitation should open new possibilities in our effort to understand the molecular bases behind HSC self-renewal. Overall design: Examining 3 cellular subsets: EPCR+, EPCRlow, EPCR- derived form CD34+CD45RA- cord blood cells after 7 day expansion in UM171

Publication Title

EPCR expression marks UM171-expanded CD34<sup>+</sup> cord blood stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP156739
Single-cell RNA-sequencing of mouse double-negative developing thymocytes
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed a single-cell transcriptome analysis of double-negative developing thymocytes from the DN2, DN3 and DN4 populations Overall design: Double-negative developing thymocytes from the DN2, DN3 and DN4 populations were sorted from six WT mice and used for single cell RNA Seq (10x genomics platform)

Publication Title

The transcription factor Duxbl mediates elimination of pre-T cells that fail β-selection.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP156218
RNA-sequencing of mouse double-negative developing thymocytes [WT and Duxbl[ind]xpTa[Cre]]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed a transcriptome comparison of double-negative developing thymocytes from the DN3-4 population, from mice overexpressing the transcription factor Duxbl and wild type mice Overall design: Double-negative developing thymocytes from both WT and Duxbl[ind]xpTa[Cre] mice were gated for CD4-, CD8-, CD3-, B220-, CD25int, CD44low and CD117low expression, which define the DN3-4 stage of thymocyte development. The experiment was performed in four replicates, giving a total of 8 samples.

Publication Title

The transcription factor Duxbl mediates elimination of pre-T cells that fail β-selection.

Sample Metadata Fields

Sex, Cell line, Subject

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accession-icon GSE146039
Expression data of intestinal polyps and intestinal normal tissue from Ubc9+/+ and Ubc9+/- Villin-CreERT2;Apcf/+ mice 12 weeks after 4-OHT treatment
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Most human cancers present hyperactivated sumoylation, and cancer cell lines are usually highly sensitive to the lack of it, supporting potential application of sumoylation chemical inhibitors in cancer therapy. Here, we explored the impact of hyposumoylation (Ubc9 haploinsufficiency) on cancer development in mice using Apc loss-driven intestinal tumorigenesis model.

Publication Title

An unanticipated tumor-suppressive role of the SUMO pathway in the intestine unveiled by Ubc9 haploinsufficiency.

Sample Metadata Fields

Specimen part

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accession-icon SRP069185
The mammalian LINC complex controls mechanosensing at a genome-wide level: RNA-Seq
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Mechanical cues influence the shape, growth, and function of tissues and organs and are necessary for the development of engineered tissues. Yet, how cells sense mechanical cues and transduce them into changes in gene expression is not well understood. It is known that mechanical forces transmitted to the nucleus induce chromatin remodeling, promote DNA repair, contribute to the motion of intranuclear organelles and cause direct dissociation of protein complexes inside nuclei. Yet, the extent to which such signals impact gene expression is not understood. Because mechanical forces from the cytoskeleton to the nucleus interior are transmitted by the LINC (linker of nucleoskeleton-to-cytoskeleton) complex, we disrupted the LINC complex and performed genome wide expression studies using RNA sequencing. LINC disruption altered the expression of hundreds of genes at a genome-wide scale. We asked how LINC disruption affected the mechanosensitivity of individual genes by quantifying fold changes in gene expression on soft and stiff substrates. Remarkably, LINC disruption tended to preserve gene mechanosensitivity, but to reverse its direction. LINC disruption did not cause changes in nuclear shape, nor eliminated nuclear shape sensitivity to substrate rigidity. Our results show for the first time that the LINC complex regulates mechano-sensing at a genome-wide level, and argue for a distinct mechanism that does not require changes in nuclear morphology. Overall design: mRNA profiles of NIH 3T3 TetON cells that were induced to express either SS-GFP-KDEL (control) or SS-HA-Sun1L-KDEL by the addition of doxycycline. Two (2) substrate stiffnesses were used (1 kPa and 308 kPa), Y27632 or blebbistatin was used for certain samples to inhibit myosin II activity. A total of 6x3 reps= 18 samples were analyzed.

Publication Title

The mammalian LINC complex regulates genome transcriptional responses to substrate rigidity.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE146106
Expression data from FACS-purified Lgr5-EGFP+ intestinal cells from Ubc9+/+ and Ubc9+/- mice
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The Lgr5+ intestinal stem cell, Paneth and transit-amplifying cell compartment constitute the intestinal crypt which is the constant source of differentiated epithelial cells that replenish the intestinal villi ensuring organ maintenance and regeneration. The Lgr5+ crypt-based columnar (CBC) cells have been identified as the intestinal stem cells (ISCs) and, importantly, as cells-of-origin of intestinal cancer.

Publication Title

An unanticipated tumor-suppressive role of the SUMO pathway in the intestine unveiled by Ubc9 haploinsufficiency.

Sample Metadata Fields

Specimen part

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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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