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GSE90620
Pseudomonas aeruginosa pao1
12 Downloadable Samples
Affymetrix Pseudomonas aeruginosa Array (paeg1a)
Description
This study examines the mechanisms underlying fumarate- and glyoxylate-mediated changes in tobraymcyin sensitivity in PAO1 cells
Publication Title
Carbon Sources Tune Antibiotic Susceptibility in Pseudomonas aeruginosa via Tricarboxylic Acid Cycle Control.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Clariom S Human array (clariomshuman)
Description
Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.
Publication Title
Cigarette Smoke Extract Disturbs Mitochondria-Regulated Airway Epithelial Cell Responses to Pneumococci.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In theses experimetns we have analized the differential gene expression profile in human trabecular meshwork cells phagocytically challenged to E. coli and pigment under physiological and oxidative stress conditions using affymetrix microarrays
Publication Title
Up-regulated expression of extracellular matrix remodeling genes in phagocytically challenged trabecular meshwork cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The transmission of information about the photic environment to the circadian clock involves a complex array of neurotransmitters, receptors, and second messenger systems. Using laser capture microscopy and microarray analysis, a population of genes rapidly induced by light in the suprachiasmatic nucleus is identified.
Publication Title
Identification of novel light-induced genes in the suprachiasmatic nucleus.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 144 Downloadable Samples
- Illumina humanRef-8 v2.0 expression beadchip
Description
Human toxicogenomic studies to date have been of limited size, have mainly addressed exposures at the upper end of typical ranges of human exposure, and have often lacked precise, individual estimates of exposure. Previously, we identified genes associated with exposure to high (>10 ppm) levels of the leukemogen, benzene, through transcriptomic analyses of blood cells from small numbers of occupationally exposed workers. Here, we have expanded the study to 125 workers exposed to a wide range of benzene levels, including <1 ppm. Study design, and analysis with a mixed effects model, removed sources of biological and experimental variability and revealed highly significant widespread perturbation of gene expression at all exposure levels. Benzene is an established cause of acute myeloid leukemia (AML), and may cause one or more lymphoid malignancies in humans. Interestingly, acute myeloid leukemia was among the most significant pathways impacted by benzene exposure in the present study. Further, at most exposure levels, immune response pathways including T cell receptor signaling, B cell receptor signaling, and Toll like receptor signaling were impacted, providing support for the biological plausibility of an association between lymphoma and benzene exposure. We also identified a 16-gene expression signature modified by all levels of benzene exposure, comprising genes with roles in immune response, inflammatory response, cell adhesion, cell-matrix adhesion, and blood coagulation. Overall, these findings support, and expand upon, our current understanding of the mechanisms by which benzene may induce hematotoxicity, leukemia and lymphoma. Furthermore, this study shows that with good study design and analysis, transcriptome profiling of the blood of chemically-exposed humans can identify relevant biomarkers across a range of exposures and inform about potential associations with disease risks.
Publication Title
Global gene expression profiling of a population exposed to a range of benzene levels.
Sample Metadata Fields
Sex, Age, Subject
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Determination of gene expression changes in hindlimb muscle (gastrocnemius/soleus) of mdx (dystrophin-deficient) mice at postnatal ages 7, 14, 23, 28, 56, and 112.
Publication Title
Dissection of temporal gene expression signatures of affected and spared muscle groups in dystrophin-deficient (mdx) mice.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 32 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
An important component of time course microarray studies is the identification of genes that demonstrate significant time-dependent variation in their expression levels. Until recently available methods for performing such significance tests required replicates of individual time points. This paper describes a replicate-free method that was developed as part of a study of the estrous cycle in the rat mammary gland in which no replicate data was collected.
Publication Title
Identifying significant temporal variation in time course microarray data without replicates.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Determination of gene expression changes in extraocular muscle of mdx (dystrophin-deficient) mice at postnatal ages 14, 28, 56, and 112 days. 3 independent replicates/age/strain.
Publication Title
Dissection of temporal gene expression signatures of affected and spared muscle groups in dystrophin-deficient (mdx) mice.
Sample Metadata Fields
No sample metadata fields
View Samples- Macaca mulatta
- 16 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Rhesus monkey extraocular muscle. Data set includes: (a) whole medial and lateral rectus muscle and (b) global and orbital muscle layers separately microdissected using a Leica LSM. All samples were expression profiled here using the Affymetrix human U133 A&B arrays. Data form part of publication: Investigative Ophthalmology and Visual Science 45, 2004.
Publication Title
Genome-wide transcriptional profiles are consistent with functional specialization of the extraocular muscle layers.
Sample Metadata Fields
No sample metadata fields
View Samples- Saccharomyces cerevisiae
- 11 Downloadable Samples
Illumina HiSeq 2000
Description
PUF proteins have become a leading scaffold for designing RNA-binding proteins to contact and control RNAs at will. We analyze the effects of that reengineering across the transcriptome in vivo for the first time. We show, by HITS-CLIP and PAR-CLIP, that S. cerevisiae Puf2p, a non-canonical PUF protein, binds more than 1000 mRNA targets. Puf2p binds multiple UAAU elements, unlike canonical PUF proteins. We also perform CLIP-seq on truncations of Puf2p, showing that its prion domain is dispensable for WT binding. We design a modified Puf2p to bind UAAG rather than UAAU, which allows us to align the protein with the binding site. In vivo, the redesigned protein binds UAAG sites. Its altered specificity redistributes the protein away from 3'UTRs, such that the protein tracks with its sites and binds throughout the mRNA. We use RNA-seq to determine that R1 SNE Puf2p represses a novel RNA network. Overall design: CLIP-seq was performed in BY4742 S. cerevisiae grown in log phase, and using 2 replicates of TAP-tagged proteins. RNA-seq was performed to determine the regulatory effect of WT or mutant Puf2p, using 4 replicates of the control (no Puf2p), 3 of WT Puf2p and 4 of R1 SNE Puf2p.
Publication Title
Target selection by natural and redesigned PUF proteins.
Sample Metadata Fields
Cell line, Subject
View Samples