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SRP133667
Zea mays
40 Downloadable Samples
Illumina HiSeq 3000
Description
We tracked the gene expression events following treatment of maize seedlings with the endoplasmic reticulum (ER) stress agent tunicamycin. ER stress elicits the unfolded protein response (UPR) and when plants are faced with persistent stress, the UPR transitions from an adaptive or cell survival phase to programmed cell death. Overall design: Each sample was collected in 3 biological replicates and two technical replicates.
Publication Title
Response to Persistent ER Stress in Plants: A Multiphasic Process That Transitions Cells from Prosurvival Activities to Cell Death.
Sample Metadata Fields
Subject, Time
View Samples- Drosophila melanogaster
- 5 Downloadable Samples
Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
FoxA transcription factors play major roles in organ-specific gene expression. How FoxA proteins achieve specificity is unclear, given their broad expression patterns and requirements in multiple cell types. Here, we characterize Sage, a basic helix-loop-helix (bHLH) transcription factor expressed exclusively in the Drosophila salivary gland (SG). We identify Sage targets and show that not only are both Sage and the single Drosophila FoxA protein, Fork head (Fkh), required for expression of these genes, but coexpression of Sage and Fkh is sufficient to drive target gene expression in multiple other cell types. Sage and Fkh drive expression of the bZip transcription factor Senseless (Sens), which boosts expression of Sage/Fkh targets. Importantly, Sage, Fkh and Sens colocalize on salivary gland polytene chromosomes. Thus, Fkh drives cell-type specific gene expression as part of a tissue-specific transcription module that includes Sage and Sens, providing a new paradigm for how mammalian FoxA proteins acheive specificity.
Publication Title
Organ-specific gene expression: the bHLH protein Sage provides tissue specificity to Drosophila FoxA.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Microarray analysis of gene expression in the olfactory epithelium of Harlequin mouse as a model of oxidative-stress induced neurodegeneration of olfactory sensory neurons
Publication Title
Cellular and molecular characterization of oxidative stress in olfactory epithelium of Harlequin mutant mouse.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 203 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This is the expression dataset for two studies: 1) Characterization of visceral and subcutaneous adipose tissue transcriptome and biological pathways in pregnant and non-pregnant women: Evidence for pregnancy-related regional-specific differences in adipose tissue and 2) Characterization of visceral and subcutaneous adipose tissue transcriptome in pregnant women with and without spontaneous labor at term: Implication of alternative splicing in the metabolic adaptations of adipose tissue to parturition.
Publication Title
Characterization of visceral and subcutaneous adipose tissue transcriptome in pregnant women with and without spontaneous labor at term: implication of alternative splicing in the metabolic adaptations of adipose tissue to parturition.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
acLDL loading of mouse peritoneal macrophage is an in vitro foam cell model.
Publication Title
Cholesterol accumulation regulates expression of macrophage proteins implicated in proteolysis and complement activation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The mammalian gastrointestinal tract harbors thousands of bacterial species that include symbionts as well as potential pathogens. The immune responses that limit access of these bacteria to underlying tissue remain poorly defined.
Publication Title
Gammadelta intraepithelial lymphocytes are essential mediators of host-microbial homeostasis at the intestinal mucosal surface.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2000
Description
The targeting of oncogenic ‘driver’ kinases with small molecule inhibitors has proven to be a highly effective therapeutic strategy in selected non-small cell lung cancer (NSCLC) patients. However, acquired resistance to targeted therapies invariably arises and is a major limitation to patient care. ROS1 fusion proteins are a recently described class of oncogenic driver, and NSCLC patients that express these fusions generally respond well to ROS1-targeted therapy. In this study, we sought to determine mechanisms of acquired resistance to ROS1 inhibition. To accomplish this, we generated a ROS1 inhibition-resistant derivative of the initially sensitive NSCLC cell line HCC78.
Publication Title
Resistance to ROS1 inhibition mediated by EGFR pathway activation in non-small cell lung cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Background: High density lipoprotein (HDL) protects the artery wall by removing cholesterol from lipid-laden macrophages. However, recent evidence suggests that it might also inhibit atherogenesis by combating inflammation. Methods and Results: To identify potential anti-inflammatory mechanisms, we challenged macrophages with lipopolysaccharide (LPS), an inflammatory microbial ligand for Toll-like receptor 4 (TLR4). HDL inhibited the expression of 33% (301 of 911) of the genes normally induced by LPS, microarray analysis revealed. One of its major targets was the type I interferon response pathway, a family of potent viral immunoregulators controlled by TLR4 and the TRAM/TRIF signaling pathway. Unexpectedly, HDLs ability to inhibit gene expression was independent of cellular cholesterol stores. Moreover, it was unaffected by downregulation of two ATP-binding cassette transporters, ABCA1 and ABCG1, that promote cholesterol efflux. To examine the pathways potential in vivo relevance, we used mice deficient in apolipoprotein (apo) A-I, HDLs major protein. After infection with Salmonella (a Gram-negative bacterium that expresses LPS), apoA-Ideficient mice had 6-fold higher plasma levels of interferon-beta-a key regulator of the type I interferon response than did wild-type mice. Conclusions: HDL inhibits a subset of LPS-stimulated macrophage genes that regulate the type I interferon response, and its action is independent of sterol metabolism. These findings raise the possibility that regulation of macrophage genes by HDL might link innate immunity and cardioprotection.
Publication Title
High-density lipoprotein suppresses the type I interferon response, a family of potent antiviral immunoregulators, in macrophages challenged with lipopolysaccharide.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Changes in the transcript profile due to ABCA1 expression in murine liver samples was evaluated in LDL receptor -/- genetic backgrounds.
Publication Title
ABCA1 overexpression in the liver of LDLr-KO mice leads to accumulation of pro-atherogenic lipoproteins and enhanced atherosclerosis.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 25 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
The ecto-enzyme CD38 is a marker of unfavorable prognosis for chronic lymphocytic leukemia (CLL) patients and an indicator of activation and proliferation of leukemic cells. Here we show that CD38 is enzymatically active in primary CLL cells and that its forced expression increases disease aggressiveness in a xenograft model. The effect is completely lost when using an enzyme deficient version of CD38 with a single amino-acid mutation. Through the enzymatic conversion of NAD, CD38 increases cytoplasmic Ca2+ concentrations, positively influencing proliferation, chemotaxis, adhesion and matrix digestion. Inhibition of the enzymatic activities of CD38 using the flavonoid kuromanin blocks CLL homing. In a short-term xenograft model using primary cells, kuromanin treatment traps CLL cells in the blood, increasing responses to chemotherapy.
Publication Title
The enzymatic activities of CD38 enhance CLL growth and trafficking: implications for therapeutic targeting.
Sample Metadata Fields
No sample metadata fields
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