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GSE51452
Homo sapiens
12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Use of formalin-fixed paraffin-embedded samples for gene expression studies in breast cancer patients.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The use of Affymetrix U133 2.0 Plus chips on FFPE samples when coupled with a qPCR-based sample pre-assessment step, yielded satisfactory results from the point of view of biological reliability. When compared with the Illumina DASL WG platform, specifically designed for degraded RNA, the data generated with the Affymetrix platform showed a wider interquartile range (IQR 1.32 vs 0.57, p<2.2x10-16) suggesting a superior discriminatory power within samples as indicated by the good agreement with the immunohistiochemically derived ER status.
Publication Title
Use of formalin-fixed paraffin-embedded samples for gene expression studies in breast cancer patients.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
Illumina HiSeq 2000
Description
The objective of this study was to determine the effects of LANA on the expressions of the cellular genes. Overall design: BJAB cells were transduced with lentiviral vector expressing LANA or the control vector, total RNA was extracted for the detection of relative expression of cellular genes in LANA expressing cells.
Publication Title
KSHV LANA upregulates the expression of epidermal growth factor like domain 7 to promote angiogenesis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
SREBF-1c is a transcription factor regulating fatty acid biosynthesis. We have charaterized the impact of the abcence of SREBF-1c on the development of peripheral neuropathy
Publication Title
Lack of sterol regulatory element binding factor-1c imposes glial Fatty Acid utilization leading to peripheral neuropathy.
Sample Metadata Fields
Age
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
M cells are the main site of bacterial translocation in the intestine. We used the in vitro M cell model to study the effect of the commensal bacteria; Lactobacillus salivarius, Eschericha coli and Bacteroides fragilis, on M cell gene expression.
Publication Title
Differential intestinal M-cell gene expression response to gut commensals.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 228 Downloadable Samples
- Illumina HiSeq 2000
Description
Bone marrow-derived macrophages derived from C57Bl/6, Myd88-/- and Trif-/-, Ifnar-/-, Atm-/-, Sting-/-, Scid, Irf3-/-, Irf1-/-, p53-/-, Nrf2-/-mice were irradiated with 6Gray ioninzing radiation; C57Bl/6 macrophages were Irradiated in the presence of MAPK inhibitors or Reactive Oxygen Species Scavenger (N-Acetyl Cysteine), Two biological replicates were generated for each time point. RNA samples were collected at 0 (unirradiated), 0.5, 1, 2, 6, and 24h post irradiation except where ever mentioned. Overall design: Bone marrow-derived macrophages derived from C57Bl/6, Myd88-/- and Trif-/-, Ifnar-/-, Atm-/-, Sting-/-, Scid, Irf3-/-, Irf1-/-, p53-/-, Nrf2-/-mice were irradiated with 6Gray ioninzing radiation; C57Bl/6 macrophages were Irradiated in the presence of MAPK inhibitors or Reactive Oxygen Species Scavenger (N-Acetyl Cysteine), Two biological replicates were generated for each time point. RNA samples were collected at 0 (unirradiated), 0.5, 1, 2, 6, and 24h post irradiation except where ever mentioned.
Publication Title
Defined Sensing Mechanisms and Signaling Pathways Contribute to the Global Inflammatory Gene Expression Output Elicited by Ionizing Radiation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina HiSeq 2000
Description
The goal of the study was to understand how integrin beta1 expressed in epithelial cells directs developmental angiogenesis. Integrin beta1 was deleted specifically in the pituitary glands of embryonic mice. RNA was isolated from knockout and WT control pituitaries dissected at e12.5, one day prior to the initiation of developmental angiogenesis. Overall design: RNA from the e12.5 pituitaries of 3 WT and 2 KO littermate embryos was profiled.
Publication Title
Epithelial cell integrin β1 is required for developmental angiogenesis in the pituitary gland.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 68 Downloadable Samples
- Illumina HiSeq 2000
Description
Successful host defense against pathogens requires innate immune recognition of the correct pathogen associated molecular patterns (PAMPs) by pathogen recognition receptors (PRRs) to trigger the appropriate gene program tailored to the pathogen. While many PRR pathways have been shown to contribute to the innate immune response to specific pathogens, the relative importance of each pathway for the complete transcriptional program elicited has not been examined in detail. Herein, we used RNA-sequencing with wildtype and mutant macrophages to delineate the innate immune pathways responsible for the early transcriptional response to Staphylococcus aureus, a ubiquitous microorganism that can activate a wide variety of PRRs. Unexpectedly, only two PRR pathways – the Toll-like receptor (TLR) and Stimulator of Interferon Gene (STING) pathways - were identified as dominant regulators of approximately 95% of the genes that were potently induced within the first four hours of macrophage infection with live S. aureus. TLR signaling predominantly activated an inflammatory program, STING signaling activated an antiviral/type I interferon response, and both pathways contributed to a program linking innate and adaptive immunity. Only a small number of genes were induced in the absence of TLR or STING signaling, and these genes possessed a strong hypoxia signature. STING pathway activation required live S. aureus and was largely dependent on the DNA sensor cyclic guanosine-adenosine synthase (cGAS) recognition of S. aureus DNA. Interestingly, using a cutaneous infection model, we found that the TLR and STING pathways played opposite roles in host defense to S. aureus, with TLR signaling being required for protective interleukin (IL)-1? and neutrophil recruitment and STING signaling having an opposite effect. These results provide novel insights into the complex interplay of innate immune signaling pathways triggered byS. aureus and uncover opposing roles of TLR and STING in cutaneous host defense to S. aureus. Overall design: Files are labeled according to the figures in which they were used. Note, that many data files were used in multiple figures or figure panels. Files are labeled by genotype of macrophages (WT=wildtype; KO= StingGt/Gt; DKO=MyD88-/-TRIF-/-) and whether the macrophages were treated with live (Live) or heat killed (HK) or uninfected (zero hour). Labeling of time points is in the order of "minutes_replicate #." For example, "WT_HK_30_2" indicates that this is wild type mouse macrophages stimulated with heat killed bacteria at the 30-minute time point and is replicate number 2. Reads were converted into RPKM, and the RPKM for all replicates listed for a given time point were averaged to obtain the average RPKM that was used for figures and analyses. For samples listed as contributing to either figure 3 or supplemental figure 2, the replicates that do NOT end in either KO_analysis nor DKO analysis were used to determine induced genes in wild type macrophages. In contrast, the replicates that end in KO_analysis or DKO_analysis were used to determine dependence on either STING signaling or MyD88/TRIF signaling, respectively. If a replicate was used in the STING or MyD88/TRIF dependence analysis for both live and heat-killed S. aureus, "live_and_hk" was added after the dependence analysis it contributed to. Some 0h samples were used in both live and heat-killed analyses.
Publication Title
Opposing roles of Toll-like receptor and cytosolic DNA-STING signaling pathways for Staphylococcus aureus cutaneous host defense.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In some organs, adult stem cells are uniquely poised to serve as cancer cells of origin1-4. It is unclear, however, whether tumorigenesis is influenced by the activation state of the adult stem cell. Hair follicle stem cells (HFSCs) act as cancer cells of origin for cutaneous squamous cell carcinoma (SCC) and undergo defined cycles of quiescence and activation. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to the gain of oncogenes (Ras) or the loss of tumor suppressors (p53). Furthermore, Pten activity is necessary for quiescence based tumor suppression, as its deletion alleviates tumor suppression without affecting proliferation. These data demonstrate that stem cell quiescence is a form of tumor suppression in HFSCs, and that Pten plays a role in maintaining quiescence in the presence of tumorigenic stimuli. This experiment includes RNA profiling of hair follicle stem cells at various stages of tumorigenesis
Publication Title
Stem cell quiescence acts as a tumour suppressor in squamous tumours.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
In many organs, adult stem cells are uniquely poised to serve as cancer cells of origin. In the epidermis, hair follicle stem cells (HFSCs) cycle through stages of quiescence (telogen) and proliferation (anagen) to drive hair growth. Within the hair follicle, HFSCs are capable of initiating squamous cell carcinoma, yet it is unclear how the hair cycle contributes to tumorigenesis. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to gain of oncogenes (Ras) or loss of tumor suppressors (p53). Instead, prolonged oncogenic stimuli only exert their effects when HFSC quiescence mechanisms are removed by normal HFSC activation. Furthermore, Pten activity is necessary for quiescence based tumor suppression, since Pten deletion alleviates this stem cell specific ability without affecting proliferation per se. Overall design: Small RNAs were cloned from Trizol-lysed cells sorted from mouse skin and sequenced with the Illumina HiSeq2000.
Publication Title
Stem cell quiescence acts as a tumour suppressor in squamous tumours.
Sample Metadata Fields
No sample metadata fields
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