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SRP070433
Mus musculus
13 Downloadable Samples
Illumina HiSeq 2500
Description
The goals of this study is to test whether NICD presence protects the RBPjk-null Hair Follicles by altering gene expression via association with other DNA binding proteins at P3, just before the conversion to TSLP-producing keratin cysts. Overall design: Methods: Skin samples were embedded in OCT. Sectioned at 20µm thickness. Dehydrated in EtOH, and equilibrated to Xylene before the LCM procedure. Laser capture was performed with Arcturus Veritas. Methods: ~100 hair follicles from Notch-null, PS-null, RBPjk-null and wild-type samples were pooled into 3 biological replicates for each genotype and subjected to RNA isolation followed by RNA-Seq. Conclusions: A total of 2047 genes were differentially expressed (=1.5 fold) in three or more biological replicates of Notch mutant hair follicles compared to wild-type controls (p-value<0.05). Unsupervised hierarchical clustering analysis failed to distinguish between the mutants.
Publication Title
The Notch Intracellular Domain Has an RBPj-Independent Role during Mouse Hair Follicular Development.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 45 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST Gene Chips. In this dataset we include expression data obtained from 8 normal adrenal medulla and 45 PHEOs/PGLs patient samples.
Publication Title
Genotype and tumor locus determine expression profile of pseudohypoxic pheochromocytomas and paragangliomas.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
RNAseq analysis of human bone marrow derived stromal cells (MSCs) treated for 24 hours with or wihout 10ng/ml Fibroblast Growth Factor 2 (FGF2) MSCs were derived from 4 different healthy donors. Cells were expanded to passage 3-4. Then cells were treated with FGF-2. 24 hours later, total RNA was extracted (total 8 samples). Overall design: RNA was submitted to BGI Americas for RNAseq. Here, QC was performed using Agilent 2100. All samples had a RIN above 8.0. For preparation for library, mRNA was enriched by using the oligo (dT) magnetic beads. mRNA was enriched by using the oligo (dT) magnetic beads. mRNA was fragmented into short fragments (about 200bp) using a fragmentation buffer. Then the first strand of cDNA was synthesized by random hexamer-primer using the mRNA fragments as templates. Buffer, dNTSPs, RNase H and DNA polymerase I were added to synthesize the second strand. The double strand cDNA was purified with QiaQuick PCR extraction kit and washed with EB buffer for end repair and base A addition. Finally, sequencing adapters were ligated to the fragments. The fragments are purified by Agarose gel electrophoresis and enriched by PCR amplification. The library products are ready for sequencing analysis via 2 sE50 lanes in Illumina HiSeqâ„¢ 2000.
Publication Title
FGF2 Induces Migration of Human Bone Marrow Stromal Cells by Increasing Core Fucosylations on N-Glycans of Integrins.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Arabidopsis thaliana
- 48 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Auxin-dependent transcript abundance was assayed by transferring 6 day old Arabidopsis grown on a a nylon mesh to IAA-containing or control media
Publication Title
A kinetic analysis of the auxin transcriptome reveals cell wall remodeling proteins that modulate lateral root development in Arabidopsis.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We were interested in characterizing the transcriptional changes that occur on a genome-wide scale following treatment of EGFR-mutant lung cancer cells with targeted therapies.
Publication Title
Inhibition of mutant EGFR in lung cancer cells triggers SOX2-FOXO6-dependent survival pathways.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus, Homo sapiens
- 24 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Antiviral Protection via RdRP-Mediated Stable Activation of Innate Immunity.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Previously, we reported that mice made transgenic for a picornaviral RdRP the 3Dpol protein of Theilers murine encephalomyelitis virus (TMEV) suppress infection by diverse viral families. How the picornaviral RdRP transgene exerted antiviral protection in vivo was not known. To investigate the molecular mechanism, we determined gene expression profiles in spinal cords of WT and RdRP transgenic mice prior to (baseline) and after (2 days) infection with Encephalomyocarditis Virus (EMCV).
Publication Title
Antiviral Protection via RdRP-Mediated Stable Activation of Innate Immunity.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Previously, we reported that mice made transgenic for a picornaviral RdRP the 3Dpol protein of Theilers murine encephalomyelitis virus (TMEV) suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPrna). Another mutant, RdRPcat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPrna, and RdRPcat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated.
Publication Title
Antiviral Protection via RdRP-Mediated Stable Activation of Innate Immunity.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Previously, we reported that mice made transgenic for a picornaviral RdRP the 3Dpol protein of Theilers murine encephalomyelitis virus (TMEV) suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPrna). Another mutant, RdRPcat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPrna, and RdRPcat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated.
Publication Title
Antiviral Protection via RdRP-Mediated Stable Activation of Innate Immunity.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Previously, we reported that mice made transgenic for a picornaviral RdRP the 3Dpol protein of Theilers murine encephalomyelitis virus (TMEV) suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNR-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPrna). Another mutant, RdRPcat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPrna, and RdRPcat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated.
Publication Title
Antiviral Protection via RdRP-Mediated Stable Activation of Innate Immunity.
Sample Metadata Fields
Specimen part
View Samples