Filters
Technology
Platform
SRP120600
Homo sapiens
49 Downloadable Samples
Illumina HiSeq 2500, NextSeq 500
Description
Purpose: the goal of this study was to test whether the amounts of genome-encoded Line-1s are influenced by TUTases and Mov10 Methods: RNA-Seq data were obtained for PA-1 or Hek293 Flp-IN T-Rex cells in which wild-type or mutant TUTases or Mov10 were overexpressed or the proteins were depleted by RNA interference Results: Minor changes (less than 0.4-fold) were observed in the amounts of mRNAs of Homo sapiens-specific Line-1 families in Hek293 Flp-IN T-Rex and PA-1 either overexpressing or depleted of TUTases and Mov10 Overall design: LINE-1 repetitive elements profiles of Hek293 Flp-IN T-Rex and PA-1 generated by deep sequencing, in triplicate, using Illumina NextSeq 500 and Illumina HiSeq 2500.
Publication Title
Uridylation by TUT4/7 Restricts Retrotransposition of Human LINE-1s.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 14 Downloadable Samples
Affymetrix Mouse Expression 430A Array (moe430a)
Description
Three types of stimuli -- heat shock, Lipofectamine 2000 and benzyl alcohol -- induce activity of some stress genes (hsp) in mouse B16-F10 cells. Besides hsp genes induction, each stimulus causes gene expression changes of different sets of genes. We used microarrays to analyze global gene expression changes in mouse B16-F10 cells treated with elevated temperature (heat shock, HS), with Lipofectamine 2000 (LA) or with 40mM benzyl alcohol (BA).
Publication Title
Liposome-based DNA carriers may induce cellular stress response and change gene expression pattern in transfected cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
Description
The exosome-independent exoribonuclease DIS3L2 is mutated in Perlman syndrome. Here we used extensive global transcriptomic and targeted biochemical analyses to identify novel DIS3L2 substrates in human cells. We show that DIS3L2 regulates pol II transcripts, comprising selected canonical and histone-coding mRNAs, and a novel FTL_short RNA from the ferritin mRNA 5'' UTR. Importantly, DIS3L2 contributes to surveillance of pre-snRNAs during their cytoplasmic maturation. Among pol III transcripts, DIS3L2 particularly targets vault and Y RNAs and an Alu-like element BC200 RNA, but not Alu repeats, which are removed by exosome-associated DIS3. Using 3'' RACE-Seq, we demonstrate that all novel DIS3L2 substrates are uridylated in vivo by TUT4/TUT7 poly(U) polymerases. Uridylation-dependent DIS3L2-mediated decay can be recapitulated in vitro, thus reinforcing the tight cooperation between DIS3L2 and TUTases. Together these results indicate that catalytically inactive DIS3L2, characteristic of Perlman syndrome, can lead to deregulation of its target RNAs to disturb transcriptome homeostasis. Overall design: To investigate DIS3L2 functions genome-wide, total RNA samples were collected from model cell lines producing either WT or mut DIS3L2 three days after induction with doxycycline. The RNA samples were rRNA-depleted before preparation of strand-specific total RNA libraries according to the standard TruSeq (Illumina) protocol. TruSeq library preparation favours RNA molecules longer than 200 nt, and shorter transcripts are suboptimal for sequencing via this protocol. Thus, to obtain information about potential DIS3L2 RNA substrates with lengths between 20 and 220 nt, another RNA-Seq was carried out in parallel (with size selection through gel purification). The stable inducible HEK293 cell lines producing DIS3L2 variants were obtained using “pAL_01” and “pAL_02” plasmid constructs and the Flp-In™ T-REx™ system according to the manufacturer’s guidelines. “pAL_01” and “pAL_02” plasmids are vectors for co-expression of recoded C-terminal FLAG-tagged DIS3L2 [wild type (WT) variant or its catalytic mutant counterpart (mut), respectively] and sh-miRNAs directed against endogenous DIS3L2 mRNA.
Publication Title
Perlman syndrome nuclease DIS3L2 controls cytoplasmic non-coding RNAs and provides surveillance pathway for maturing snRNAs.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 25 Downloadable Samples
- Illumina HiSeq 4000
Description
Astrocytes were purified from postnatal day 2 mouse cortices by immunopanning with HepaCAM. Inhibitors and DMSO were added on in-vitro day 2. HBEGF was depleted on the cell prep day and till in-vitro day 7. In-vitro day 2, 7 and 14 samples were collected on designed timepointed. Overall design: Three EGFR inhibitor samples and three relative DMSO control samples, three P53 inhibitor samples and three relative DMSO control samples, two HBEGF samples and two HBEGF withdrawal samples, three samples for each in-vitro day 2, 7 and 14.
Publication Title
Astrocyte-to-astrocyte contact and a positive feedback loop of growth factor signaling regulate astrocyte maturation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Expression data from this experiment is part of a larger project aimed at defining the individual effects and synergistic effects of ROCK inhibitor Y-27632 and conditioned media from irradiated J2 cells when applied to epithelial cells. This data set consists of four individual samples, each of which are total RNA collected from human foreskin keratinocyte cells, either grown in F medium (control), treated with Y-27632, grown in conditioned medium (as described in associated publication), or both treatments.
Publication Title
Multifactorial analysis of conditional reprogramming of human keratinocytes.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Hypertension is a dominating risk factor for cardiovascular disease. To characterize the genomic response to hypertension, we administered vehicle or angiotensin II to mice and performed gene expression analyses. AngII treatment resulted in a robust increase in blood pressure and altered expression of 235 genes in the aorta, including Gucy1a3 and Gucy1b3 which encode subunits of soluble guanylyl cyclase (sGC). Western blotting and immunohistochemistry confirmed repression of sGC associated with curtailed relaxation via sGC activation. Analysis of transcription factor binding motifs in promoters of differentially expressed genes identified enrichment of motifs for RBPJ, a component of the Notch signaling pathway, and the Notch coactivators FRYL and MAML2 were reduced. Gain and loss of function experiments demonstrated that JAG/NOTCH signaling controls sGC expression together with MAML2 and FRYL. Reduced expression of sGC, correlating with differential expression of MAML2 in stroke prone and spontaneously hypertensive rats was also seen and RNA-Seq data demonstrated correlations between JAG1, NOTCH3, MAML2 and FRYL and the sGC subunits GUCY1A3 and GUCY1B3 in human coronary artery. Notch signaling thus provides a constitutive drive on expression of the major nitric oxide receptor (GUCY1A3/GUCY1B3) in arteries from mice, rats, and humans, and this control mechanism is disturbed in hypertension.
Publication Title
Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway.
Sample Metadata Fields
Specimen part
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- Homo sapiens
- 6 Downloadable Samples
- NextSeq 500
Description
We analysed the effect of depriving the human cell of the catalytic activity of the nuclear 5' to 3' exoribonuclease XRN2. Catalytic amino acids in this protein had been defined previously, so it was possible to design a mutated catalytically inactive form of the protein (XRN2D233A-D235A) (PMID: 19194460). We created 293 Flp-In T-REx stable cell lines that induciby silence endogenous XRN2, and concomitantly express wild-type or inactive XRN2 in fusion with EGFP at the C-terminus. Thus, complementation of silencing of endogenous XRN2 with the expression of mutant version of the protein allows to directly link potential phenotypes with the lack of XRN2 enzymatic activity. To this end we isolated total RNA from tetracycline-treated cells, depleted it from rRNA and conducted strand-specific deep sequencing. Overall design: 6 samples were analysed. 3 replicates of control cells (endogenous copy of XRN2 gene is silenced and catalytically active exogenous XRN2-EGFP is expressed) and 3 replicates of cells deprived of XRN2 ribonucleolytic activity (endogenous copy of XRN2 gene is silenced and catalytically inactive exogenous XRN2(D233AD235A)-EGFP is expressed)
Publication Title
Versatile approach for functional analysis of human proteins and efficient stable cell line generation using FLP-mediated recombination system.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
A control vs. genetic knockout experiment aimed at determining what RNAs are upregulated or downregulated in e11.5 mouse proximal limb tissue lacking the Lmx1b gene. Because Lmx1b is required for dorsal-ventral patterning of the limb, this screen gives insight into what putative downstream targets of Lmx1b contribute to dorsal-ventral patterning.
Publication Title
Identification of genes controlled by LMX1B in the developing mouse limb bud.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 38 Downloadable Samples
- Illumina HiSeq 2500
Description
Genes and pathways in which inactivation dampens tissue inflammation present new opportunities for understanding the pathogenesis of common human inflammatory diseases, including inflammatory bowel disease, rheumatoid arthritis and multiple sclerosis. We identified a mutation in the gene encoding the deubiquitination enzyme USP15 (Usp15L749R) that protected mice against both experimental cerebral malaria (ECM) induced by Plasmodium berghei and experimental autoimmune encephalomyelitis (EAE). Combining immunophenotyping and RNA sequencing in brain (ECM) and spinal cord (EAE) revealed that Usp15L749R-associated resistance to neuroinflammation was linked to dampened type I interferon responses in situ. In hematopoietic cells and in resident brain cells, USP15 was coexpressed with, and functionally acted together with the E3 ubiquitin ligase TRIM25 to positively regulate type I interferon responses and to promote pathogenesis during neuroinflammation. The USP15-TRIM25 dyad might be a potential target for intervention in acute or chronic states of neuroinflammation. Overall design: Sequencing of RNA extracted from target tissue in two experimental neuroinflammation models in wild-type (B6), USP15(L749R) and Trim25 KO mutant mice: (1) brains at day 3 and 5 following Plasmodium berghei ANKA (PbA) infection for the cerebral malaria model (ECM); and (2) spinal cords at day 7 following induction of experimental autoimmune encephalomyelitis (EAE) for B6 and Usp15 mutant mice only.
Publication Title
USP15 regulates type I interferon response and is required for pathogenesis of neuroinflammation.
Sample Metadata Fields
Sex, Specimen part, Treatment, Subject
View Samples