Filters
Technology
Platform
GSE94417
Homo sapiens
195 Downloadable Samples
Affymetrix Human Genome U219 Array (hgu219)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 86 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Corticosteroids are the current standard of care to improve short-term mortality in severe alcoholic hepatitis (AH), although nearly 40% of the patients do not respond and accurate pre-treatment predictors are lacking. We developed 123-gene prognostic score based on molecular and clinical variables before initiation of corticosteroids. Furthermore, The gene signature was implemented in an FDA-approved platform (NanoString), and verified for technical validity and prognostic capability. Here we demonstrated that a Nanostring-based gene expressoin risk classification is useful to predict mortality in patients with severe alcoholic hepatitis who were treated by corticosteroid
Publication Title
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 71 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Corticosteroids are the current standard of care to improve short-term mortality in severe alcoholic hepatitis (AH), although nearly 40% of the patients do not respond and accurate pre-treatment predictors are lacking. We developed 123-gene prognostic score based on molecular and clinical variables before initiation of corticosteroids. Furthermore, The gene signature was implemented in an FDA-approved platform (NanoString), and verified for technical validity and prognostic capability. Here we demonstrated that a Nanostring-based gene expressoin risk classificatoin is useful to predict mortality in patients with severe alcoholic hepatitis who were treated by corticosteroid
Publication Title
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 38 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Corticosteroids are the current standard of care to improve short_term mortality in severe alcoholic hepatitis (AH), although nearly 40% of the patients do not respond and accurate pre_treatment predictors are lacking. We developed 123_gene prognostic score based on molecular and clinical variables before initiation of corticosteroids. Furthermore, The gene signature was implemented in an FDA_approved platform (NanoString), and verified for technical validity and prognostic capability. Here we demonstrated that a Nanostring_based gene expressoin risk classificatoin is useful to predict mortality in patients with severe alcoholic hepatitis who were treated by corticosteroid
Publication Title
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
NextSeq 500
Description
Before birth B-cells develop in the fetal liver (FL). Here we show that Gli3 activity in the FL stroma is required for B-cell development. In the Gli3-deficient FL B-cell development was reduced at multiple stages, whereas the Sonic hedgehog (Shh)-deficient FL showed increased B-cell development, and Gli3 functioned to repress Shh transcription. Use of a transgenic Hedgehog (Hh)-reporter mouse showed that Shh signals directly to developing B-cells, and that Hh pathway activation was increased in developing B-cells from Gli3-deficient fetal liver. RNAsequencing confirmed that Hh-mediated transcription is increased in B-lineage cells from Gli3-deficient FL, and showed that these cells expressed reduced levels of B-lineage transcription factors and BCR/pre-BCR-signalling genes. We showed that expression of the master regulators of B-cell development, Ebf1 and Pax5, is reduced in developing B-cells from Gli3-deficient FL and increased in Shh-deficient FL, and that in vitro Shh-treatment or neutralisation can repress or induce their expression respectively. Overall design: Wildtype and Gli3 mutant (Gli3+/- and Gli3-/-) (n=2) embryonic day 17.5 fetal livers were sorted for CD19+B220+ cells. RNA extracted from these cells was sequenced to help understand the transcriptional changes governing B cell development in the Gli3 mutants.
Publication Title
The transcription factor Gli3 promotes B cell development in fetal liver through repression of Shh.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Despite Hedgehogs influence on T-cell activation and proliferation, the transcriptional targets of Gli2 in lymphocytes are not known. We therefore examined the Hedgehog-dependent transcriptional response of resting and early-stage activated T-cells in order to define their transcriptional response to Hedgehog pathway activation.
Publication Title
Tissue-derived hedgehog proteins modulate Th differentiation and disease.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
We used Affymetrix microarrays to understand the genome wide differences in Wildtype and Gli3 mutant (Gli3+/- and Gli3-/-) (n=2) embryonic day 18.5 DP CD69-, DP CD69+ and SP4 thymocytes.
Publication Title
Gli3 in fetal thymic epithelial cells promotes thymocyte positive selection and differentiation by repression of <i>Shh</i>.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 3 Downloadable Samples
- IlluminaHiSeq2000
Description
This experiment sought to determine the genome-wide interactome of CTCF in human cells. Overall design: PAR-CLIP seq for CTCF was performed in U2OS cells in 2 biological replicates
Publication Title
CTCF regulates the human p53 gene through direct interaction with its natural antisense transcript, Wrap53.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 146 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
Dietary gluten proteins (prolamins) from wheat, rye, and barley are the driving forces behind celiac disease, an organ-specific autoimmune disorder that targets both the small intestine and organs outside the gut. In the small intestine, gluten induces inflammation and a typical morphological change of villous atrophy and crypt hyperplasia. Gut lesions improve and heal when gluten is excluded from the diet and the disease relapses when patients consume gluten. Oral immune tolerance towards gluten may be kept for years or decades before breaking tolerance in genetically susceptible individuals. Celiac disease provides a unique opportunity to study autoimmunity and the transition in immune cells as gluten breaks oral tolerance. Seventy-three celiac disease patients on a long-term gluten-free diet ingested a known amount of gluten daily for six weeks. A peripheral blood sample and intestinal biopsies were taken before and six weeks after initiating the gluten challenge. Biopsy results were reported on a continuous numeric scale that measured the villus height to crypt depth ratio to quantify gluten-induced gut mucosal injury. Pooled B and T cells were isolated from whole blood, and RNA was analyzed by DNA microarray looking for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth, as patients maintained or broke oral tolerance in the face of a gluten challenge.
Publication Title
A B-Cell Gene Signature Correlates With the Extent of Gluten-Induced Intestinal Injury in Celiac Disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We have demonstrated that the oncogenic activation of B-RAF (using a truncated delta-BRAF-ER version inducible with tamoxifen) in the melan-a melanocyte cell line triggers the activation of Zeb1 and Twist1 at the expanse of Zeb2 and Snail2. Enforced maintenance of Zeb2 or Snail2 expression reduces the B-RAF oncogenic potential while ectopic expression of Zeb1 or Twist1 cooperates with B-RAF in melan-a cell transformation. To get an insight into the properties of these embryonic transcription factors, gene expression profiles of melan-a-derived cell lines either expressing a non-activated B-RAF (- tamoxifen) or an activated BRAF (+ tamoxifen) alone or in combination with Snail2, Zeb2, Twist1 or Zeb1 have been established.
Publication Title
A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.
Sample Metadata Fields
Cell line
View Samples