This SuperSeries is composed of the SubSeries listed below.
Oxidative stress activates a specific p53 transcriptional response that regulates cellular senescence and aging.
Age, Specimen part
View SamplesWe describe here a male infant with a 100 kb de novo Xq28 deletion encompassing parts of the TMEM187 and MECP2 protein-coding genes and the IRAK1 protein-coding gene, as well as the MIR3202-1, MIR3202-2, and MIR718 RNA-coding genes. We analyzed the impact of human IRAK-1 deficiency on a genome-wide gene expression in human fibroblasts in response to TLR2/6, TLR4 agonists as well as to IL-1 and TNF-, using primary fibroblasts from healthy controls and IRAK-4-, MyD88- and MECP2-deficient patients for comparison.
Inherited human IRAK-1 deficiency selectively impairs TLR signaling in fibroblasts.
No sample metadata fields
View SamplesIFNs are highly pleiotropic cytokines also endowed with marked anti-angiogenic activity. In this study, the mRNA expression profiles of endothelial cells (EC) exposed in vitro to IFN-alpha, IFN-beta, or
Identification of genes selectively regulated by IFNs in endothelial cells.
No sample metadata fields
View SamplesSeventeen T-ALL patients out of 120 (14.2%) presented CRLF2 expression 5 times higher than the median (CRLF2-high) with a significantly inferior 5-y EFS and an increased CIR compared to CRLF2-low patients.GEP of 15 T-ALL patients with (CRLF2-high) were compared to 15 CRLF2-low patients. GSEA identified cell cycle deregulating gene sets.
CRLF2 over-expression is a poor prognostic marker in children with high risk T-cell acute lymphoblastic leukemia.
Disease
View SamplesGene expression from WT and NFAT5 KO primary macrophage cultures.
Gene expression induced by Toll-like receptors in macrophages requires the transcription factor NFAT5.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
Specimen part, Disease
View SamplesCorticosteroids 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
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
Specimen part, Disease
View SamplesCorticosteroids 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
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
No sample metadata fields
View SamplesCorticosteroids 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
Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.
No sample metadata fields
View SamplesThe inhibitor of DNA binding 2 (Id2) is essential for NK cell development with its canonical role in this pathway being to antagonize E-proteins, silencing E-box gene expression and subsequent commitment to the T and B cell lineages. However, how E-box genes prevent NK cell development and homeostasis remains enigmatic. Here we identify a key role for Id2 in regulating the threshold for IL-15 receptor signaling and homeostasis of NK cells by repressing multiple E-protein target genes including Socs3. Deletion of Id2 in mature NK cells was incompatible with their homeostasis due to impaired IL-15 receptor signaling. Id2-null NK cells displayed impaired IL-15 mediated JAK1/STAT5 phosphorylation, compromised metabolic function and enhanced apoptosis. Remarkably, Id2-null NK cell homeostasis could be fully rescued in vivo by IL-15 receptor stimulation and partially rescued by genetic ablation of Socs3. During normal NK cell maturation we observed an inverse correlation between the expression levels of E-protein target genes and Id2. These results shift the current paradigm on the role of Id2, indicating that it is not only required to antagonize E-proteins during NK cell commitment, but constantly required to titrate E-protein activity to regulate NK cell fitness and responsiveness to IL-15. Overall design: Transcriptional profiling of wild type and Id2-null natural killer (NK) cells using RNA sequencing
The Helix-Loop-Helix Protein ID2 Governs NK Cell Fate by Tuning Their Sensitivity to Interleukin-15.
Specimen part, Cell line, Subject
View Samples