Understanding the structure and interplay of cellular signalling pathways is one of the great challenges in molecular biology. Boolean Networks can infer signalling networks from observations of protein activation. In situations where it is difficult to assess protein activation directly, Nested Effect Models are an alternative. They derive the network structure indirectly from downstream effects of pathway perturbations. To date, Nested Effect Models cannot resolve signalling details like the formation of signalling complexes or the activation of proteins by multiple alternative input signals. Here we introduce Boolean Nested Effect Models (B-NEM). B-NEMs combine the use of downstream effects with the higher resolution of signalling pathway structures in Boolean Networks. We show that B-NEMs accurately reconstruct signal flows in simulated data. Using B-NEM we then resolve BCR signalling via PI3K and TAK1 kinases in BL2 lymphoma cell lines.
Analyzing synergistic and non-synergistic interactions in signalling pathways using Boolean Nested Effect Models.
Specimen part, Cell line, Treatment
View SamplesIdentification of genes up or down regulated in LPS stimulated samples in comparison to control samples.
Genomic data integration using guided clustering.
Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A comparative study of RNA-Seq and microarray data analysis on the two examples of rectal-cancer patients and Burkitt Lymphoma cells.
Cell line, Treatment
View SamplesRNA-Seq profiling of Burkitt Lymphoma cell line (BL2) with B-cell activating factor (BAFF) for 24 hrs . The Burkitt Lymphoma cell line were either only cultured in cell culture medium supplemented with 10 mM HEPES at 1 × 106 cells/ml or additionally incubated with B-cell activating factor (BAFF) for 24 hrs Overall design: Two conditions of BL2 cells each in 3 replicates: 1. non-stimulated control (BL2), 2. Baff stimulated (BL2Baff)
A comparative study of RNA-Seq and microarray data analysis on the two examples of rectal-cancer patients and Burkitt Lymphoma cells.
Treatment, Subject
View SamplesMicroarray profiling of Burkitt Lymphoma cell line (BL2) with B-cell activating factor (BAFF) for 24 hrs .
A comparative study of RNA-Seq and microarray data analysis on the two examples of rectal-cancer patients and Burkitt Lymphoma cells.
Cell line
View SamplesIn this study, we have investigated the effect of LMP2A on gene expression in normal human GC B cells using a non-viral vector based system
Suppression of the LMP2A target gene, EGR-1, protects Hodgkin's lymphoma cells from entry to the EBV lytic cycle.
Specimen part, Subject
View SamplesTranscriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s). Overall design: mRNA profiles of group 2 innate lymphoid cells (ILC2s) sort-purified from small intestinal lamina propria and mesenteric white adipose tissue of 9-week-old wild type (WT) mice were generated by sequencing, in duplicate, using Illumina HiSeq1500.
Innate Lymphoid Cells in the Induction of Obesity.
Age, Specimen part, Subject
View SamplesIn this study we investigated to which extend aberrant c Myc activity plays a functional role in other aNHL and whether it is independent from MYC translocations. Based on a combined microarray analysis of human germinal centre (GC) B cells transfected with c Myc and 220 aNHLs cases, we developed a c Myc index.
High Myc activity is an independent negative prognostic factor for diffuse large B cell lymphomas.
Specimen part, Treatment
View SamplesGene expression was compared between four B-cell derived HL cell lines (L428, L1236, L591, KMH2) and GC B cells from three different patients.
The Epstein-Barr virus oncoprotein, latent membrane protein-1, reprograms germinal centre B cells towards a Hodgkin's Reed-Sternberg-like phenotype.
No sample metadata fields
View SamplesIn this study, we have investigated the effect of BLIMP1 on gene expression, cell differentiation and pathogenesis in normal human GC B cells using a non-viral vector based system
Down-regulation of BLIMP1α by the EBV oncogene, LMP-1, disrupts the plasma cell differentiation program and prevents viral replication in B cells: implications for the pathogenesis of EBV-associated B-cell lymphomas.
Specimen part
View Samples