Canakinumab is a human anti-interleukin-1 beta (IL-1 beta) monoclonal antibody neutralizing IL-1 beta. Systemic juvenile idiopathic arthritis (SJIA) is a rare, multigenic, autoinflammatory disease of unknown etiology characterized by chronic arthritis; intermittent high-spiking fever, rash, and elevated levels of acute-phase reactants. Blood samples of SJIA patients were obtained from two phase 3 clinical trials conducted by the members of the Pediatric Rheumatology International Trials Organization (PRINTO) and the Pediatric Rheumatology Collaborative Study Group (PRCSG) (Clinicaltrials.gov: NCT00886769 and NCT00889863). For patients, baseline and day 3 samples were analyzed for either placebo or canakinumab (Ilaris) treatment.
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Specimen part, Disease, Treatment, Subject
View SamplesThe goal is the characterization of the off-target activity of BKM120 observed in A2058 human melanoma cell line at IC90 concentration (3.606 M) but not at lower concentrations. Controls are BEZ235, GDC0941, showing no off-target activity.
Characterization of the mechanism of action of the pan class I PI3K inhibitor NVP-BKM120 across a broad range of concentrations.
Cell line
View SamplesMLL1 WT or KO MEF with and without HSP90 inhibitor treatment
Identification of mixed lineage leukemia 1(MLL1) protein as a coactivator of heat shock factor 1(HSF1) protein in response to heat shock protein 90 (HSP90) inhibition.
Treatment
View SamplesTo understand the underlying mechanism by which Alox15 gene is required by HSCs, we performed a comparative DNA microarray analysis using total RNA isolated from wild type Lin-Sca-1+c-Kit+, SELP-/- Lin-Sca-1+c-Kit+. The result was validated by quantitative real-time PCR analysis of wild type Lin-Sca-1+c-Kit+ and SELP-/- Lin-Sca-1+c-Kit+.
Arachidonate 15-lipoxygenase is required for chronic myeloid leukemia stem cell survival.
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View SamplesExtracellular signal regulated kinases, ERK1 and ERK2 are often considered as redundant due to their high homology, large number of overlapping substrates, and ability to substitute for each other in genetically engineered mouse models. We have investigated the individual contribution of ERK1 and ERK2 to the survival of human melanoma cell lines driven by oncogenic BRAF. ERK2, but not ERK1 activity, was crucial to drive survival and maintain transcriptional output of the MAPK pathway. Furthermore, we found that ERK2 DEF-domain interactions were crucial for transcriptional regulation and survival in some cells, but not in others, whereas ERK2-substrate interactions at the D-docking motif were largely dispensable.
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Cell line, Treatment, Time
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