Transcription profiling of human fibrosarcoma cells to study the relative contributions of Jak1 and Jak2 in IFNg signaling
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ABSTRACT: General impact of Jak1 and Jak2 inhibition on IFNg-mediated target gene expression. U4C-Jak1AS and g2A-Jak2AS cells were stimulated with IFNg and treated with either 1NM-PP1 (to inhibit the activity only of the analog-sensitive mutant) or JI1 (to suppress both wild-type and analog-sensitive Jaks) for 24h.
Project description:A global microRNA expression profile was obtained from gradient-purified granulocytes (>95% pure) collected at the time of screening and at cycle 4 of treatment Protocol #18424-256 is a Phase 2 study of the JAK1 and JAK2 inhibitor INCB01842 in patients with advanced polycythemia vera (PV) and essential thrombocythemia (ET) refractory to hydroxyurea; The aim was to to determine whether treatment with INC180424 was associated with changes in the global microRNA expression profile we compared granulocytes collected at baseline (screening) and at cycle 4
Project description:Timecourse analysis of Interferon-Gamma (IFNg) signalling in mice deficient for IFNg or both IFNg and Suppressor of Cytokine Signalling-1 (SOCS1).
Project description:We have examined the transcriptional events in mouse bone marrow derived macrophages (MBDM) with interferon-gamma (Ifng)at 2, 4 & 8 h following treatment or pre-treatment (0 h).
Project description:Using Affinity Purification in tandem to targeted LC-MS/MS analysis, we identified possible succination sites of JAK1 and IKK2 proteins follwoing DMF treatement. We looked for the specific 2-Dimethylsuccinyl modifications of Cysteins residues.
Project description:The present study show the impact of macrophages activation by IFN-Gamma on the gene regulation in intracellularly replicating L. monocytogenes and provide an overview about additionally adaption mechanisms of L. monocytogenes to immune response.
Project description:Gene expression profiling experiments were performed using the Agilent 44K whole human genome microarrays (Agilent Biotechnologies, Diegem, Belgium) according to the two-color gene expression analysis (Quick Amp labeling) protocol (version 5.7) from the manufacturer. Hybridizations were performed by comparing 300 ng of total RNA extracted from HEL cells treated with either 5 ?M of JI1 or 10 ?M of Erlotinib with that obtained from untreated cells. For each treatment, three biological replicates were analyzed in duplicate including a dye swap. Only high quality RNAs with a ribosomal RNA ratio greater than 1.9 and no evidence of degradation, as evaluated using the Agilent Bioanalyzer 2100 RNA 6000 nano assay, were used in this study. Microarray images were quantified using the GenePix Pro 6.1 software (Molecular Devices, Sunnyvale, CA, USA) as described in supplemental information.
Project description:We performed bulk RNA-Seq to investigate global transcriptional changes upon overexpression of the centromeric H3 variant CenH3/CENP-A in p53 wild-type and defective cells, and after X-irradiation treatment. We established clonal MCF-10-2A TetOn-CENPA-FLAG-HA cell lines where CENP-A can be reversibly induced by Doxycycline (Dox) treatment. Upon CENP-A overexpression, these cells exhibit different radiosensitivity depending on p53 status. In order to profile global changes in expression, we compared MCF-10-2A TetOn-CENPA-FLAG-HA cells expressing either empty vector (p53-WT) or dominant-negative p53 (p53-DN) with 0X Dox (no Dox), 1X Dox (10 ng/ml), or 10X Dox (100 ng/ml) for 24h. At time 0, we irradiated one set of cells by X-ray generator (4gy) while a control set remained un-irradiated (0gy). 6h later, we extracted RNA for RNA-seq.
Project description:In order to identify genes dysregulated by the aberrant transcriptional activity of RUNX1-RUNX1T1, we used microarrays to determine the effect of this mutation on gene expression during myeloid and erythroid development of normal human progenitor cells.
Project description:We established the transcriptional profile of brain aging and examine the global effects of vitamin E supplementation on age-related alterations in expression in the aged mouse brain. Experiment Overall Design: Gene expression profiles were obtained from the neocortex tissues of 5-month-old controls, 30-month-old controls and 30-month old B6C3F1 mice with middle age-onset supplementation of alpha-tocopherol or a mixture of alpha and gamma-tocopherol (500mg/kg of each tocopherol).