Project description:We investigated the ability of the NFkB protein p65 to bind RNA and what its target transcrips were. In this CLIP-seq experiment we demonstrated that p65 is capable of binding RNA and it has a preference to introns and exons, suggesting it binds unspliced RNA.
Project description:WT mice and Nfkb/p65 S534A were exposed to 1mg/kg LPS and their gene expression measured. Affymetrix Mouse 1.0ST chips were used to measure gene expression.
Project description:WT mice and Nfkb/p65 S534A were exposed to 1µg/kg LPS and their gene expression measured. Affymetrix Mouse 1.0ST chips were used to measure gene expression
Project description:Nuclear factor kappa B and C/EBP are two important transcription factors that independently and synergistically regulate different genes. In this experiment the expression of genes will be examined with the overexpression of NFKB (p65) and CEBP alone and in combination.
Project description:We used microarrays to assess gene expression in p65-knockout 3T3 fibroblasts, after stable reconstitution with normal and engineered forms of NFkB p65, and knock-down of Zbtb7a using stable shRNA interference. Cells were treated with 5ng/ml mouse TNF-alpha to stimulate NFkB pathway activation.
Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array Analysis of gene expression in lewis lung carcinoma cells resected from lungs of WT and RelA/p65 deficient mice exposed to smoke or air. Four different samples were analyzed (3 replicates each).
Project description:We investigated the ability of the NFkB protein p65 to bind DNA after RNA digestion. In this ChIP-seq experiment, we investigated the genome-wide binding profiles of p65 in Jurkat cells. We demonstrated that p65 binding to promoters and promoter proximal regions is enhanced by digestion of RNA with RNase A.
Project description:Smoking is the most important risk factor for both lung cancer (LC) and chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the role of myeloid cell NF-kB in the regulation of tumor cell growth signaling. We subjected mice lacking myeloid RelA/p65 to a metastatic LC model. Cigarette smoke (CS) exposure significantly increased the proliferation of Lewis lung carcinoma cell (LLC) tumors in wild type mice. In CS exposed mice lacking myeloid RelA/p65, the tumor growth was largely inhibited. Transcriptome and pathway analysis of cancer tissue revealed a fundamental impact of myeloid cells on various growth signaling pathways. Myeloid RelA/p65 is necessary to link smoke-induced inflammation with LC growth. Keywords: Expression profiling by array