![]() Urban environments are plagued by complex mixtures of anthropogenic volatile organic compounds (VOCs), such as mixtures of benzene, toluene, ethylene, and xylene (BTEX). ![]() Data are representative of three experiments. The arrow indicates the NF-kB DNA binding complex composed of RelA heterodimers. (F) Nfkbia −/− fibroblasts expressing the indicated constructs were treated with LPS alone (L) or were costimulated with LPS and aLTbR (LB) for the indicated times before being subjected to RelA-EMSA. Data are means ± SEM of three biological replicates. (E) Nfkbia −/− fibroblasts expressing the indicated constructs were treated with LPS for the indicated times before being subjected to RT-PCR analysis of Nfkb2 mRNA abundance. Data are representative of three independent experiments. (D) Nfkbia −/− fibroblasts expressing the indicated constructs were treated with LPS for the indicated times before being subjected to RelA-EMSA. LPS-induced changes in Nfkbia mRNA abundance expressed by the endogenous (Endo) promoter in WT fibroblasts were measured as a control. (C) WT and Nfkbia −/− fibroblasts expressing the indicated constructs were treated with LPS for 1 hour before being subjected to RT- PCR analysis of Nfkbia mRNA abundance normalized to that of Actb mRNA. Blots are representative of two technical replicates. (B) Western blotting analysis of IkBa proteins in Nfkbia −/− fibroblasts expressing transgenic (tg) constructs containing promoters with either one or five kB sites. The differences in the RelA activity induced for a given value of the rate constant and the nominal value were computed and plotted along the y axis. The activity of RelA at late time points was determined as the area under the respective time-course curve measured between 16 and 24 hours. (A) Computational simulations showing changes in the nuclear activity of RelA (RelAn) at late times in response to the indicated stimuli as a function of the rate constant corresponding to the NFkB–induced expression of Nfkbia mRNA (which encodes IkBa). Enhancing the NF-kB responsiveness of the Nfkbia promoter in fibroblasts abrogates cross-talk by reducing the expression of Nfkb2 mRNA.
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