The effect of sodium salicylate and aspirin on NF-κB

B Frantz, EA O'Neill - Science, 1995 - science.org
B Frantz, EA O'Neill
Science, 1995science.org
DNA into our laboratory. Our conclusion that BCA16 was an ancient isolate is not based
solely on sequence comparisons, but on several lines of evidence that include phenetic and
phylogenetic analysis. Furthermore, a compelling case can be made by comparing the
putatively ancient B. sphaericus isolate (BCA16) with the sequence of the amplicon PD_Ex6
(GenBank accession number L38655) obtained from the abdominal tissue of bees in the
same amber specimen. These sequences were essentially identical (figures 1 and 2 of our …
DNA into our laboratory. Our conclusion that BCA16 was an ancient isolate is not based solely on sequence comparisons, but on several lines of evidence that include phenetic and phylogenetic analysis. Furthermore, a compelling case can be made by comparing the putatively ancient B. sphaericus isolate (BCA16) with the sequence of the amplicon PD_Ex6 (GenBank accession number L38655) obtained from the abdominal tissue of bees in the same amber specimen. These sequences were essentially identical (figures 1 and 2 of our report), which suggests that the BCA16 DNA (or that of a similar organism) was present in the amber inclusion before the organism was cultivated in the laboratory. Although further tests must be done, when all the evidence gathered thus far are evaluated and weighed, they appear to support our claim that BCA16 is indeed ancient.
12-myristate 13-acetate (PMA)/ionomycindependent induction of NF-KB DNA binding activity (not shown) and similarly induced transcription from an NF-KB-dependent enhancer (Fig. lA). To ascertain the nature of this event, we examined the specificity of salicylate. Salicylate inhibited transcription from an AP-l-dependent enhancer induced by PMA/ionomycin (Fig. 1B). This effect is not secondary to the inhibition of NF-KB, as in these cells the immunosuppressive drug FK-506 also inhibits induction of NF-KB-dependent promoter activity by PMA/ionomycin, but has no inhibitory effect on induction of AP-1-dependent activity (2). As activation of NF-KB and AP-l share. the same stimuli,
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