There seem to be clear evolutionary advantages of fortuitously adapting toxic reactions for signaling pathways. This may imply that every cytotoxic or genotoxic reaction has such potential. In the case of reactive oxygen and NO, new biological reactions continue to be described. Some of these involve new signaling mechanisms. Others are merely new examples of previously known mechanisms. In the particular case of DNICs, we note their broad occurrence in a wide range of different cells after exposure to NO. The DNICs appear wherever FeS
Reduced >Fei_lF(0F^ Inactive
Fig. 5. Scheme for SoxR activation by various stimuli. SoxR with reduced [2Fe—2S] centers binds the soxS promoter but does not stimulate transcription. Oxidation of the metal centers converts SoxR to a strongly active form, as does nitrosylation by nitric oxide to form DNIC. Removal of the metal centers by chelation or mutational substitution of the iron-anchoring cysteine residues also activates SoxR, although this form has lower transcriptional activity than oxidized or nitrosylated SoxR. The structural transitions in the C-terminus due to these modifications are symbolized, as is a proposed reorientation of the subunits accompanying activation.
Chelators, Iron deficiency
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