Member of the two-component regulatory system NreB/NreC involved in the control of dissimilatory nitrate/nitrite reduction in response to oxygen. NreB functions as a direct oxygen sensor histidine kinase which is autophosphorylated, in the absence of oxygen, probably at the conserved histidine residue, and transfers its phosphate group probably to a conserved aspartate residue of NreC. NreB/NreC activates the expression of the nitrate (narGHJI) and nitrite (nir) reductase operons, as well as the putative nitrate transporter gene narT. ATP + protein L-histidine = ADP + protein N-phospho-L-histidine. Binds 1 [4Fe-4S] cluster. Activated by cysteine desulfurase, Fe(2+) ions and cysteine and inhibited by oxygen and ADP. Autophosphorylated. NreB may sense the oxygen concentration directly via the disassembly and reassembly of the FNR-type 4Fe-4S cluster. The iron-sulfur cluster controls the functional state of the kinase domain. Under oxic conditions, the iron-sulfur cluster is destroyed and the autophosphorylation activity of NreB is decreased. However, under anoxic conditions and in the presence of iron ions, the iron-sulfur cluster is formed and NreB is autophosphorylated (Probable).