Member of the two-component regulatory system GlnK/GlnL that positively regulates the expression of the glsA-glnT operon in response to glutamine (PubMed:11717295, PubMed:15995196). It seems that autophosphorylated GlnK transfers a phosphoryl group to GlnL, which positively regulates the expression of the glsA-glnT operon (PubMed:11717295, PubMed:15995196). Interaction between GlnK-AmtB complex and TnrA protects TnrA from proteolytic degradation (PubMed:17001076, PubMed:21435182). ATP + protein L-histidine = ADP + protein N-phospho-L-histidine. Homotrimer (PubMed:17001076, PubMed:25691471). Under poor nitrogen source such as nitrate, the complex between GlnK and AmtB, which are the transmembrane ammonium transporter and its cognate regulator, respectively, interacts with TnrA (PubMed:17001076, PubMed:21435182, PubMed:25691471). GlnK-ATP complex are not able to bind TnrA (PubMed:21435182). ATP concentrations are sensed by GlnK and affect its cellular localization. In the absence of nitrogen source, cells lacking this gene do not show degradation of TnrA, which is entirely soluble.