Wang, YZ (reprint author), Chinese Acad Sci, SIBS, Inst Neurosci,Grad Sch, Lab Neural Signal Transduct, 320 Yue Yang Rd, Shanghai 200031, Peoples R China,firstname.lastname@example.org
Low intracellular K+ concentration ([K+](i)) promotes apoptosis and blocking K+ loss prevents apoptosis, but the mechanism of action of low [K+](i) remains unclear. Here, we show that low [K+](i) increases NF-kappa B transcriptional activity by enhancing its binding to the promoter of target genes without affecting its activation and nuclear translocation in cortical neurons deprived of serum. Low K+ concentration promotes NF-kappa B/DNA binding through direct effects on the interaction of NF-kappa B dimers with DNA. Up-regulation of proapoptotic protein Bcl-X-S and neuronal apoptosis induced by serum deprivation are blocked by inhibition and/or downregulation of NF-kappa B and by prevention of K+ loss. Thus, a direct action of K+ on NF-kappa B/DNA binding regulates gene transcription related to neuronal apoptosis.