B/DNA Binding in Neuronal Apoptosis Induced by K+ Loss
Dong Yan,
Qiaoyun Yang,
Rui Zeng, and
Yizheng Wang*
Laboratory of Neural Signal Transduction, Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 200031, People's Republic of China
Received 22 June 2005/ Returned for modification 14 August 2005/ Accepted 12 November 2005
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-
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-
B/DNA binding through direct effects on the interaction of NF-
B dimers with DNA. Up-regulation of proapoptotic protein Bcl-XS and neuronal apoptosis induced by serum deprivation are blocked by inhibition and/or down-regulation of NF-
B and by prevention of K+ loss. Thus, a direct action of K+ on NF-
B/DNA binding regulates gene transcription related to neuronal apoptosis.
Y.T. and D.Y. contributed equally to this work.
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