The transcriptional activation of specific genes by transciption factor proteins is an important factor in
the determination of cell-type specific patterns of gene expression. In one form or another, transcription factors
comprising the Rel-family of proteins (responsible for the activity referred to as “NF-κB”) are present in every
cell type examined. However, studies of NF-κB often rely solely on a single endpoint (e.g., nuclear translocation)
as an index of activation. Careful examination of CNS neuronal populations indicates that the initial components
of NF-κB activation, up to and including nuclear translocation, are often dissociated from transcriptional
activation. Indeed, there are few, if any, circumstances in which classical transcriptional activation by NF-κB has
been documented in CNS neurons. In addition to the mechanistic intrigue this disjunction inspires, it is possible
that this phenomenon contributes to important cell-type specificity distinguishing neurons from other cell types. It
also suggests several implications for pharmacotherapeutic manipulation of NF-κB in the CNS.
Keywords: Artifact, cell culture, Glia, neurons, nuclear factor kappa B, rel family, reporter gene, specificity protein
transcription factor (Sp1), specificity protein 4 transcription factor (Sp4), transcription.
