Retrograde Transport of Transcription Factor NF-κB in Living Neurons*

By H. Wellmann, B. Kaltschmidt, C. Kaltschmidt. Journal of Biological Chemistry, 2001

117 citations recorded by the source corpus.

The mechanism by which signals such as those produced by glutamate are transferred to the nucleus may involve direct transport of an activated transcription factor to trigger long-term transcriptional changes. Ionotropic glutamate receptor activation or depolarization activates transcription factor NF-κB and leads to translocation of NF-κB from the cytoplasm to the nucleus. We investigated the dynamics of NF-κB translocation in living neurons by tracing the NF-κB subunit RelA (p65) with jellyfish green fluorescent protein. We found that green fluorescent protein-RelA was located in either the nucleus or cytoplasm and neurites, depending on the coexpression of the cognate inhibitor of NF-κB, IκB-α. Stimulation with glutamate, kainate, or potassium chloride resulted in a redistribution of NF-κB from neurites to the nucleus. This transport depended on an intact nuclear localization signal on RelA. Thus, in addition to its role as a transcription factor, NF-κB may be a signal transducer, transmitting transient glutamatergic signals from distant sites to the nucleus.

Subfields: Cancer Research

View Paper: https://www.semanticscholar.org/paper/e9bc507001d4cf96c89d6ccb90143b67994c90e0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Chuen-Mao Yang
2. Ruey-Horng Shih
3. Chen-Yu Wang

Citations in the corpus

• NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review (2015, background): “Thus, NF-κB is involved in translation of short-lasting synaptic signals to persistent changes in gene expression (Wellmann et al., 2001; Meffert et al., 2003).”
• Regulation of transcription factors by neuronal activity (2002, unknown): “NF-κB is activated by membrane depolarization and glutamate stimulation in both cultured cerebellar granule cells and hippocampal neuron”