PMID: 9185529Jul 1, 1997Paper

An NF-kappaB-like transcription factor in axoplasm is rapidly inactivated after nerve injury in Aplysia

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
M PovelonesR T Ambron

Abstract

We found a protein in Aplysia neurons that has many characteristics of the transcription factor NF-kappaB. Thus, the protein recognized a radiolabeled probe containing the kappaB sequence from the human interferon-beta gene enhancer element (PRDII), and the binding was not affected by PRDIV, an ATF-2 enhancer sequence from the same gene. Binding was efficiently inhibited, however, by nonradioactive oligonucleotides containing H2, the kappaB site from the major histocompatibility complex I gene promotor. In addition, recombinant mammalian IkappaB-alpha, which associates specifically with the P65 subunit of NF-kappaB, inhibited the binding to the PRDII probe in a dose-dependent manner. The nuclear form of the Aplysia protein was constitutively active. Axoplasm, however, contained the constitutively active form as well as a latent form. The latter was activated by treatment with deoxycholate under the same conditions as mammalian NF-kappaB. Based on these findings, we believe the protein to be a homolog of NF-kappaB. To investigate the role of apNF-kappaB in the axon, we crushed the peripheral nerves to the body wall. Surprisingly, there was a rapid loss of apNF-kappaB binding at the crush site and, within 15 min, as far as 2.5 cm...Continue Reading

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