An NF-κB-Like Transcription Factor in Axoplasm is Rapidly Inactivated after Nerve Injury inAplysia

Journal of Neuroscience - Tập 17 Số 13 - Trang 4915-4920 - 1997
Michael Povelones1, Kathy May Tran2, Dimitris Thanos2, Richard T. Ambron1
1Departments of Anatomy and Cell Biology, and
2Biochemistry and Molecular Biophysics, College of Physicians and Surgeons of Columbia University, New York, New York 10032

Tóm tắt

We found a protein in Aplysia neurons that has many characteristics of the transcription factor NF-κB. Thus, the protein recognized a radiolabeled probe containing the κB sequence from the human interferon-β 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 κB site from the major histocompatibility complex I gene promotor. In addition, recombinant mammalian IκB-α, which associates specifically with the P65 subunit of NF-κB, 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-κB. Based on these findings, we believe the protein to be a homolog of NF-κB. To investigate the role of apNF-κB in the axon, we crushed the peripheral nerves to the body wall. Surprisingly, there was a rapid loss of apNF-κB binding at the crush site and, within 15 min, as far as 2.5 cm along the axon. In contrast, exposing either the intact animal or the nervous systemin situto levels of 5-HT that induce synaptic facilitation did not affect apNF-κB activity.

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Journal of Neuroscience

Tập 17 Số 13

4915-4920

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