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Papers In Press, published online ahead of print September 8, 2000
J. Biol. Chem, 10.1074/jbc.C000507200
Submitted on July 31, 2000
Accepted on September 7, 2000

The NF-kappa B-inducing kinase NIK induces PC12 cell differentiation and prevents apoptosis

Erik D. Foehr, Jan Bohuslav, Lin-Feng Chen, Carlos DeNoronha, Romas Geleziunas, Xin Lin, Alison O'Mahony, and Warner C. Greene

Virology and Immunology, J. David Gladstone Institute, San Francisco, CA 94141-9100

Corresponding Author: efoehr{at}gladstone.ucsf.edu

NF-kappa B has been implicated in the survival and differentiation of PC12 cells. In this study, we examined the effect of the NF-kappa B inducing kinase (NIK) on these processes. When inducibly expressed in PC12 cells, a kinase-proficient but not kinase deficient form of NIK promoted neurite process formation and mediated anti-apoptotic signaling. As expected, NIK expression led to IKK activation and induced nuclear translocation of NF-kappa B. However, NIK-induced neurite outgrowth was only partially blocked by concamitant expression of a nondegradable form of Ikappa Balpha that completely blocks NF-kappa B induction. In search of additional signaling pathways activated by NIK, we now demonstrate that NIK activates MEK1 phosphorylation and induces the Erk1/Erk2 MAPK pathway. Treatment of PC12 cells with PD98059, a MEK1 inhibitor, potently blocked neurite process formation; however, a dominantly interfering mutant of the upstream Shc adapter failed to alter this response. These findings reveal a new function for NIK as a MEK1 -dependent activator of the MAPK pathway and implicate both the IKK and MAPK signaling cascades in NIK-induced differentiation of PC12 cells.


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