p62 modulates Akt activity via association with PKC{zeta} in neuronal survival and differentiation
- Department of Biology, Hanseo University, Seosan, Chungnam 352-820 (Korea, Republic of)
- Department of Biology and Research Institute for Basic Sciences, Kyunghee University, Seoul 130-701 (Korea, Republic of)
p62 is a ubiquitously expressed phosphoprotein that interacts with a number of signaling molecules and a major component of neurofibrillary tangles in the brain of Alzheimer's disease patients. It has been implicated in important cellular functions such as cell proliferation and anti-apoptotic pathways. In this study, we have addressed the potential role of p62 during neuronal differentiation and survival using HiB5, a rat neuronal progenitor cell. We generated a recombinant adenovirus encoding T7-epitope tagged p62 to reliably transfer p62 cDNA into the neuronal cells. The results show that an overexpression of p62 led not only to neuronal differentiation, but also to decreased cell death induced by serum withdrawal in HiB5 cells. In this process p62-dependent Akt phosphorylation occurred via the release of Akt from PKC{zeta} by association of p62 and PKC{zeta}, which is known as a negative regulator of Akt activation. These findings indicate that p62 facilitates cell survival through novel signaling cascades that result in Akt activation. Furthermore, we found that p62 expression was induced during neuronal differentiation. Taken together, the data suggest p62 is a regulator of neuronal cell survival and differentiation.
- OSTI ID:
- 20710937
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 334, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2005.06.138; PII: S0006-291X(05)01374-4; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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