Journal
CURRENT NEUROPHARMACOLOGY
Volume 12, Issue 3, Pages 213-218Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570159X11666131225000518
Keywords
Hypoxia; neuroprotection; PKN; PRK; protein kinase C-related kinase; purine nucleosides; review
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Funding
- Austrian Science Fund (FWF) [T 421-B18, P 19578-B05, P 26002-B24]
- Austrian Science Fund (FWF) [P26002] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [T 421] Funding Source: researchfish
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Serine/threonine protein kinase C-related kinase (PKN/PRK) is a family of three isoenzymes (PKN1, PKN2, PKN3), which are widely distributed in eukaryotic organisms and share the same overall domain structure. The N-terminal region encompasses a conserved repeated domain, termed HR1a-c as well as a HR2/C2 domain. The serine/threonine kinase domain is found in the C-terminal region of the protein and shows high sequence homology to other members of the PKC superfamily. In neurons, PKN1 is the most abundant isoform and has been implicated in a variety of functions including cytoskeletal organization and neuronal differentiation and its deregulation may contribute to neuropathological processes such as amyotrophic lateral sclerosis and Alzheimer's disease. We have recently identified a candidate role of PKN1 in the regulation of neuroprotective processes during hypoxic stress. Our key findings were that: 1) the activity of PKN1 was significantly increased by hypoxia (1% O-2) and neurotrophins (nerve growth factor and purine nucleosides); 2) Neuronal cells, deficient of PKN1 showed a decrease of cell viability and neurite formation along with a disturbance of the F-actin-associated cytoskeleton; 3) Purine nucleoside-mediated neuroprotection during hypoxia was severely hampered in PKN1 deficient neuronal cells, altogether suggesting a potentially critical role of PKN1 in neuroprotective processes. This review gives an up-to-date overview of the PKN family with a special focus on the neuroprotective role of PKN1 in hypoxia.
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