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Pro-apoptotic action of PAR-4 involves inhibition of NF-?B activity and suppression of BCL-2 expression

2000; Wiley; Volume: 61; Issue: 2 Linguagem: Inglês

10.1002/1097-4547(20000715)61

1097-4547

Simonetta Camandola, Mark P. Mattson,

Immune Response and Inflammation

Journal of Neuroscience ResearchVolume 61, Issue 2 p. 134-139 Article Pro-apoptotic action of PAR-4 involves inhibition of NF-κB activity and suppression of BCL-2 expression Simonetta Camandola, Simonetta Camandola Sanders-Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, LexingtonSearch for more papers by this authorMark P. Mattson, Corresponding Author Mark P. Mattson [email protected] Sanders-Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, Baltimore, MarylandLaboratory of Neurosciences, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224Search for more papers by this author Simonetta Camandola, Simonetta Camandola Sanders-Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, LexingtonSearch for more papers by this authorMark P. Mattson, Corresponding Author Mark P. Mattson [email protected] Sanders-Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, Baltimore, MarylandLaboratory of Neurosciences, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224Search for more papers by this author First published: 27 June 2000 https://doi.org/10.1002/1097-4547(20000715)61:2 3.0.CO;2-PCitations: 69AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract Par-41 (prostate apoptosis response 4) is known to function at an early stage in apoptosis in several different cell types, including neurons. On the other hand, activation of the transcription factor NF-κB can prevent apoptosis in various cancer cells and neurons. We now report that overexpression of full-length Par-4 in cultured PC12 cells results in a suppression of basal NF-κB DNA-binding activity and NF-κB activation following trophic factor withdrawal (TFW). The decreased NF-κB activity is correlated with enhanced apoptosis. Conversely, NF-κB activity is increased and vulnerability to apoptosis reduced in cells overexpressing a dominant-negative form of Par-4. Par-4 overexpression or functional blockade had no effect on AP-1 DNA-binding activity. Expression of the antiapoptotic protein Bcl-2 was dramatically reduced in PC12 cells overexpressing Par-4. Our data suggest that suppression of NF-κB activation plays a major role in the proapoptotic function of Par-4. \ J. Neurosci. Res. 2:134–139, 2000. © 2000 Wiley-Liss, Inc. Citing Literature Volume61, Issue215 July 2000Pages 134-139 RelatedInformation