Alteration of NF-kappaB activity leads to mitochondrial apoptosis after infection with pathological prion protein.

ABSTRACT: Nuclear factor kappa B (NF-kappaB) is a key regulator of the immune response, but in almost the same manner it is involved in induction of inflammation, proliferation and regulation of apoptosis. In the central nervous system activated NF-kappaB plays a neuroprotective role. While in some neurodegenerative disorders the role of NF-kappaB is well characterized, there is poor knowledge on the role of NF-kappaB in prion disease. We found binding but no transcriptional activity of the transcription factor in vitro. Characterizing the mechanism of cell death after infection with pathological prion protein increased caspase-9 and caspase-3 activity was detected and the lack of NF-kappaB activity resulted in the inability to activate target genes that usually play an important role in neuroprotec

SUBMITTER: Bourteele S 

PROVIDER: S-EPMC2048569 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature