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. Author manuscript; available in PMC: 2007 Sep 19.
Published in final edited form as: Biochim Biophys Acta. 2007 Mar 2;1772(6):629–644. doi: 10.1016/j.bbadis.2007.02.011

FIGURE 1. Possible mechanisms for PrP suppression of Bax-induced apoptosis.

FIGURE 1

PrPC may inhibit Bax-mediated apoptotic pathways at several different points, either by a direct interaction between the two proteins or by involvement of additional, intermediary proteins. PrPC on the cell surface (GPI-PrP) may bind to a putative transmembrane receptor, initiating a signal transduction cascade that culminates in inhibition of Bax mitochondrial translocation, conformational change, or oligomerization (A). Cytoplasmic forms of PrP may produce similar effects via a direct interaction with Bax (B). PrP may inhibit pro-apoptotic, BH3-only proteins (C), or enhance an interaction between Bax and anti-apoptotic, multi-domain proteins such as Bcl-2 and Bcl-XL (D). PrP may suppress downstream events in the Bax pathway, such as cytochrome c (cyto. c) release, or activation of Apaf-1 and caspases (E). Finally, PrP in the ER may alter Bax function in this organelle, via effects on intracellular calcium and the unfolded protein response (UPR) (F).