Figures
Somatic accumulation of primed PKC is an early step in prion neurotoxicity
This immunofluorescence micrograph catches a cultured neuron 30 minutes after exposure to pathogenic prions (PrP Sc ). Protein Kinase C (PKC) primed by phosphorylation at serine-660 rapidly accumulates in specialized endosomes within the cell body, prior to its redistribution to dendritic spines. Colocalization of the primed PKC (red) with total PKC (green) produces striking yellow/orange fluorescence in the cell body. A similar effect is elicited by other strong PKC activators like phorbol ester. This acute spatial rearrangement of a key signaling kinase highlights a crucial, pre-degenerative window prior to neuronal fragmentation and death. Le et al. 2026
Image Credit: Nhat T. T. Le
Citation: (2026) PLoS Pathogens Issue Image | Vol. 22(6) July 2026. PLoS Pathog 22(6): ev22.i06. https://doi.org/10.1371/image.ppat.v22.i06
Published: July 8, 2026
Copyright: © 2026 . This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This immunofluorescence micrograph catches a cultured neuron 30 minutes after exposure to pathogenic prions (PrP Sc ). Protein Kinase C (PKC) primed by phosphorylation at serine-660 rapidly accumulates in specialized endosomes within the cell body, prior to its redistribution to dendritic spines. Colocalization of the primed PKC (red) with total PKC (green) produces striking yellow/orange fluorescence in the cell body. A similar effect is elicited by other strong PKC activators like phorbol ester. This acute spatial rearrangement of a key signaling kinase highlights a crucial, pre-degenerative window prior to neuronal fragmentation and death. Le et al. 2026
Image Credit: Nhat T. T. Le