5 ms·

The hypothesis for many prion diseases is that of "seeding" whereby a small number (or maybe even a single) prion protein acts as a template to induce misfoldin

The hypothesis for many prion diseases is that of "seeding" whereby a small number (or maybe even a single) prion protein acts as a template to induce misfolding of other proteins with similar sequence but native folds [1,2]. This causes a chain reaction in the proliferation of the prion protein inside the cell, and then in other cells as prion proteins are transported/secreted to the surrounding tissue. [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665718/#S1title https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665718/#S1titl... [2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449729/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449729/

LambdaComplex 7y ago
>whereby a small number (or maybe even a single) prion protein acts as a template to induce misfolding of other proteins So, maybe Vonnegut was onto something when he wrote Cat's Cradle
sandworm101 7y ago
There is an advantage in thinking about prions, and proteins more generally, as crystals rather than biological systems. A vat of fluid can sit for decades without ever forming a crystal. But then the addition of a single seed can give rise to an infinitely large, growing, structure.