Associated Papers
Changed membrane integration and catalytic site conformation are two mechanisms behind the increased Aβ42/Aβ40 ratio by presenilin 1 familial Alzheimer-linked mutations.
Wanngren J et al.
Febs Open Bio, 2014
Ultrahigh and high resolution structures and mutational analysis of monomeric Streptococcus pyogenes SpeB reveal a functional role for the glycine-rich C-terminal loop.
González-Páez GE et al.
The Journal of Biological Chemistry, 2012
The mechanism of γ-Secretase dysfunction in familial Alzheimer disease.
Chávez-Gutiérrez L et al.
The Embo Journal, 2012
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