Associated Papers
Decrease in catalytic capacity of γ-secretase can facilitate pathogenesis in sporadic and Familial Alzheimer's disease.
Svedružić ŽM et al.
Molecular and Cellular Neurosciences, 2015
Alzheimer presenilin-1 mutations dramatically reduce trimming of long amyloid β-peptides (Aβ) by γ-secretase to increase 42-to-40-residue Aβ.
Fernandez MA et al.
The Journal of Biological Chemistry, 2014
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
Molecular consequences of amyloid precursor protein and presenilin mutations causing autosomal-dominant Alzheimer's disease.
Weggen S et al.
Alzheimer's Research & Therapy, 2012
Amyloid precursor protein gene mutations responsible for early-onset autosomal dominant Alzheimer's disease.
Kowalska A
Folia Neuropathologica, 2003
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