Differential contribution of the three Aph1 genes to γ-secretase activity in vivo

By L. Serneels, T. Dejaegere, K. Craessaerts, Katrien Horré, E. Jorissen, T. Tousseyn, Sébastien S. Hébert, Marcel W. Coolen, G. Martens, A. Zwijsen and 3 more. 2005

170 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/3654dda1453bcc835ddff522e99e66dd8719b5f2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Ilya Bezprozvanny

In Molecular Biology

1. B. de Strooper

In Physiology

1. E. Karran
2. M. Mercken
3. Ilya Bezprozvanny
4. B. de Strooper

Citations in the corpus

• Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations. (2006, background): “Moreover, the filling state of ER Ca2+ stores was normal in Aph-1abc / MEF cells (Figure 6B and Figure 7B), which completely lack g-secretase activity (Serneels et al., 2005).”
• The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics (2011, background): “There are two homologues of APH1 in humans — APH1A and APH1B — so in total there are four different γ-secretase complexes possibl”