Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations.

By Huiping Tu, Omar Nelson, A. Bezprozvanny, Zhengnan Wang, Sheu-Fen Lee, Yi‐Heng Hao, L. Serneels, Bart de Strooper, Gang Yu, Ilya Bezprozvanny. Cell, 2006

700 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/7c5336c04a009c8363fcda6bbaca28aaa512b0b5

Citations in the corpus

• Aβ plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks (2008, unknown): “Finally, PS1-mediated effects on calcium regulation might also occur independently of gamma secretase activity (Akbari et al., 2004; Tu et al., 2006).”
• An Overview of APP Processing Enzymes and Products (2010, unknown): “…about the exact mechanism, as PS1 may act as a calcium leak channel or it may enhance the opening of the inositol-3-phosphate receptor (IP3R); however, it does seem clear that PS1 causes an increase in cytosolic calcium concentrations (Tu et al., 2006, Nelson et al., 2007, Cheung et al., 2008).”