A physiologic signaling role for the γ-secretase-derived intracellular fragment of APP
By M. Leissring, M. Murphy, Tonya R. Mead, Yama Akbari, Michael C. Sugarman, M. Jannatipour, B. Anliker, U. Müller, P. Saftig, B. de Strooper and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2002
257 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/8c1bbac689936b7f0f1809bb3db824572f99032a
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Citations in the corpus
- Picomolar amyloid-β positively modulates synaptic plasticity and memory in hippocampus (2008, background): “…1994; Furukawa et al., 1996; Ishida et al., 1997; Meziane et al., 1998), and the intracellular CTF may regulate gene transcription, calcium signaling, synaptic plasticity, and memory (Cao and Südhof, 2001; Gao and Pimplikar, 2001; Kimberly et al., 2001; Leissring et al., 2002; Ma et al., 2007).”
- Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations. (2006, background): “Another hypothesis states that the APP intracellular domain (AICD) released by g-secretase cleavage affects Ca2+ signaling by regulating expression of neuronal Ca2+ signaling proteins (Leissring et al., 2002).”
- Calcium dyshomeostasis and intracellular signalling in alzheimer's disease (2002, background): “However, data from my laboratory indicate that alterations in Aβ formation precede the changes in calciu”