APP at a glance
Author:
Affiliation:
1. Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
2. Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Charlestown, MA, USA
Publisher
The Company of Biologists
Subject
Cell Biology
Link
http://journals.biologists.com/jcs/article-pdf/120/18/3157/1370580/3157.pdf
Reference77 articles.
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2. Ando, K., Iijima, K. I., Elliott, J. I., Kirino, Y. and Suzuki, T. (2001). Phosphorylation-dependent regulation of the interaction of amyloid precursor protein with Fe65 affects the production of beta-amyloid. J. Biol. Chem.276, 40353-40361.
3. Annaert, W. and De Strooper, B. (1999). Presenilins: molecular switches between proteolysis and signal transduction. Trends Neurosci.22, 439-443.
4. Araki, Y., Miyagi, N., Kato, N., Yoshida, T., Wada, S., Nishimura, M., Komano, H., Yamamoto, T., De Strooper, B., Yamamoto, K. et al. (2004). Coordinated metabolism of Alcadein and amyloid beta-protein precursor regulates FE65-dependent gene transactivation. J. Biol. Chem.279, 24343-24354.
5. Asaumi, M., Iijima, K., Sumioka, A., Iijima-Ando, K., Kirino, Y., Nakaya, T. and Suzuki, T. (2005). Interaction of N-terminal acetyltransferase with the cytoplasmic domain of beta-amyloid precursor protein and its effect on A beta secretion. J. Biochem.137, 147-155.
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