Role of the Presenilin1mediated cleavage of Ephrin B proteins

Anastasios Georgakopoulos, PhD
Mount Sinai School of Medicine (New York, NY)
Year Awarded:
Grant Duration:
April 1, 2003 to March 31, 2005
Alzheimer's Disease
Award Amount:
Grant Reference ID:
Award Type:
Award Region:
US Northeastern

Role of the Presenilin1mediated cleavage of Ephrin B proteins


Alzheimer's disease (AD) is a neurodegenerative disorder of the central nervous system (CNS). There are at least two forms of AD: the sporadic form, which inflicts most AD patients and usually occurs after the age of 65 or 70, and the familial form, which occurs at earlier stages and follows a more rapid progressive course than the sporadic disease. Familial AD (FAD) is caused by mutations in certain genes, including the amyloid precursor protein (APP) gene, presenilin-1 (PS1), and presenilin-2 (PS2). PS1 mutations are responsible for most cases of FAD. It was recently demonstrated that PS1 controls the γ-secretase-mediated cleavage of several type I transmembrane proteins like the APP, Notch, erbB4, CD44 and E-cadherin. EphrinB proteins are type I transmembrane proteins that are ligands for the ephrinB receptors (EphBs). Both proteins are expressed in the CNS and are also found at the neuronal synapses, where they play a very important role in the synaptic function affecting memory. The goal of this study is to investigate the role of PS1-dependent γ-secretase-like activity in the processing and function of ephrinB proteins.


Georgakopoulos A, Litterst C., Baki L, Xu CJ, Serban J, and Robakis, NK (2005) PS1/y-secretase mediate the EphB-induced phosphorylation of Src and ephrinB: Effects of FAD mutations. [PMID: nd][link not available]
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