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Journal of Bacteriology|June 1, 1988
Identification of a site of ATP requirement for signal processing in bacterial chemotaxisJ M Smith, E H Rowsell, J Shioi, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|July 1, 1997
Appican expression induces morphological changes in C6 glioma cells and promotes adhesion of neural cells to the extracellular matrixA Wu, M N Pangalos, S Efthimiopoulos, et al.
Neurodegeneration : a Journal for Neurodegenerative Disorders, Neuroprotection, and Neuroregeneration|December 1, 1996
Characterization of appican, the chondroitin sulfate proteoglycan form of the Alzheimer amyloid precursor proteinM N Pangalos, J Shioi, S Efthimiopoulos, et al.
Journal of Neuroscience Research|October 1, 1992
Evidence for intracellular cleavage of the Alzheimer's amyloid precursor in PC12 cellsK Sambamurti, J Shioi, J P Anderson, et al.
Annals of the New York Academy of Sciences|September 24, 1993
Cellular processing and proteoglycan nature of amyloid precursor proteinsN K Robakis, D Vassilacopoulou, S Efthimiopoulos, et al.
The American Journal of Pathology|February 1, 1997
Presenilin-1-immunoreactive neurons are preserved in late-onset Alzheimer's diseaseP Giannakopoulos, C Bouras, E Kövari, et al.
Acta Neuropathologica|December 14, 1999
Presenilin-1 expression in Pick's diseaseP Giannakopoulos, E Kövari, L Buée, et al.
The Journal of Biological Chemistry|August 2, 2001
Appican, the proteoglycan form of the amyloid precursor protein, contains chondroitin sulfate E in the repeating disaccharide region and 4-O-sulfated galactose in the linkage regionK Tsuchida, J Shioi, S Yamada, et al.
The Journal of Biological Chemistry|May 19, 1995
The Alzheimer amyloid precursor proteoglycan (appican) is present in brain and is produced by astrocytes but not by neurons in primary neural culturesJ Shioi, M N Pangalos, J A Ripellino, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|November 21, 1998
Overexpression in neurons of human presenilin-1 or a presenilin-1 familial Alzheimer disease mutant does not enhance apoptosisS Bursztajn, R DeSouza, D L McPhie, et al.
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