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Neuron, v.17 no.5, 1996년, pp.1023 - 1030
Doan, Andrew (Department of Neuroscience, The Johns Hopkins University, School of Medicine, Baltimore, Maryland, 21205, USA) , Thinakaran, Gopal (Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland, 21205, USA) , Borchelt, David R (Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland, 21205, USA) , Slunt, Hilda H (The Neuropathology Laboratory, The Johns Hopkins University, School of Medicine, Baltimore, Maryland, 21205, USA) , Ratovitsky, Tamara (The Neuropathology Laboratory, The Johns Hopkins University, School of Medicine, Baltimore, Maryland, 21205, USA) , Podlisny, Marcia (Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts, 02115, USA) , Selkoe, Dennis J (Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts, 02115, USA) , Seeger, Mary (Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York, 10021, USA) , Gandy, Samuel E (Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York, 10021, USA) , Price, Donald L (Department of Neurosci) , Sisodia, Sangram S
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AbstractMutations in a gene encoding a multitransmembrane protein, termed presenilin 1 (PS1), are causative in the majority of early-onset cases of AD. To determine the topology of PS1, we utilized two strategies: first, we tested whether putative transmembranes are sufficient to export a protease-s...
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