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P2‐135: Loss of NPC1 leads to decreased expression of APP at the cell surface and alters APP distribution within endosome compartments
Author(s) -
Lisica Ana,
Krolo Ana,
Malnar Martina,
Kosicek Marko,
Hecimovic Silva
Publication year - 2009
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2009.04.446
Subject(s) - endosome , microbiology and biotechnology , npc1 , colocalization , lipid raft , amyloid precursor protein , chemistry , lysosome , biology , biochemistry , intracellular , medicine , enzyme , signal transduction , alzheimer's disease , disease
deletion mutants confirmed that biophysical interaction depends on intact PTB domain and YENPTY-motif. Moreover, presence of APP altered GULPs cellular distribution indicating an affinity of the adaptor to APP. Functional assays revealed that GULP overexpression in turn decreases surface levels of APP and generation of Ab. Conclusions: Together these data identify GULP as a novel APP interacting protein and indicate that GULP alters APP trafficking and may therefore play a role in APP processing by secretases and subsequent Ab generation.