Abstract
Presenilin 1 (PS1) interacts with telencephalin (TLN)
and the amyloid precursor protein via their transmembrane
domain.
Here, we
demonstrate that TLN is not a substrate for
γ-secretase
cleavage, but displays a prolonged half-life in PS1⁻/⁻ hippocampal
neurons. TLN accumulates in intracellular structures
bearing characteristics of autophagic vacuoles including
the presence of Apg12p and LC3. Importantly, the TLN accumulations
are suppressed
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