Abstract
Alcadein (Alc) are type I membrane protein like amyloid β–protein precursor (APP), and the metabolism and trafficking of both proteins are regulated by their cytoplasmic domain through interaction with cytoplasmic adaptor proteins. We previously reported that APP and Alc form complex via cytoplasmic interaction with X11–like protein (X11L) in neuron, and both proteins are subject to coordinated metabolism when X11L is released from the complex. However, the process of complex formation remained unclear in cells. Here we found that APP and Alcα, a member of Alc family proteins, are subjected to an independent vesicular transport at different speeds with kinesin I motor. Furthermore, we found that JIP1b, a member of JNK–interacting proteins, plays an important role in the selection of cargos containing APP or Alca by kinesin I. Molecular mechanisms of intracellular trafficking and metabolism of APP and Alc will be discussed.
Published Version
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