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Published on: October 30, 2013
Mu 1A deficiency induces a profound increase in MPR300/IGF-II receptor internalization rate
C Meyer1, E L Eskelinen, M R Guruprasad
1Zentrum für Biochemie und Molekulare Zellbiologie, Biochemie II, Universität Göttingen, Heinrich-Düker-Weg 12, D-37073 Göttingen, Germany.
Journal of Cell Science
|January 17, 2002
Summary
Defects in AP-1 transport disrupt mannose-6-phosphate/IGF-II receptor (MPR300) recycling. This leads to increased MPR300 endocytosis, impacting lysosomal enzyme sorting and IGF-II hormone uptake.
Area of Science:
- Cell Biology
- Molecular Biology
- Receptor Trafficking
Background:
- The mannose-6-phosphate/IGF-II receptor (MPR300) is crucial for lysosomal enzyme sorting and IGF-II endocytosis.
- AP-1 adaptor protein complex mediates transport between endosomes and the trans-Golgi network (TGN).
Purpose of the Study:
- To investigate the role of AP-1 in MPR300 trafficking.
- To analyze MPR300 transport in mu1A-adaptin-deficient fibroblasts lacking functional AP-1.
Main Methods:
- Analysis of MPR300 transport in mu1A-adaptin-deficient fibroblasts.
- Assessment of receptor endocytosis rates and localization.
- Comparison with other AP-2-mediated endocytosis pathways.
Main Results:
- MPR300 endocytosis is significantly enhanced in mu1A-adaptin-deficient cells.
- Increased internalization rate, not plasma membrane concentration, drives enhanced endocytosis.
- MPR300 accumulates in endosomes, with increased presence in clathrin-coated pits at the plasma membrane.
Conclusions:
- AP-1-mediated retrograde transport from endosomes to the TGN is essential for controlling MPR300 recycling rate.
- Disruption of AP-1 function leads to impaired MPR300 trafficking and altered endocytosis dynamics.
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