Abstract
Progression of activated EGF receptor (EGFR) through the endocytic pathway regulates EGFR signaling. Here we show that a non-ubiquitinated EGFR mutant, unable to bind the endosomal-sorting complex required for transport (ESCRT) component, Hrs, is not efficiently targeted onto intraluminal vesicles (ILVs) of multivesicular endosomes/bodies (MVBs). Moreover, ubiquitination and ESCRT engagement of activated EGFR are required for EGF-stimulated ILV formation. Non-ubiquitinated EGFRs enter clathrin-coated tubules emanating from MVBs and show enhanced recycling to the plasma membrane, compared to wild-type EGFR.
© 2011 John Wiley & Sons A/S.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aorta / cytology
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Cell Membrane / metabolism
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Cells, Cultured
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Clathrin / genetics
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Clathrin / metabolism
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Endosomal Sorting Complexes Required for Transport / metabolism
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Endosomes / metabolism
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Endothelial Cells / drug effects
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Endothelial Cells / metabolism
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Epidermal Growth Factor / metabolism
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Epidermal Growth Factor / pharmacology
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ErbB Receptors / genetics
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ErbB Receptors / metabolism*
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Humans
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Mitogen-Activated Protein Kinase 1 / metabolism
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Mitogen-Activated Protein Kinase 3 / metabolism
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Multivesicular Bodies / drug effects
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Multivesicular Bodies / metabolism
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Multivesicular Bodies / ultrastructure
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Mutation / physiology
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Phosphorylation / drug effects
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Protein Binding / drug effects
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Protein Binding / physiology
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Protein Subunits / metabolism
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Protein Transport / drug effects
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Protein Transport / physiology*
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Sus scrofa
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Transfection
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Transferrin / metabolism
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Ubiquitination / physiology*
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Vesicular Transport Proteins / genetics
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Vesicular Transport Proteins / metabolism
Substances
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Clathrin
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Endosomal Sorting Complexes Required for Transport
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Protein Subunits
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Transferrin
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Vesicular Transport Proteins
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early endosome antigen 1
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Epidermal Growth Factor
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EGFR protein, human
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ErbB Receptors
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3