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Effect of receptor kinase inactivation on the rate of internalization and degradation of PDGF and the PDGF beta-receptor.
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MedLine Citation:
PMID:  1846866     Owner:  NLM     Status:  MEDLINE    
The complementary DNAs for wildtype and tyrosine kinase-inactivated (K634A) forms of the PDGF beta-receptor were expressed in porcine aortic endothelial cells. We examined the internalization and degradation of ligands and receptors after exposure of receptor expressing cells to PDGF-BB, which binds to the beta-receptor with high affinity, and PDGF-AB, which binds with lower affinity. Cells expressing wildtype beta-receptors were able to internalize and degrade the receptor, as well as the ligand, after exposure to PDGF-BB or -AB. Cells expressing the kinase-inactivated mutant receptor also internalized and degraded both receptor and ligand, but with lower efficiency compared with the wildtype receptor cells. The degradation of either form of receptor was inhibited by treatment of the cells with the lysosomotropic drug chloroquine. Exposure of wildtype and K634A receptor expressing cells to PDGF-AB resulted in a twofold slower rate of internalization of this ligand as compared with PDGF-BB, whereas the relative rate of degradation was similar for the two ligands. Our data indicate that tyrosine kinase activity promotes, but is not a prerequisite for, ligand-induced internalization and degradation of the ligand-receptor complex.
A Sorkin; B Westermark; C H Heldin; L Claesson-Welsh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of cell biology     Volume:  112     ISSN:  0021-9525     ISO Abbreviation:  J. Cell Biol.     Publication Date:  1991 Feb 
Date Detail:
Created Date:  1991-03-08     Completed Date:  1991-03-08     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0375356     Medline TA:  J Cell Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  469-78     Citation Subset:  IM    
Department of Pathology, University Hospital, Uppsala, Sweden.
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MeSH Terms
Cell Line
Chloroquine / pharmacology
Endothelium, Vascular
Fibroblasts / metabolism
Fluorescent Antibody Technique
Platelet-Derived Growth Factor / metabolism*
Protein Kinases / genetics,  metabolism*
Receptors, Cell Surface / drug effects,  genetics,  metabolism*
Receptors, Platelet-Derived Growth Factor
Reg. No./Substance:
0/Platelet-Derived Growth Factor; 0/Receptors, Cell Surface; 54-05-7/Chloroquine; EC 2.7.-/Protein Kinases; EC, Platelet-Derived Growth Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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Journal Information
Journal ID (nlm-ta): J Cell Biol
Journal ID (publisher-id): J. Cell Biol.
ISSN: 0021-9525
ISSN: 1540-8140
Publisher: The Rockefeller University Press
Article Information
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Print publication date: Day: 1 Month: 2 Year: 1991
Volume: 112 Issue: 3
First Page: 469 Last Page: 478
ID: 2288834
Publisher Id: 91123300
PubMed Id: 1846866

Effect of receptor kinase inactivation on the rate of internalization and degradation of PDGF and the PDGF beta-receptor

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