Disruption of PDGF receptor trafficking by mutation of its PI-3 kinase binding sites.

doi:10.1126/science.8303278

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Article

Disruption of PDGF receptor trafficking by mutation of its PI-3 kinase binding sites.

Science (New York, N.Y.) - 4 Feb 1994

Joly M, Kazlauskas A, Fay F S, Corvera S

Abstract excerpt

Human platelet-derived growth factor receptors (PDGFRs) expressed in human Hep G2 cells internalized and concentrated in a juxtanuclear region near the Golgi network within 10 minutes after the cells were treated with PDGF. A PDGFR mutant (F5) that lacks high-affinity binding sites for the Src ho...

Topics

Binding Sites
Cell Membrane
Endocytosis
GTPase-Activating Proteins
Golgi Apparatus
Humans
Intracellular Signaling Peptides and Proteins
Isoenzymes
Mutation
Phosphatidylinositol 3-Kinases
Phospholipase C gamma
Phosphotransferases (Alcohol Group Acceptor)
Platelet-Derived Growth Factor
Protein Tyrosine Phosphatase, Non-Receptor Type 11
Protein Tyrosine Phosphatase, Non-Receptor Type 6
Protein Tyrosine Phosphatases
Proteins
Receptors, Platelet-Derived Growth Factor

Source

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Identifiers

PMID: 8303278
DOI: 10.1126/science.8303278

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-8303278-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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