Downregulation of platelet-derived growth factor receptor-beta in Shp-2 mutant fibroblast cell lines - PubMed (original) (raw)
. 1998 Jul 30;17(4):441-8.
doi: 10.1038/sj.onc.1201988.
Affiliations
- PMID: 9696037
- DOI: 10.1038/sj.onc.1201988
Downregulation of platelet-derived growth factor receptor-beta in Shp-2 mutant fibroblast cell lines
X Lu et al. Oncogene. 1998.
Abstract
The SH2-containing tyrosine phosphatase Shp-2 appears to function downstream of a variety of growth factor receptors and might play a positive role in cell proliferation. Here we report that expression of the beta subunit of platelet-derived growth factor receptor (PDGFR-beta) was specifically downregulated in mutant fibroblasts lacking a functional Shp-2, while the levels of PDGFR-alpha EGFR and IGFIR were not changed. PDGF-stimulated DNA synthesis and extracellular signal regulated kinase (Erk) activation was severely suppressed in mutant cells. RasGAP, that responds to activation of PDGFR-beta but not PDGFR-alpha, was not phosphorylated on tyrosine in mutant cells upon PDGF-treatment. Northern blot analysis failed to detect PDGFR-beta mRNA in mutant cells. The transcription initiation from the PDGFR-beta gene promoter was not significantly changed, but the half-life of its mRNA was shortened in Shp-2 mutant cells. These observations indicate that Shp-2 not only participates in transmission of signals from growth factor receptors but also plays a specific role in the control of the PDGFR-beta expression. We propose that this is an important mechanism for the positive control of cell proliferation by Shp-2.
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