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Expression of trans...
Expression of transforming growth factor b1, b2, b3 in neuroendocrine tumors of the digestive system
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Chaudhry, A (author)
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- Öberg, Kjell (author)
- Uppsala universitet,Institutionen för medicinska vetenskaper,Onkologisk endokrinologi, K Öberg
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- Gobl, Anders (author)
- Uppsala universitet,Institutionen för medicinska vetenskaper,Onkologisk endokrinologi, K Öberg
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- Heldin, Carl-Henrik (author)
- Ludwiginstitutet för Cancerforskning
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- Funa, Keiko (author)
- Ludwiginstitutet för Cancerforskning
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(creator_code:org_t)
- 1994
- 1994
- English.
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In: Anticancer Res. ; 14, s. 2085-
- Related links:
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https://urn.kb.se/re...
Abstract
Subject headings
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- Ligand induced activation of the beta-receptor for platelet-derived growth factor (PDGF) leads to activation of Src family tyrosine kinases. We have explored the possibility that the receptor itself is a substrate for Src. We show that Tyr934 in the kinase domain of the PDGF receptor is phosphorylated by Src. Cell lines expressing a beta-receptor mutant, in which Tyr934 was replaced with a phenyalanine residue, showed reduced mitogenic signaling in response to PDGF-BB. In contrast, the mutant receptor mediated increased signals for chemotaxis and actin reorganization. Whereas the motility responses of cells expressing wild-type beta-receptors were attenuated by inhibition of phosphatidylinositol 3'-kinase, those of cells expressing the mutant receptor were only slightly influenced. In contrast, PDGF-BB-induced chemotaxis of the cells with the mutant receptor was attenuated by inhibition of protein kinase C, whereas the chemotaxis of cells expressing the wild-type beta-receptor was less affected. Moreover, the PDGF-BB-stimulated tyrosine phosphorylation of phospholipase C-gamma was increased in the mutant receptor cells compared with wild-type receptor cells. In conclusion, the characteristics of the Y934F mutant suggest that the phosphorylation of Tyr934 by Src negatively modulates a signal transduction pathway leading to motility responses which involves phospholipase C-gamma, and shifts the response to increased mitogenicity.
Keyword
- 1-Phosphatidylinositol 3-Kinase
- Chemotaxis
- Phospholipase C
- Platelet-Derived Growth Factor
Publication and Content Type
- ref (subject category)
- art (subject category)
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