Engineered High-Affinity Affibody Molecules Targeting Platelet-Derived Growth Factor Receptor β In Vivo

2011 ◽  
Vol 407 (2) ◽  
pp. 298-315 ◽  
Author(s):  
M. Lindborg ◽  
E. Cortez ◽  
I. Höidén-Guthenberg ◽  
E. Gunneriusson ◽  
E. von Hage ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Affibody Molecules ◽  
High Affinity

scholarly journals Platelet-Derived Growth Factor-Receptor α Strongly Inhibits Melanoma Growth In Vitro and In Vivo

Neoplasia ◽  
2009 ◽  
Vol 11 (8) ◽  
pp. 732-W7 ◽  
Author(s):  
Debora Faraone ◽  
Maria Simona Aguzzi ◽  
Gabriele Toietta ◽  
Angelo M. Facchiano ◽  
Francesco Facchiano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Melanoma Growth

scholarly journals Evidence for glutathione involvement in platelet-derived growth-factor-mediated signal transduction

1997 ◽  
Vol 324 (3) ◽  
pp. 791-796 ◽  
Author(s):  
Stefania RIGACCI ◽  
Teresa IANTOMASI ◽  
Patrizia MARRACCINI ◽  
Andrea BERTI ◽  
Maria Teresa VINCENZINI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Activation ◽  
Platelet Derived Growth Factor ◽  
Glutathione Depletion ◽  
Physiological Processes ◽  
Buthionine Sulphoximine ◽  
Precise Relationship

Recent studies show that glutathione, while being involved in the well-known physiological processes of amino acid transport and detoxification, can also play a part in cell proliferation events. Cell treatment with l-buthionine sulphoximine, which causes glutathione depletion, is accompanied by a decrease in cell proliferation. At present no precise relationship between this thiol and any critical intermediate of the mitogenic cascade has been proved. In this study, conducted on NIH/3T3 murine fibroblasts, we demonstrate a strict correlation between glutathione levels and platelet-derived growth-factor-receptor activation in response to stimulation and cell proliferation. The receptor autophosphorylation is severely impaired at low glutathione cellular levels. The interaction of glutathione with this growth-factor receptor in vivo, while being rather specific, is complex and may involve both cytosolic and extracellular receptor domains.

scholarly journals Platelet-Derived Growth Factor Receptor Transactivation Mediates the Trophic Effects of Angiotensin II In Vivo

Hypertension ◽  
2004 ◽  
Vol 44 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Darren J. Kelly ◽  
Alison J. Cox ◽  
Renae M. Gow ◽  
Yuan Zhang ◽  
Bruce E. Kemp ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Trophic Effects ◽  
Receptor Transactivation

scholarly journals Sustained Platelet-Derived Growth Factor Receptor α Signaling in Osteoblasts Results in Craniosynostosis by Overactivating the Phospholipase C-γ Pathway

2008 ◽  
Vol 29 (3) ◽  
pp. 881-891 ◽  
Author(s):  
Anne Moenning ◽  
Richard Jäger ◽  
Angela Egert ◽  
Wolfram Kress ◽  
Eva Wardelmann ◽  
...  
Keyword(s):  
Growth Factor ◽  
Phospholipase C ◽  
Bone Matrix ◽  
Growth Factor Receptor ◽  
Specific Inhibitor ◽  
Platelet Derived Growth Factor ◽  
Cranial Sutures ◽  
First Time

ABSTRACT The development and growth of the skull is controlled by cranial sutures, which serve as growth centers for osteogenesis by providing a pool of osteoprogenitors. These osteoprogenitors undergo intramembranous ossification by direct differentiation into osteoblasts, which synthesize the components of the extracellular bone matrix. A dysregulation of osteoblast differentiation can lead to premature fusion of sutures, resulting in an abnormal skull shape, a disease called craniosynostosis. Although several genes could be linked to craniosynostosis, the mechanisms regulating cranial suture development remain largely elusive. We have established transgenic mice conditionally expressing an autoactivated platelet-derived growth factor receptor α (PDGFRα) in neural crest cells (NCCs) and their derivatives. In these mice, premature fusion of NCC-derived sutures occurred at early postnatal stages. In vivo and in vitro experiments demonstrated enhanced proliferation of osteoprogenitors and accelerated ossification of osteoblasts. Furthermore, in osteoblasts expressing the autoactivated receptor, we detected an upregulation of the phospholipase C-γ (PLC-γ) pathway. Treatment of differentiating osteoblasts with a PLC-γ-specific inhibitor prevented the mineralization of synthesized bone matrix. Thus, we show for the first time that PDGFRα signaling stimulates osteogenesis of NCC-derived osteoblasts by activating the PLC-γ pathway, suggesting an involvement of this pathway in the etiology of human craniosynostosis.

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