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FGF and ROR2 receptor tyrosine kinase signaling in human skeletal development

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons50578

Stricker,  S.
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50437

Mundlos,  S.
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Zitation

Stricker, S., & Mundlos, S. (2011). FGF and ROR2 receptor tyrosine kinase signaling in human skeletal development. Curr Top Dev Biol, 97, 179-206. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22074606.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-7818-9
Zusammenfassung
Skeletal malformations are among the most frequent developmental disturbances in humans. In the past years, progress has been made in unraveling the molecular mechanisms that govern skeletal development by the use of animal models as well as by the identification of numerous mutations that cause human skeletal syndromes. Receptor tyrosine kinases have critical roles in embryonic development. During formation of the skeletal system, the fibroblast growth factor receptor (FGFR) family plays major roles in the formation of cranial, axial, and appendicular bones. Another player of relevance to skeletal development is the unusual receptor tyrosine kinase ROR2, the function of which is as interesting as it is complex. In this chapter, we review the involvement of FGFR signaling in human skeletal disease and provide an update on the growing knowledge of ROR2.