Project information
Identification of new treatment options for achondroplasia through the analysis of interaction between FGFR3 and adapter protein Frs2

Information

This project doesn't include Faculty of Science. It includes Faculty of Medicine. Official project website can be found on muni.cz.
Project Identification
15-33232A (kod CEP: NV15-33232A)
Project Period
5/2015 - 12/2018
Investor / Pogramme / Project type
Ministry of Health of the CR
MU Faculty or unit
Faculty of Medicine

Activating mutations in the FGFR3 receptor tyrosine kinase cause the most common form of dwarfism in humans, achondroplasia. Excessive activation of FGFR3 causes premature termination of chondrocyte growth, abnormal extracellular matrix homeostasis and abnormal chondrocyte differentiation, leading to achondroplasia. Although achondroplasia is considered a treatable condition, no treatment currently exists. This is primarily due to our lack of understanding of the fundamental mechanisms governing FGFR3 signal transduction in cartilage. Uncontrolled activation of the Erk MAP kinase, mediated by the signalling adaptor protein Frs2, represents the main mediator of FGFR3 activation in achondroplasia. The molecular mechanisms underlying this phenotype are unknown. The dynamics of the interaction between Frs2 and FGFR3, Erk and other proteins represent a key to understanding the pathology of achondroplasia, and are addressed in this proposal. Through the systematic mapping of interactions between FGFR3, Frs2, Erk and other proteins, we aim to identify new treatment options for achondroplasia.

Publications

Total number of publications: 21


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