Cell responses to FGFR3 signalling: growth, differentiation and apoptosis.

摘要: FGFR3 is a receptor tyrosine kinase (RTK) of the FGF family, known to have negative regulatory effect on long bone growth. Fgfr3 knockout mice display longer bones and, accordingly, most germline-activating mutations in man are associated with dwarfism. Somatically, some same activating human cancers multiple myeloma, cervical carcinoma and bladder. How signalling through can lead either chondrocyte apoptosis or cancer cell proliferation not fully understood. Although be expressed as two main splice isoforms (IIIb IIIc), there no apparent link specific responses, which may rather type its differentiation status. Depending type, differential activation STAT proteins has been observed. STAT1 phosphorylation seems involved inhibition while ERK pathway inhibits B-cell (as myeloma). The role epithelial (bladder cervix) known. Some specificity arise via modulation by crosstalk other pathways. Recently, achondroplastic provided hope for an approach treatment Further understanding ability trigger different responses depending cellular context treatments both skeletal dysplasias cancer.