Publication details

FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence

Investor logo
Authors

KREJČÍ Pavel PROCHÁZKOVÁ Jiřina SMUTNÝ Jiří CHLEBOVÁ Katarína LIN Patricia AKLIAN Anie BRYJA Vítězslav KOZUBÍK Alois WILCOX William R.

Year of publication 2010
Type Article in Periodical
Magazine / Source Bone
MU Faculty or unit

Faculty of Science

Citation
Field Genetics and molecular biology
Keywords FGFR3; Oncogene; Skeletal dysplasia; Cartilage; MAP kinase; Senescence
Description FGFR3 signaling is capable of inducing premature senescence in chondrocytes, manifested as reversible, ERK-dependent growth arrest accompanied by alteration of cellular shape, loss of the extracellular matrix, upregulation of senescence markers (alpha-GLUCOSIDASE, FIBRONECTIN, CAVEOLIN 1, LAMIN A, SM22alpha and TIMP 1), and induction of senescence-associated beta-GALACTOSIDASE activity. Our data support a model whereby FGFR3 signaling inhibits cartilage growth via exploiting cellular response originally designed to eliminate cells harboring activated oncogenes.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.

More info