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@article{889689,
author = {Krejčí, Pavel and Procházková, Jiřina and Smutný, Jiří and Chlebová, Katarína and Lin, Patricia and Aklian, Anie and Bryja, Vítězslav and Kozubík, Alois and Wilcox, William R.},
article_location = {USA},
article_number = {47},
keywords = {FGFR3; Oncogene; Skeletal dysplasia; Cartilage; MAP kinase; Senescence},
language = {eng},
issn = {8756-3282},
journal = {Bone},
title = {FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence},
volume = {neuveden},
year = {2010}
}
TY - JOUR
ID - 889689
AU - Krejčí, Pavel - Procházková, Jiřina - Smutný, Jiří - Chlebová, Katarína - Lin, Patricia - Aklian, Anie - Bryja, Vítězslav - Kozubík, Alois - Wilcox, William R.
PY - 2010
TI - FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence
JF - Bone
VL - neuveden
IS - 47
SP - 102-110
EP - 102-110
PB - Elsevier Science
SN - 87563282
KW - FGFR3
KW - Oncogene
KW - Skeletal dysplasia
KW - Cartilage
KW - MAP kinase
KW - Senescence
N2 - 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.
ER -
KREJČÍ, Pavel, Jiřina PROCHÁZKOVÁ, Jiří SMUTNÝ, Katarína CHLEBOVÁ, Patricia LIN, Anie AKLIAN, Vítězslav BRYJA, Alois KOZUBÍK a William R. WILCOX. FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence. \textit{Bone}. USA: Elsevier Science, 2010, neuveden, č.~47, s.~102-110. ISSN~8756-3282.
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