Foxp1/2/4 regulate endochondral ossification as a suppresser complex.
Foxp1/2/4 regulate endochondral ossification as a suppresser complex.
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Foxp1/2/4 作为抑制复合物调节软骨内骨化。
DOI：
10.1016/j.ydbio.2014.12.007
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发表时间：
2015-02-15
影响因子：
2.7
通讯作者：
Guo, Xizhi
中科院分区：
文献类型：
--
作者：
Zhao, Haixia;Zhou, Wenrong;Yao, Zhengju;Wan, Yong;Cao, Jingjing;Zhang, Lingling;Zhao, Jianzhi;Li, Hanjun;Zhou, Rujiang;Li, Baojie;Wei, Gang;Zhang, Zhenlin;French, Catherine A.;Dekker, Joseph D.;Yang, Yingzi;Fisher, Simon E.;Tucker, Haley O.;Guo, Xizhi
Osteoblast induction and differentiation in developing long bones is dynamically controlled by the opposing action of transcriptional activators and repressors. In contrast to the long list of activators that have been discovered over past decades, the network of repressors is not well-defined. Here we identify the expression of Foxp1/2/4 proteins, comprised of Forkhead-box (Fox) transcription factors of the Foxp subfamily, in both perichondrial skeletal progenitors and proliferating chondrocytes during endochondral ossification. Mice carrying loss-of-function and gain-of-function Foxp mutations had gross defects in appendicular skeleton formation. At the cellular level, over-expression of Foxp1/2/4 in chondroctyes abrogated osteoblast formation and chondrocyte hypertrophy. Conversely, single or compound deficiency of Foxp1/2/4 in skeletal progenitors or chondrocytes resulted in premature osteoblast differentiation in the perichondrium, coupled with impaired proliferation, survival, and hypertrophy of chondrocytes in the growth plate. Foxp1/2/4 and Runx2 proteins interacted in vitro and in vivo, and Foxp1/2/4 repressed Runx2 transactivation function in heterologous cells. This study establishes Foxp1/2/4 proteins as coordinators of osteogenesis and chondrocyte hypertrophy in developing long bones and suggests that a novel transcriptional repressor network involving Foxp1/2/4 may regulate Runx2 during endochondral ossification.
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影响因子：
11.8
作者：
Correa, Diego;Hesse, Eric;Seriwatanachai, Dutmanee;Kiviranta, Riku;Saito, Hiroaki;Yamana, Kei;Neff, Lynn;Atfi, Azeddine;Coillard, Lucie;Sitara, Despina;Maeda, Yukiko;Warming, Soren;Jenkins, Nancy A.;Copeland, Neal G.;Horne, William C.;Lanske, Beate;Baron, Roland
通讯作者：
Baron, Roland
DOI：
10.1016/0922-3371(90)90079-c
发表时间：
1990-05-01
期刊：
CELL DIFFERENTIATION AND DEVELOPMENT
影响因子：
--
作者：
ATSUMI, T;MIWA, Y;IKAWA, Y
通讯作者：
IKAWA, Y
影响因子：
30.5
作者：
Hu, Hui;Wang, Bin;Rao, Anjana
通讯作者：
Rao, Anjana
影响因子：
15.9
作者：
Kode, Aruna;Mosialou, Ioanna;Kousteni, Stavroula
通讯作者：
Kousteni, Stavroula
影响因子：
11.8
作者：
Bialek, P;Kern, B;Karsenty, G
通讯作者：
Karsenty, G