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本文引用的文献

1
Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.转录因子NFATc1（NFAT2）的诱导与激活在破骨细胞终末分化过程中整合RANKL信号。
Dev Cell. 2002 Dec;3(6):889-901. doi: 10.1016/s1534-5807(02)00369-6.
2
Impaired intervertebral disc formation in the absence of Jun.在没有Jun的情况下椎间盘形成受损。
Development. 2003 Jan;130(1):103-9. doi: 10.1242/dev.00186.
3
JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation-dependent and -independent mechanisms.JNK1通过c-Jun磷酸化依赖性和非依赖性机制调节破骨细胞生成。
J Cell Sci. 2002 Nov 15;115(Pt 22):4317-25. doi: 10.1242/jcs.00082.
4
AP-1 as a regulator of cell life and death.作为细胞生死调节因子的活化蛋白-1
Nat Cell Biol. 2002 May;4(5):E131-6. doi: 10.1038/ncb0502-e131.
5
Reaching a genetic and molecular understanding of skeletal development.达成对骨骼发育的基因和分子层面的理解。
Dev Cell. 2002 Apr;2(4):389-406. doi: 10.1016/s1534-5807(02)00157-0.
6
RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-beta.核因子κB受体活化因子配体（RANKL）通过依赖于c-Fos的干扰素-β诱导来维持骨稳态。
Nature. 2002 Apr 18;416(6882):744-9. doi: 10.1038/416744a.
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Genetic control of skeletal development.骨骼发育的遗传控制
Curr Opin Genet Dev. 2001 Oct;11(5):527-32. doi: 10.1016/s0959-437x(00)00228-8.
8
AP-1 in mouse development and tumorigenesis.AP-1在小鼠发育和肿瘤发生中的作用
Oncogene. 2001 Apr 30;20(19):2401-12. doi: 10.1038/sj.onc.1204389.
9
T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-gamma.通过RANKL与干扰素-γ之间的信号串扰实现T细胞介导的破骨细胞生成调节。
Nature. 2000 Nov 30;408(6812):600-5. doi: 10.1038/35046102.
10
Fra-1 replaces c-Fos-dependent functions in mice.Fra-1在小鼠中取代了c-Fos依赖的功能。
Genes Dev. 2000 Nov 1;14(21):2695-700. doi: 10.1101/gad.187900.

Signalling in osteoclasts and the role of Fos/AP1 proteins.

作者信息

Wagner E F, Matsuo K

机构信息

IMP, Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, A-1030 Vienna, Austria.

出版信息

Ann Rheum Dis. 2003 Nov;62 Suppl 2(Suppl 2):ii83-5. doi: 10.1136/ard.62.suppl_2.ii83.

DOI:10.1136/ard.62.suppl_2.ii83
PMID:14532157
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1766737/
Abstract
摘要