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Negative autoregulation of RANKL and c-Src signaling in osteoclasts.

作者信息

Yogo Keiichiro, Ishida-Kitagawa Norihiro, Takeya Tatsuo

机构信息

Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0192, Japan.

出版信息

J Bone Miner Metab. 2007;25(4):205-10. doi: 10.1007/s00774-007-0751-2. Epub 2007 Jun 25.

DOI:10.1007/s00774-007-0751-2
PMID:17593489
Abstract
摘要

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本文引用的文献

1
Type I interferons in host defense.宿主防御中的I型干扰素。
Immunity. 2006 Sep;25(3):373-81. doi: 10.1016/j.immuni.2006.08.007.
2
Calcitonin plays a critical role in regulating skeletal mineral metabolism during lactation.降钙素在哺乳期骨骼矿物质代谢调节中起关键作用。
Endocrinology. 2006 Sep;147(9):4010-21. doi: 10.1210/en.2005-1616. Epub 2006 May 4.
3
RANKL stimulates inducible nitric-oxide synthase expression and nitric oxide production in developing osteoclasts. An autocrine negative feedback mechanism triggered by RANKL-induced interferon-beta via NF-kappaB that restrains osteoclastogenesis and bone resorption.
RANKL刺激发育中的破骨细胞中诱导型一氧化氮合酶的表达和一氧化氮的产生。RANKL诱导的干扰素-β通过NF-κB触发一种自分泌负反馈机制,该机制抑制破骨细胞生成和骨吸收。
J Biol Chem. 2006 Jun 9;281(23):15809-20. doi: 10.1074/jbc.M513225200. Epub 2006 Apr 12.
4
Src homology 2 (SH2)-containing 5'-inositol phosphatase localizes to podosomes, and the SH2 domain is implicated in the attenuation of bone resorption in osteoclasts.含Src同源2(SH2)结构域的5'-肌醇磷酸酶定位于足体,且SH2结构域与破骨细胞骨吸收的减弱有关。
Endocrinology. 2006 Jul;147(7):3307-17. doi: 10.1210/en.2005-1309. Epub 2006 Apr 6.
5
Podosome and sealing zone: specificity of the osteoclast model.足体与封闭区:破骨细胞模型的特异性
Eur J Cell Biol. 2006 Apr;85(3-4):195-202. doi: 10.1016/j.ejcb.2005.09.008. Epub 2005 Oct 24.
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Podosomes as smart regulators of cellular adhesion.作为细胞黏附智能调节因子的足体
Eur J Cell Biol. 2006 Apr;85(3-4):191-4. doi: 10.1016/j.ejcb.2005.08.005. Epub 2005 Sep 19.
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NFATc1 regulation of the human beta3 integrin promoter in osteoclast differentiation.破骨细胞分化过程中NFATc1对人β3整合素启动子的调控
Gene. 2006 May 10;372:92-102. doi: 10.1016/j.gene.2005.12.012. Epub 2006 Mar 2.
8
RANKL-RANK signaling in osteoclastogenesis and bone disease.破骨细胞生成及骨疾病中的RANKL-RANK信号传导
Trends Mol Med. 2006 Jan;12(1):17-25. doi: 10.1016/j.molmed.2005.11.007. Epub 2005 Dec 13.
9
CCR1 acts downstream of NFAT2 in osteoclastogenesis and enhances cell migration.CCR1在破骨细胞生成过程中作用于NFAT2下游,并增强细胞迁移。
J Bone Miner Res. 2006 Jan;21(1):48-57. doi: 10.1359/JBMR.051001. Epub 2005 Oct 10.
10
The role(s) of Src kinase and Cbl proteins in the regulation of osteoclast differentiation and function.Src激酶和Cbl蛋白在破骨细胞分化和功能调节中的作用。
Immunol Rev. 2005 Dec;208:106-25. doi: 10.1111/j.0105-2896.2005.00335.x.