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人多发性骨髓瘤细胞缺乏核因子-κB受体激活剂配体(RANKL)的表达及功能性产生。

Lack of receptor activator of nuclear factor-kB ligand (RANKL) expression and functional production by human multiple myeloma cells.

作者信息

Giuliani Nicola, Colla Simona, Morandi Francesca, Barille-Nion Sophie, Rizzoli Vittorio

出版信息

Haematologica. 2005 Feb;90(2):275-8.

PMID:15710592
Abstract

The direct expression and production of the critical osteoclastogenic factor, the receptor activator of NF-kB ligand (RANKL), is a matter of controversy. In this study we definitively demonstrate by both qualitative and quantitative polymerase chain reaction analysis that human myeloma cells do not express significant levels of RANKL mRNA or produce RANKL able to stimulate osteoclast formation.

摘要

关键破骨细胞生成因子——核因子κB受体活化因子配体(RANKL)的直接表达和产生存在争议。在本研究中,我们通过定性和定量聚合酶链反应分析明确证明,人骨髓瘤细胞不会表达显著水平的RANKL mRNA,也不会产生能够刺激破骨细胞形成的RANKL。

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Lack of receptor activator of nuclear factor-kB ligand (RANKL) expression and functional production by human multiple myeloma cells.人多发性骨髓瘤细胞缺乏核因子-κB受体激活剂配体(RANKL)的表达及功能性产生。
Haematologica. 2005 Feb;90(2):275-8.
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Expression of receptor activator of nuclear factor kappaB ligand on bone marrow plasma cells correlates with osteolytic bone disease in patients with multiple myeloma.核因子κB受体活化因子配体在骨髓浆细胞上的表达与多发性骨髓瘤患者的溶骨性骨病相关。
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IFN-gamma-producing human T cells directly induce osteoclastogenesis from human monocytes via the expression of RANKL.产生干扰素-γ的人T细胞通过RANKL的表达直接诱导人单核细胞形成破骨细胞。
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Soluble glucocorticoid-induced tumor necrosis factor receptor (sGITR) stimulates osteoclast differentiation in response to receptor activator of NF-kappaB ligand (RANKL) in osteoclast cells.可溶性糖皮质激素诱导的肿瘤坏死因子受体(sGITR)在破骨细胞中响应核因子κB受体激活剂配体(RANKL)刺激破骨细胞分化。
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