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Cell migration towards CXCL12 in leukemic cells compared to breast cancer cells.与乳腺癌细胞相比,白血病细胞向CXCL12的细胞迁移。
Cell Signal. 2016 Apr;28(4):316-24. doi: 10.1016/j.cellsig.2016.01.006. Epub 2016 Jan 21.
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Novel biological insights in T-cell acute lymphoblastic leukemia.T细胞急性淋巴细胞白血病的新生物学见解。
Exp Hematol. 2015 Aug;43(8):625-39. doi: 10.1016/j.exphem.2015.05.017. Epub 2015 Jun 26.
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A critical role of Src family kinase in SDF-1/CXCR4-mediated bone-marrow progenitor cell recruitment to the ischemic heart.Src家族激酶在SDF-1/CXCR4介导的骨髓祖细胞募集至缺血心脏过程中的关键作用。
J Mol Cell Cardiol. 2015 Apr;81:49-53. doi: 10.1016/j.yjmcc.2015.01.024. Epub 2015 Feb 3.
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Update on biology and treatment of T-cell acute lymphoblastic leukaemia.T细胞急性淋巴细胞白血病的生物学特性与治疗进展
Curr Opin Pediatr. 2015 Feb;27(1):44-9. doi: 10.1097/MOP.0000000000000171.
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Stromal cell-derived factor-1α/C-X-C chemokine receptor type 4 axis promotes endothelial cell barrier integrity via phosphoinositide 3-kinase and Rac1 activation.基质细胞衍生因子-1α/C-X-C 趋化因子受体 4 轴通过磷酸肌醇 3-激酶和 Rac1 的激活促进内皮细胞屏障完整性。
Arterioscler Thromb Vasc Biol. 2014 Aug;34(8):1716-22. doi: 10.1161/ATVBAHA.114.303890. Epub 2014 Jun 12.
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Cyclovirobuxinum D suppresses lipopolysaccharide-induced inflammatory responses in murine macrophages in vitro by blocking JAK-STAT signaling pathway.环维黄杨星D通过阻断JAK-STAT信号通路抑制体外培养的小鼠巨噬细胞中脂多糖诱导的炎症反应。
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Jak3 enables chemokine-dependent actin cytoskeleton reorganization by regulating cofilin and Rac/Rhoa GTPases activation.Jak3 通过调节丝切蛋白和 Rac/Rhoa GTPases 的激活来实现趋化因子依赖的细胞骨架重排。
PLoS One. 2014 Feb 3;9(2):e88014. doi: 10.1371/journal.pone.0088014. eCollection 2014.
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International Union of Basic and Clinical Pharmacology. [corrected]. LXXXIX. Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors.国际基础和临床药理学联合会。[更正]。LXXXIX. 趋化因子受体大家族的更新及为非典型趋化因子受体引入新的命名法。
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CXC chemokine receptor 4 expression, CXC chemokine receptor 4 activation, and wild-type nucleophosmin are independently associated with unfavorable prognosis in patients with acute myeloid leukemia.CX 趋化因子受体 4 表达、CX 趋化因子受体 4 激活以及野生型核磷蛋白与急性髓系白血病患者的不良预后独立相关。
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一氧化氮在基质细胞衍生因子-1诱导的细胞骨架变化及 Jurkat 细胞迁移中发挥作用。

Nitric oxide functions in stromal cell-derived factor-1-induced cytoskeleton changes and the migration of Jurkat cells.

作者信息

Luo Jixian, Wei Dan, Li Dingyun, Wang Lan

机构信息

Department of Biology, School of Life Science, Shanxi University, Taiyuan, Shanxi 030006, P.R. China.

出版信息

Oncol Lett. 2018 Nov;16(5):6685-6690. doi: 10.3892/ol.2018.9429. Epub 2018 Sep 11.

DOI:10.3892/ol.2018.9429
PMID:30405809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6202483/
Abstract

Stromal cell-derived factor-1 (SDF-1) regulates multiple cell signal pathways in a variety of cellular functions, including cell migration, proliferation, survival and angiogenesis. SDF-1-induced chemotaxis is an important step of lymphocyte migration. However, the molecular mechanisms that modulate SDF-1-mediated lymphocyte migration are not well identified. Nitric oxide (NO) has been found to function as a signaling molecule in a number of signaling pathways, including migration. In the present study, the potential role of NO in SDF-1-induced migration and the association between NO and the cytoskeletal changes of Jurkat cells was investigated. The present study demonstrated that Jurkat cells induced the production of NO by SDF-1 stimulation, using Griess reaction method and western blot analysis, and that NO was involved in SDF-1-induced rearrangement and polymerization of the cytoskeleton, using NOS inhibitor L-NMMA. Furthermore, NO was required for the migration of Jurkat cells. The research suggested that NO signaling pathways exerted a critical role in SDF-1-induced cytoskeleton changes and the migration of Jurkat cells. This work provides insight into the migration mechanism of acute lymphoblastic leukemia and provides an effective theoretical basis for therapy strategies for acute lymphoblastic leukemia.

摘要

基质细胞衍生因子-1(SDF-1)在多种细胞功能中调节多个细胞信号通路,包括细胞迁移、增殖、存活和血管生成。SDF-1诱导的趋化作用是淋巴细胞迁移的重要步骤。然而,调节SDF-1介导的淋巴细胞迁移的分子机制尚未完全明确。一氧化氮(NO)已被发现在包括迁移在内的许多信号通路中作为信号分子发挥作用。在本研究中,研究了NO在SDF-1诱导的迁移中的潜在作用以及NO与Jurkat细胞细胞骨架变化之间的关联。本研究表明,使用格里斯反应法和蛋白质印迹分析,SDF-1刺激可诱导Jurkat细胞产生NO,并且使用一氧化氮合酶抑制剂L-NMMA表明,NO参与了SDF-1诱导的细胞骨架重排和聚合。此外,Jurkat细胞的迁移需要NO。该研究表明,NO信号通路在SDF-1诱导的细胞骨架变化和Jurkat细胞迁移中发挥关键作用。这项工作为急性淋巴细胞白血病的迁移机制提供了见解,并为急性淋巴细胞白血病的治疗策略提供了有效的理论基础。