MICROTUBULES ROLE IN MACROPHAGE RESPONSE TO LPS

微管在巨噬细胞对 LPS 反应中的作用

基本信息

  • 批准号:
    2065488
  • 负责人:
  • 金额:
    $ 12.31万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1990
  • 资助国家:
    美国
  • 起止时间:
    1990-07-01 至 1995-04-30
  • 项目状态:
    已结题

项目摘要

The goal of this proposal is to further understand the mechanisms involved in LPS-mediated actions in leukocytes, focusing on the interaction between LPS and the microtubule (MT) network of murine macrophages (Mphi). LPS is known to have profound, multiple effects on Mphis. Preliminary findings that drugs (e.g. colchicine and taxol) which are known to affect microtubule organization can mimic LPS in inducing (a) down-regulation of Mphi TNFalpha receptors, (b) release of TNFalpha, and (c) secretion of nitrite, and that LPS-hyporesponsive C3H/HeJ mice lack these responses to taxol, raise the possibilities that MT may play an important role in LPS- mediated actions. The specific aims of this study are to answer how LPS's actions are related to MT organization, and whether there is any structural or functional association between MT and LPS-binding protein(s). The proposed experiments include: (1) To determine the functional interaction between LPS and MT by examining the effect of LPS on MT modification (tyrosinolation and phosphorylation), and the effect of MT-active agents (i.e., colchicine, nocodazole, taxol) on lPS-mediated activation of Mphis (release of IL-1, TNFalpha, reactive oxygen or nitrogen intermediates; changes in intracellular calcium, Ia expression; and translocation of protein kinase c). (2) To examine whether any of the MY components can serve as an LPS-receptor or associate with an LPS receptor, by colocalizing MT and LPS binding sites with double immunofluorescent staining, by measuring the binding of labeled LPS to isolated MT, and by co- precipitating an LPS receptor with MT in the presence of taxol. (3) To determine the genetic linkage between LPS- and taxol-responsiveness in the mouse by examining the closeness of these two responses in Mphis from the F2 generation of a cross between C5/BL/6J and C3H/HeJ, possibly leading to the identification of the defective protein(s) in C3H/HeJ mice.
本提案的目的是进一步了解所涉及的机制 在LPS介导的白细胞作用中, LPS和小鼠巨噬细胞(Mphi)的微管(MT)网络。 LPS是 对姆菲斯有着深远的多重影响 初步调查结果 已知影响的药物(如秋水仙碱和紫杉醇) 微管组织可以模拟LPS诱导(a)微管的下调, Mphi TNF α受体,(B)TNF α的释放,和(c)TNF α的分泌, 亚硝酸盐,而LPS低反应C3 H/HeJ小鼠缺乏这些反应, 紫杉醇,提出MT可能在LPS-1中发挥重要作用的可能性。 调解行动。 本研究的具体目的是回答LPS如何 行动与MT组织有关,以及是否有任何结构性 或MT和LPS结合蛋白之间的功能性关联。 的 建议的实验包括:(1)确定功能相互作用 通过检查LPS对MT修饰的影响来研究LPS与MT之间的关系 (酪氨酸化和磷酸化),以及MT活性剂的作用 (i.e.,秋水仙碱、诺考达唑、紫杉醇)对LPS介导的Mphis活化的影响 (IL-1、TNF α、活性氧或氮中间体的释放; 细胞内钙离子的变化,Ia表达; 蛋白激酶c)。 (2)要检查任何MY组件是否可以 作为LPS受体或与LPS受体结合,通过共定位 MT和LPS结合位点的双重免疫荧光染色, 测量标记的LPS与分离的MT的结合,并通过共- 在紫杉醇存在下用MT沉淀LPS受体。 (3)到 确定LPS和紫杉醇反应性之间的遗传联系, 通过检查Mphis中这两种反应的接近程度, C5/BL/6 J和C3 H/HeJ之间杂交的F2代,可能导致 C3 H/HeJ小鼠中缺陷蛋白的鉴定。

项目成果

期刊论文数量(26)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(1)
Regulation of tumor necrosis factor receptors on phagocytes.
吞噬细胞上肿瘤坏死因子受体的调节。
Identification of genes involved in innate responsiveness to bacterial products by differential display.
通过差异展示鉴定涉及对细菌产物的先天反应的基因。
  • DOI:
    10.1006/meth.1998.0694
  • 发表时间:
    1998
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Jin,F;Nathan,C;Ding,A
  • 通讯作者:
    Ding,A
Paradoxical preservation of a lipopolysaccharide response in C3H/HeJ macrophages: induction of matrix metalloproteinase-9.
C3H/HeJ 巨噬细胞中脂多糖反应的矛盾保存:基质金属蛋白酶 9 的诱导。
Pseudomonas aeruginosa ExoT ADP-ribosylates CT10 regulator of kinase (Crk) proteins.
铜绿假单胞菌 ExoT ADP-核糖基化激酶 (Crk) 蛋白的 CT10 调节因子。
  • DOI:
    10.1074/jbc.m304290200
  • 发表时间:
    2003
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Sun,Jianjun;Barbieri,JosephT
  • 通讯作者:
    Barbieri,JosephT
Association of mitogen-activated protein kinases with microtubules in mouse macrophages.
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Aihao Ding其他文献

Aihao Ding的其他文献

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{{ truncateString('Aihao Ding', 18)}}的其他基金

MECHANISMS OF NOVEL ANTI-INFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    7239622
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTI-INFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    7068658
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTIINFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    6636492
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTIINFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    6520299
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTI-INFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    6897998
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTIINFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    6166901
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTIINFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    6387213
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
MECHANISMS OF NOVEL ANTI-INFLAMMATORY ACTIONS OF SLPI
SLPI 的新型抗炎作用机制
  • 批准号:
    6781461
  • 财政年份:
    2000
  • 资助金额:
    $ 12.31万
  • 项目类别:
Molecular Responses of Macrophages-- Lipopolysaccharides
巨噬细胞的分子反应——脂多糖
  • 批准号:
    6326408
  • 财政年份:
    1990
  • 资助金额:
    $ 12.31万
  • 项目类别:
MOLECULAR RESPONSES OF MACROPHAGES TO LIPOPOLYSACCHARIDE
巨噬细胞对脂多糖的分子反应
  • 批准号:
    2672025
  • 财政年份:
    1990
  • 资助金额:
    $ 12.31万
  • 项目类别:

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