Chemokines and Chemokine Receptors

趋化因子和趋化因子受体

基本信息

  • 批准号:
    6572636
  • 负责人:
  • 金额:
    $ 0.5万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2003
  • 资助国家:
    美国
  • 起止时间:
    2003-01-15 至 2003-12-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): Chemokines are members of a family of chemotactic cytokines, which mediate their function through seven transmembrane G protein-coupled receptors. While these small proteins were initially characterized as modulators of leukocyte trafficking, they have since been associated with inflammatory disorders, allergic disease, infectious diseases, atherosclerosis, wound healing, angiogenesis, and tumorigenesis. The mechanisms for activation, trafficking, signal transduction, and modulation of gene expression mediated through chemokines are under intense study. One benefit of learning more about these processes will be the more rational design of small molecules to block responses to these factors. This is particularly critical, since in a number of disease processes, the failure to shut off biological response to chemokines is associated with tissue damage. This Keystone Conference on "Chemokines" will bring together scientists working on the molecular basis of chemokine responses with those working at the organismal level on problems of disease and the immune response. The resultant interaction should stimulate development of new approaches for more rational design of chemokine-directed therapeutics. Moreover, the basic scientists will benefit from learning about the small molecules, which have been developed that may be useful for additional studies into mechanism of action of chemokines.
描述(由申请人提供):趋化因子是趋化性细胞因子家族的成员,其通过七种跨膜G蛋白偶联受体介导其功能。虽然这些小蛋白最初被表征为白细胞运输的调节剂,但它们已经与炎性疾病、过敏性疾病、感染性疾病、动脉粥样硬化、伤口愈合、血管生成和肿瘤发生相关。通过趋化因子介导的基因表达的激活、运输、信号转导和调节的机制正在紧张的研究中。更多地了解这些过程的一个好处是更合理地设计小分子来阻止对这些因素的反应。这是特别关键的,因为在许多疾病过程中,未能关闭对趋化因子的生物反应与组织损伤有关。这次关于“趋化因子”的关键会议将汇集研究趋化因子反应分子基础的科学家,以及那些在生物体水平上研究疾病和免疫反应问题的科学家。由此产生的相互作用,应刺激发展的新方法,更合理的设计趋化因子导向的治疗。此外,基础科学家将受益于了解小分子,这些小分子已经开发出来,可能有助于进一步研究趋化因子的作用机制。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Ann Richmond其他文献

Ann Richmond的其他文献

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{{ truncateString('Ann Richmond', 18)}}的其他基金

BLR&D Merit Review Research Career Scientist (RCS) Award (IK6)
BLR
  • 批准号:
    10618231
  • 财政年份:
    2020
  • 资助金额:
    $ 0.5万
  • 项目类别:
BLR&D Merit Review Research Career Scientist (RCS) Award (IK6)
BLR
  • 批准号:
    10454101
  • 财政年份:
    2020
  • 资助金额:
    $ 0.5万
  • 项目类别:
Optimizing Response to Immune Checkpoint Inhibitor Therapy for Breast Cancer: A Role for Inhibitors of the PI3K pathway
优化乳腺癌免疫检查点抑制剂治疗的反应:PI3K 通路抑制剂的作用
  • 批准号:
    10305634
  • 财政年份:
    2019
  • 资助金额:
    $ 0.5万
  • 项目类别:
Optimizing Response to Immune Checkpoint Inhibitor Therapy for Breast Cancer: A Role for Inhibitors of the PI3K pathway
优化乳腺癌免疫检查点抑制剂治疗的反应:PI3K 通路抑制剂的作用
  • 批准号:
    9916443
  • 财政年份:
    2019
  • 资助金额:
    $ 0.5万
  • 项目类别:
Optimizing Response to Immune Checkpoint Inhibitor Therapy for Breast Cancer: A Role for Inhibitors of the PI3K pathway
优化乳腺癌免疫检查点抑制剂治疗的反应:PI3K 通路抑制剂的作用
  • 批准号:
    10531596
  • 财政年份:
    2019
  • 资助金额:
    $ 0.5万
  • 项目类别:
Combining Immune Therapy with Targeted Therapies to Improve Melanoma Survival
免疫治疗与靶向治疗相结合以提高黑色素瘤的生存率
  • 批准号:
    10609814
  • 财政年份:
    2013
  • 资助金额:
    $ 0.5万
  • 项目类别:
Combining Immune Therapy with Targeted Therapies to Improve Melanoma Survival
免疫治疗与靶向治疗相结合以提高黑色素瘤的生存率
  • 批准号:
    10369756
  • 财政年份:
    2013
  • 资助金额:
    $ 0.5万
  • 项目类别:
Modeling New Therapeutic Approaches for Malignant Melanoma
模拟恶性黑色素瘤的新治疗方法
  • 批准号:
    8817140
  • 财政年份:
    2013
  • 资助金额:
    $ 0.5万
  • 项目类别:
Combining Immune Therapy with Targeted Therapies to Improve Melanoma Survival
免疫治疗与靶向治疗相结合以提高黑色素瘤的生存率
  • 批准号:
    10265337
  • 财政年份:
    2013
  • 资助金额:
    $ 0.5万
  • 项目类别:
Modeling New Therapeutic Approaches for Malignant Melanoma
模拟恶性黑色素瘤的新治疗方法
  • 批准号:
    8633274
  • 财政年份:
    2013
  • 资助金额:
    $ 0.5万
  • 项目类别:

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