MECHANISMS OF LEUKOCYTE ACTIVATION AND CHEMOTAXIS
白细胞激活和趋化机制
基本信息
- 批准号:2722957
- 负责人:
- 金额:$ 23.88万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1998
- 资助国家:美国
- 起止时间:1998-02-01 至 2003-01-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION (Adapted from applicant's abstract): Leukocytes play an
important role in host defense against invading microorganisms. Their
ability to generate superoxide radicals and release degradative enzymes
following migration to sites of inflammation is essential for this
function. However, these same responses can also participate in the
formation of numerous pathological conditions. The re-introduction of
blood flow to ischaemic tissues following myocardial thrombosis, stroke or
frostbite is responsible for the observed tissue damage, which can be
alleviated by the depletion of neutrophils. Chemoattractants elicit their
effects on neutrophils by binding to cell surface receptors coupled to
guanine nucleotide-binding regulatory proteins (G proteins). The goal of
this work is to understand the molecular mechanisms involved in the
activation of leukocyte G protein-coupled chemoattractant receptors as
they pertain to receptor signaling and processing, receptor interactions
with the cytoskeleton and chemotaxis.
The specific aims of this proposal include the determination of the role
of the N-formyl peptide receptor (FPR) activation I the physical binding
of the receptor to G protein. The proposed experiments will also determine
residues responsible for the interaction of the receptor with the
cytoskeleton and one of its major components, actin. We will generate
mutations in the intracellular domains of the recombinant FPR and express
these in tissue culture cell lines for functional analysis. The roles of
specific residues, including potentially phosphorylated residues, will be
determined with respect to receptor processing and chemotaxis utilizing a
novel system we have recently developed. These complex activities likely
require interactions following receptor phosphorylation. Utilizing this
system, we will also examine the role(s) of the low MW G proteins rho, rac
and cdc42 in leukocyte chemotaxis.
Information obtained from the proposed studies is expected to extend our
knowledge of the activation of signal transduction pathways by
chemoattractant receptors with the long term goal that such knowledge will
lead to the development of therapeutic means to control neutrophil
activation and prevent the tissue damage resulting from the excessive
activation of neutrophils following reperfusion.
描述(改编自申请人摘要):白细胞起作用
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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Eric R Prossnitz其他文献
Eric R Prossnitz的其他文献
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{{ truncateString('Eric R Prossnitz', 18)}}的其他基金
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
8517052 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
8677811 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
10472699 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
10251268 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
8849761 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
10689300 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
G protein-coupled estrogen receptor GPER and breast carcinogenesis
G蛋白偶联雌激素受体GPER与乳腺癌发生
- 批准号:
9079447 - 财政年份:2012
- 资助金额:
$ 23.88万 - 项目类别:
MLP Assay for Arrestin-AP2 Inhibitors
Arrestin-AP2 抑制剂的 MLP 测定
- 批准号:
8208096 - 财政年份:2011
- 资助金额:
$ 23.88万 - 项目类别:
MLP Assay for Arrestin-AP2 Inhibitors
Arrestin-AP2 抑制剂的 MLP 测定
- 批准号:
8069438 - 财政年份:2011
- 资助金额:
$ 23.88万 - 项目类别:
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肌动蛋白和肌动蛋白结合蛋白的结构/相互作用
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