Molecular mechanisms controlling stress responses and cell adhesion in bacteria
控制细菌应激反应和细胞粘附的分子机制
基本信息
- 批准号:10614114
- 负责人:
- 金额:$ 4.86万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2019
- 资助国家:美国
- 起止时间:2019-07-01 至 2024-04-30
- 项目状态:已结题
- 来源:
- 关键词:AddressAdhesionsAnabolismBacteriaBacterial InfectionsBacterial PhysiologyBiochemicalBiologyBiophysicsCell AdhesionCellsChemicalsClinicalCommunitiesComplexCytoplasmDataDetectionEnvironmentGene Expression RegulationGeneticGrowthInfectionInvestigationMicrobial BiofilmsMolecularMolecular StructurePhysiologyPolysaccharidesProcessRouteSensorySignal TransductionStressStructureSurfaceSystemVirulenceWorkbiological adaptation to stresscell envelopegenetic regulatory proteinimprovednovel therapeuticspathogenic bacteriaresponse
项目摘要
Project Summary/Abstract
My group seeks to understand molecular mechanisms that underlie the ability of bacterial cells to survive in
complex, dynamic environments, including mammalian hosts. In the context of this project, we will specifically
focus on defining mechanisms by which bacteria (i) regulate their physiology to survive environmental stress,
and (ii) regulate and modify their envelope to control adhesion to surfaces and to other cells. We will utilize an
interdisciplinary set of genetic, biochemical, biophysical, and computational approaches to address these
questions on multiple scales, from the cellular/systems level to the level of molecular structure. The data that
emerge from our studies will enhance understanding of processes that allow bacteria to grow and survive in
complex environments, and will inform new concepts in gene regulation and cell envelope biology. More
specifically, this project will provide the scientific community with an integrative understanding of sensory
transduction mechanisms, from signal detection to cellular response. In addition, our investigations of bacterial
cell adhesion and envelope polysaccharide biosynthesis will lead to improved understanding of the molecular
mechanisms by which bacteria build the highly complex structure known as the envelope, which separates the
tightly controlled activities in the cytoplasm from the outside world. Importantly, both environmental regulatory
proteins and components of the bacterial cell envelope are well-defined virulence determinants in many
bacterial pathogens. Thus our work has the potential to inform new therapeutic routes to control certain
bacterial infections.
项目总结/文摘
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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Sean Crosson其他文献
Sean Crosson的其他文献
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{{ truncateString('Sean Crosson', 18)}}的其他基金
Molecular mechanisms controlling stress responses and cell adhesion in bacteria
控制细菌应激反应和细胞粘附的分子机制
- 批准号:
10616493 - 财政年份:2019
- 资助金额:
$ 4.86万 - 项目类别:
2020 Signal Transduction in Microorganisms Gordon Research Conference and Gordon Research Seminar
2020微生物信号转导戈登研究会议暨戈登研究研讨会
- 批准号:
9902685 - 财政年份:2019
- 资助金额:
$ 4.86万 - 项目类别:
Molecular mechanisms controlling stress responses and cell adhesion in bacteria
控制细菌应激反应和细胞粘附的分子机制
- 批准号:
10278328 - 财政年份:2019
- 资助金额:
$ 4.86万 - 项目类别:
Molecular mechanisms controlling stress responses and cell adhesion in bacteria
控制细菌应激反应和细胞粘附的分子机制
- 批准号:
10380281 - 财政年份:2019
- 资助金额:
$ 4.86万 - 项目类别:
Molecular mechanisms controlling stress responses and cell adhesion in bacteria
控制细菌应激反应和细胞粘附的分子机制
- 批准号:
10391503 - 财政年份:2019
- 资助金额:
$ 4.86万 - 项目类别:
Molecular mechanism of general stress signaling in Brucella abortus
流产布鲁氏菌一般应激信号传导的分子机制
- 批准号:
8793743 - 财政年份:2014
- 资助金额:
$ 4.86万 - 项目类别:
Molecular mechanism of general stress signaling in Brucella abortus
流产布鲁氏菌一般应激信号传导的分子机制
- 批准号:
8694631 - 财政年份:2014
- 资助金额:
$ 4.86万 - 项目类别:
Defining the functions of uncharacterized genes in priority pathogens
定义优先病原体中未表征基因的功能
- 批准号:
8891357 - 财政年份:2013
- 资助金额:
$ 4.86万 - 项目类别:
Brucella stress-response proteins as virulence factors and antimicrobial targets
布鲁氏菌应激反应蛋白作为毒力因子和抗菌靶点
- 批准号:
8549363 - 财政年份:2013
- 资助金额:
$ 4.86万 - 项目类别:
Defining the functions of uncharacterized genes in priority pathogens
定义优先病原体中未表征基因的功能
- 批准号:
8719930 - 财政年份:2013
- 资助金额:
$ 4.86万 - 项目类别:
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