REGULATION OF THE SIGNALING PHOSPHOLIPID, PHOSPHATIDYLINOSITOL 3,5 BIS PHOSPHATE
信号磷脂、磷脂酰肌醇 3,5 二磷酸酯的调节
基本信息
- 批准号:8171245
- 负责人:
- 金额:$ 0.24万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2010
- 资助国家:美国
- 起止时间:2010-09-01 至 2011-08-31
- 项目状态:已结题
- 来源:
- 关键词:Computer Retrieval of Information on Scientific Projects DatabaseDefectFundingGenerationsGeneticGoalsGrantInstitutionMembrane Protein TrafficMinorNervous System PhysiologyPathway interactionsPhosphatidylinositolsPhospholipidsPhosphorylationPhosphorylation SitePolyphosphatesProteinsRegulationResearchResearch PersonnelResourcesRisk FactorsSignal TransductionSourceUnited States National Institutes of Healthinorganic phosphate
项目摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
Phosphatidylinositol polyphosphates (PPIs) have recently emerged as key regulators of membrane trafficking pathways. We recently discovered that the PPI, phosphatidylinositol 3,5 bis phosphate (PI3,5)P2, is particularly critical for normal function of the nervous system. We found that very minor defects in the generation of (PI3,5)P2 are a significant risk factor in ALS. Moreover we recently found that the five proteins known to regulate PI3,5P2 are phosphorylated. The overall goal of this project is to determine the phosphorylation sites, and then to use a genetic approach to determine how phosphorylation regulates PI3,5P2 levels
这个子项目是许多研究子项目中的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可以在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者所在的机构。
磷脂酰肌醇多磷酸(PPIs)最近成为膜运输途径的关键调节剂。我们最近发现,PPI,磷脂酰肌醇3,5二磷酸(PI 3,5)P2,对神经系统的正常功能特别重要。 我们发现,(PI 3,5)P2生成过程中非常微小的缺陷是ALS的一个重要风险因素。 此外,我们最近发现,已知调节PI 3,5 P2的五种蛋白质被磷酸化。 本项目的总体目标是确定磷酸化位点,然后使用遗传方法确定磷酸化如何调节PI 3,5 P2水平
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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Lois S Weisman其他文献
Lois S Weisman的其他文献
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{{ truncateString('Lois S Weisman', 18)}}的其他基金
Phosphoinositide signaling: novel potential targets for Huntington disease
磷酸肌醇信号传导:亨廷顿病的新潜在靶点
- 批准号:
10183342 - 财政年份:2017
- 资助金额:
$ 0.24万 - 项目类别:
2016 Lysosome and Endocytosis Gordon Research Conference & Gordon Research Seminar
2016年溶酶体与内吞作用戈登研究会议
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9123850 - 财政年份:2016
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$ 0.24万 - 项目类别:
Inositol lipid regulation of membrane fusion and fission
肌醇脂质对膜融合和裂变的调节
- 批准号:
7810115 - 财政年份:2010
- 资助金额:
$ 0.24万 - 项目类别:
How does misregulation of PI3,5P2 signaling lead to neurodegeneration?
PI3、5P2 信号传导失调如何导致神经退行性变?
- 批准号:
8197473 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
How does misregulation of PI3,5P2 signaling lead to neurodegeneration?
PI3、5P2 信号传导失调如何导致神经退行性变?
- 批准号:
7564524 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
Roles and regulation of PI(3,5)P2 and PI5P in neurons
PI(3,5)P2和PI5P在神经元中的作用和调节
- 批准号:
8853956 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
Roles and regulation of PI(3,5)P2 and PI5P in neurons
PI(3,5)P2和PI5P在神经元中的作用和调节
- 批准号:
9052226 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
How does misregulation of PI3,5P2 signaling lead to neurodegeneration?
PI3、5P2 信号传导失调如何导致神经退行性变?
- 批准号:
7994750 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
Roles and regulation of PI(3,5)P2 and PI5P in neurons
PI(3,5)P2和PI5P在神经元中的作用和调节
- 批准号:
8768515 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
Regulation of Myosin V Interaction with Cargo
肌球蛋白 V 与货物相互作用的调节
- 批准号:
7932391 - 财政年份:2009
- 资助金额:
$ 0.24万 - 项目类别:
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