课题基金 / 基金详情

Disulfide activated protein kinase G Ialpha as a new therapeutic target in sepsis

Disulfide activated protein kinase G Ialpha as a new therapeutic target in sepsis
二硫键激活蛋白激酶 G Iα 作为脓毒症新治疗靶点
批准号:
MR/L009684/1
负责人:
Philip Eaton
金额:
$64.08万
依托单位:
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2014
资助国家:
英国
项目状态:
已结题
起止时间:
2014 至 --

项目摘要

项目成果

Philip Eaton的其他基金

相似基金

相关文献

中文摘要
翻译
败血症,通常被称为血液中毒,当细菌进入血液时就会发生。这是一种非常常见的疾病,当它发生时,存活的机会相当低。脓毒症的主要问题是患者的血压变得非常低,他们的血管变得漏水。总而言之,这会造成很大的伤害,许多身体器官没有足够的血液供应,因此它们会受伤。最近,我们发现了一种新的途径,可以降低健康人的血压并促进血管渗漏,现在我们发现,在导致器官损伤的脓毒症过程中,这一途径被过度刺激。在这些研究中,我们希望开发和测试防止这一途径在脓毒症期间被激活的新药。据预测,这种疗法可以防止器官损伤,并最终提高脓毒症患者的存活率。
英文摘要
Sepsis, often referred to as blood poisoning, occurs when bacteria get into the blood stream. This is a very common disease and when it occurs the chances of survival are rather poor. Major issues in sepsis are that the patients' blood pressure becomes very low and their blood vessels become leaky. Together this causes a lot of harm and many of the bodies organs are not supplied with enough blood and so they become injured. Recently we identified a new pathway that lowers blood pressure and promotes vessel leakiness in healthy people, and have now we have found this is over-stimulated during sepsis resulting in organ damage. In these studies we hope to develop and test new drugs that prevent this pathway being actuated during sepsis. Such therapies are predicted to prevent organ damage and ultimately enhance patient survival during sepsis.
期刊论文(10)
专著(0)
科研奖励(0)
会议论文
DOI: 10.1016/j.cub.2015.04.020
发表时间: 2015-06-01
期刊: CURRENT BIOLOGY
影响因子: 9.2
作者: [Cameron, Jenifer M., Gabrielsen, Mads, Chim, Ya Hua, Munro, June, McGhee, Ewan J., Sumpton, David, Eaton, Philip, Anderson, Kurt I., Yin, Huabing, Olson, Michael F.]
通讯作者: Olson, Michael F.
DOI: 10.1021/acs.biochem.5b00774
发表时间: 2016-02-09
期刊: BIOCHEMISTRY
影响因子: 2.9
作者: [Akashi, Soichiro, Ahmed, Khandaker Ahtesham, Akaike, Takaaki]
通讯作者: Akaike, Takaaki
DOI: 10.1016/j.pep.2018.09.001
发表时间: 2019-01
期刊: Protein expression and purification
影响因子: 1.6
作者: [Abis G, Charles RL, Eaton P, Conte MR]
通讯作者: Conte MR
BeyondSNO: Signalling beyond protein S-nitrosylation - determining the roles of nitroxyl and hydroxylamine
  • 批准号:
    EP/Y027698/1
  • 项目类别:
    Research Grant
  • 资助金额:
    $269.79万
  • 财政年份:
    2024
  • 负责人:
    Philip Eaton
  • 依托单位:
Targeting the oxidative activation of PKG Ialpha as a treatment for HFpEF
  • 批准号:
    MR/W023784/1
  • 项目类别:
    Research Grant
  • 资助金额:
    $68.89万
  • 财政年份:
    2022
  • 负责人:
    Philip Eaton
  • 依托单位:
Furthering our understanding of the redox regulation of Protein Kinase A in the cardiovascular system
  • 批准号:
    MR/P023150/2
  • 项目类别:
    Research Grant
  • 资助金额:
    $35.35万
  • 财政年份:
    2019
  • 负责人:
    Philip Eaton
  • 依托单位:
Thiol-disulfide redox switches in protein kinases and their role in cardiovascular health and disease
  • 批准号:
    MR/R01065X/2
  • 项目类别:
    Research Grant
  • 资助金额:
    $157.86万
  • 财政年份:
    2019
  • 负责人:
    Philip Eaton
  • 依托单位:
国内基金
海外基金
ASD1(Activated SAM in Darkness1)调控植物暗形态建成中茎尖分生组织活性的分子机制研究
  • 批准号:
    31970824
  • 项目类别:
    面上项目
  • 资助金额:
    60.0万元
  • 批准年份:
    2019
  • 负责人:
    刘西岗
  • 依托单位:
抑素蛋白(prohibitin)1调控蛋白酶激活受体(protease-activated receptor)1内化转运及降解的功能和机制
miR-320家族与RACK1的关系及其对乳腺癌侵袭转移的作用和机制
  • 批准号:
    81272387
  • 项目类别:
    面上项目
  • 资助金额:
    70.0万元
  • 批准年份:
    2012
  • 负责人:
    刘秀萍
  • 依托单位:
钙激活的大电流钾离子通道β1亚基影响慢性肾脏病进展的机制探讨
  • 批准号:
    81070587
  • 项目类别:
    面上项目
  • 资助金额:
    38.0万元
  • 批准年份:
    2010
  • 负责人:
    陈育青
  • 依托单位: