Signaling Processes Underlying Cardiovascular Function
心血管功能的信号传导过程
基本信息
- 批准号:7367382
- 负责人:
- 金额:$ 180.1万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2002
- 资助国家:美国
- 起止时间:2002-06-06 至 2012-12-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION (provided by applicant):
The Program Project Grant will integrate aspects of signal transduction that underlie normal and abnormal cardiovascular function and development. The Program is unified technically in using the approaches of gain- and loss-of-function in cell culture and in the mouse. Signaling pathways in normal cardiac development and function, the basic biology of cardiac signal transduction, and their intersections with the overall stress response will be studied. The Program consists of 4 Projects and 3 Cores. Project 1: Pathogenic signaling in cardiomyopathy will focus on understanding how mutations in a general chaperone, alpha-B crystallin (CryAB) can affect global cardiac function during stress response signaling. As each of the other Projects proposes to modulate specific signaling pathways, it is important to integrate the end response(s) with global cellular events in the cardiomyocyte. Project 2: The Akt-FoxO pathway in heart development will study the FoxO subfamily of the forkhead-related transcription factors. The members of this subfamily participate in regulating proliferation, differentiation and control of cell size in postnatal cardiac, skeletal and smooth muscle lineages. Project 3: The ERK-MAPK signaling branch in the heart will focus on the ERK pathway, one of the three branches of the MAPK signaling pathway. The hypothesis of the project is that ERK1/2 signaling is both necessary and sufficient in mediating physiologic and pathophysiologic cardiac hypertrophy. Although many investigators assume this is the case, with over 100 reports studying the pathway using cultured cells, a careful reading of the literature shows that almost nothing has been reported in vivo as to the necessary and sufficient functions of MEK1-ERK1/2 signaling within the adult heart. Project 4: G-protein receptor kinases in cardiac development and stress adaptation will explore the G-protein receptor kinases (GRKs), which phosphorylate ligand-occupied beta-AR, thus uncoupling them from G-protein effectors and targeting them for internalization. The Administrative Core (A) will serve as the organizational focus. The HistoPathology/Physiology Core (B) will provide an integrated central facility for the necessary histology and pathology, as well as for the physiological analyses. The Adenovirus-Cardiomyocyte Core (C) will prepare virus, rat neonatal cardiomyocytes and fetal and adult mouse cardiomyocytes for the Projects.
描述(由申请人提供):
该计划项目赠款将整合信号转导方面的基础正常和异常的心血管功能和发展。该计划在技术上统一使用细胞培养和小鼠中功能获得和丧失的方法。正常心脏发育和功能的信号通路,心脏信号转导的基础生物学,以及它们与整体应激反应的交叉点将被研究。该计划包括4个项目和3个核心。项目一:心肌病中的致病性信号传导将集中在了解一般分子伴侣α-B晶体蛋白(CryAB)的突变如何在应激反应信号传导过程中影响整体心脏功能。由于其他每个项目都提出调节特定的信号通路,因此将终末反应与心肌细胞中的全局细胞事件整合起来是很重要的。项目2:心脏发育中的Akt-FoxO通路将研究叉头相关转录因子的FoxO亚家族。该亚家族的成员参与调节出生后心脏、骨骼肌和平滑肌谱系中的增殖、分化和细胞大小的控制。项目三:心脏中的ERK-MAPK信号分支将重点关注MAPK信号通路三个分支之一的ERK通路。该项目的假设是ERK 1/2信号传导在介导生理性和病理生理性心脏肥大中是必要的和充分的。尽管许多研究者认为情况就是这样,有超过100篇报道使用培养的细胞研究了该途径,但仔细阅读文献表明,几乎没有关于成年心脏内MEK 1-ERK 1/2信号传导的必要和充分功能的体内报道。项目四:心脏发育和应激适应中的G蛋白受体激酶将探索G蛋白受体激酶(GRKs),其磷酸化配体占据的β-AR,从而将它们与G蛋白效应子解偶联并靶向它们进行内化。行政核心(A)将作为组织重点。组织病理学/生理学中心(B)将为必要的组织学和病理学以及生理学分析提供集成的中心设施。腺病毒-心肌细胞核心(C)将为项目制备病毒、大鼠新生心肌细胞以及胎儿和成年小鼠心肌细胞。
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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Jeffrey Robbins其他文献
Jeffrey Robbins的其他文献
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{{ truncateString('Jeffrey Robbins', 18)}}的其他基金
Mouse and cMyBP-C Protein Production Core
小鼠和 cMyBP-C 蛋白质生产核心
- 批准号:
8215313 - 财政年份:2011
- 资助金额:
$ 180.1万 - 项目类别:
cMyBP-C: Phosphorylation-Dependent Regulation In Vivo
cMyBP-C:体内磷酸化依赖性调节
- 批准号:
8215310 - 财政年份:2011
- 资助金额:
$ 180.1万 - 项目类别:
Mouse and cMyBP-C Protein Production Core
小鼠和 cMyBP-C 蛋白质生产核心
- 批准号:
7789884 - 财政年份:2010
- 资助金额:
$ 180.1万 - 项目类别:
cMyBP-C: Phosphorylation-Dependent Regulation In Vivo
cMyBP-C:体内磷酸化依赖性调节
- 批准号:
7789875 - 财政年份:2010
- 资助金额:
$ 180.1万 - 项目类别:
Cardiomyocyte Toxicity and Heart Failure in Desmin Related Cardiomyopathy
结蛋白相关心肌病中的心肌细胞毒性和心力衰竭
- 批准号:
7364708 - 财政年份:2008
- 资助金额:
$ 180.1万 - 项目类别:
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