Cell Identity and Signaling Research Program (Project-001)

细胞识别和信号传导研究计划(项目-001)

基本信息

  • 批准号:
    9149430
  • 负责人:
  • 金额:
    $ 3.36万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1997
  • 资助国家:
    美国
  • 起止时间:
    1997-04-01 至 2020-06-30
  • 项目状态:
    已结题

项目摘要

Cell Identity and Signaling Research Program Project Summary Since the last competitive renewal, the long standing Cell Growth and Differentiation Program, which had been in existence since 1993, was reorganized to the Cell Identity and Signaling (CIS) Program. In response to concerns expressed in the 2009 CCSG review, the Cell Growth and Differentiation Program Leaders, Senior Leadership, and Executive Committee conducted a full programmatic review in conjunction with the External Advisory Committee. A consensus was reached to reorganize the Program to address review concerns and enhance collaborative interactions. The reorganized and refocused CIS Program required new faculty recruitment to strengthen the reorganized Program and the mission of the Purdue University Center for Cancer Research (PCCR). The reorganized CIS Program serves the PCCR as the central component for basic discovery in cancer cell biology. To do this, CIS leverages Purdue University foundational strengths in the biological sciences, medicinal chemistry, pharmacy, veterinary medicine, and nutrition science, to address critical topics in cancer cell biology. Specifically, the overall mission of the CIS Program is to investigate key molecules that impact signaling pathways and gene expression programs, and to understand how cellular identity is determined or altered. CIS members are committed to understanding what is needed to maintain cellular identity and correcting the identity crisis that cancer cells undergo. The CIS membership represents 7 different Purdue academic departments and 5 colleges, and has grown from 26 members to 33 members through the addition of 14 new members since the previous CCSG review. The CIS Program has a current portfolio of ~$4.3 million (direct costs) of NCI and other peer-reviewed, cancer-related support. As a result of PCCR support and the programmatic changes initiated by the CIS Program Leaders, CIS collaborative publications have dramatically increased with intra-programmatic publications at 8% (~38% increase) and inter-programmatic at 25% (~68% increase); inter-institutional collaborations are at 17%, providing an overall strong collaborative publication rate of ~43%. The CIS Program is structured to address the issue of cellular identity by focusing on two major Research Clusters: Signaling and Cellular Growth Control and Regulation of Gene Expression. CIS Program members also share the common goal of focusing on basic science to identify and characterize key molecules for cellular processes that can be translated into cancer solutions. The biological expertise and cancer targets that CIS members study allow them to develop collaborations within the CIS Program and among members of the other PCCR Research Programs, adding considerable value to the PCCR.
细胞身份和信号研究计划 项目摘要 自从上次竞争更新以来,长期存在的细胞生长和分化计划 自1993年以来一直存在,重组为细胞身份和信号传导(CIS)程序。响应 2009年CCSG评论,细胞增长和分化计划领导者,高级 领导力和执行委员会与外部进行了完整的程序审查 咨询委员会。达成共识,以重组该计划,以解决审查问题和 增强协作互动。重组和重新集中的独联体计划需要新的教师 招聘以加强重组计划和普渡大学癌症中心的任务 研究(PCCR)。重组的CIS程序将PCCR作为基本的核心组成部分 癌细胞生物学的发现。为此,CIS利用普渡大学的基础优势 生物科学,药物化学,药房,兽医医学和营养科学,以解决 癌细胞生物学的关键主题。具体而言,独联体计划的整体任务是调查密钥 影响信号通路和基因表达程序的分子,并了解细胞 确定或改变身份。 CIS成员致力于了解维护所需的内容 细胞身份并纠正癌细胞经历的身份危机。顺式成员代表7 普渡大学的学术系和5所大学,已从26名成员增长到33名成员 自之前的CCSG审查以来,通过增加了14个新成员。 CIS程序具有当前 NCI和其他与癌症相关的支持的NCI和其他同行评审的支持约为430万美元(直接费用)。后果 PCCR支持和CIS计划负责人发起的程序化更改,CIS协作 出版物的出版物内出版物的出版物大大增加了(增长约38%),并且 跨编程间为25%(增加68%);机构间合作率为17%,提供了整体 强大的合作出版率约为43%。 CIS程序的结构是解决蜂窝的问题 通过关注两个主要的研究集群的身份:信号传导和细胞生长控制和调节 基因表达。 CIS计划成员还分享关注基础科学以识别的共同目标 并表征可以将可以翻译成癌症的细胞过程的关键分子。这 生物学专业知识和癌症目标使他们能够在境内发展合作 CIS计划以及其他PCCR研究计划的成员中,增加了相当大的价值 PCCR。

项目成果

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科研奖励数量(0)
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专利数量(0)

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SCOTT D BRIGGS其他文献

SCOTT D BRIGGS的其他文献

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{{ truncateString('SCOTT D BRIGGS', 18)}}的其他基金

SET Domain Epigenetic Factors Govern Antifungal Drug Efficacy and Fungal Pathogenesis
SET域表观遗传因素控制抗真菌药物疗效和真菌发病机制
  • 批准号:
    10229440
  • 财政年份:
    2018
  • 资助金额:
    $ 3.36万
  • 项目类别:
SET Domain Epigenetic Factors Govern Antifungal Drug Efficacy and Fungal Pathogenesis
SET域表观遗传因素控制抗真菌药物疗效和真菌发病机制
  • 批准号:
    10462528
  • 财政年份:
    2018
  • 资助金额:
    $ 3.36万
  • 项目类别:
SET Domain Epigenetic Factors Govern Antifungal Drug Efficacy and Fungal Pathogenesis
SET域表观遗传因素控制抗真菌药物疗效和真菌发病机制
  • 批准号:
    9790911
  • 财政年份:
    2018
  • 资助金额:
    $ 3.36万
  • 项目类别:
SET Domain Epigenetic Factors Govern Antifungal Drug Efficacy and Fungal Pathogenesis
SET域表观遗传因素控制抗真菌药物疗效和真菌发病机制
  • 批准号:
    9979745
  • 财政年份:
    2018
  • 资助金额:
    $ 3.36万
  • 项目类别:
Role of Set1-mediated methylation in chromatin functioin
Set1 介导的甲基化在染色质功能中的作用
  • 批准号:
    8003036
  • 财政年份:
    2010
  • 资助金额:
    $ 3.36万
  • 项目类别:
Role of Set1-mediated methylation in chromatin functioin
Set1 介导的甲基化在染色质功能中的作用
  • 批准号:
    7752593
  • 财政年份:
    2006
  • 资助金额:
    $ 3.36万
  • 项目类别:
Role of Set1-mediated methylation in chromatin function
Set1 介导的甲基化在染色质功能中的作用
  • 批准号:
    7161311
  • 财政年份:
    2006
  • 资助金额:
    $ 3.36万
  • 项目类别:
Role of Set1-mediated methylation in chromatin functioin
Set1 介导的甲基化在染色质功能中的作用
  • 批准号:
    7334736
  • 财政年份:
    2006
  • 资助金额:
    $ 3.36万
  • 项目类别:
Role of Set1-mediated methylation in chromatin functioin
Set1 介导的甲基化在染色质功能中的作用
  • 批准号:
    7540398
  • 财政年份:
    2006
  • 资助金额:
    $ 3.36万
  • 项目类别:
Role of Set1-mediated methylation in chromatin functioin
Set1 介导的甲基化在染色质功能中的作用
  • 批准号:
    7028127
  • 财政年份:
    2006
  • 资助金额:
    $ 3.36万
  • 项目类别:

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