Transcriptional Regulation by PI 3-kinase/Akt Signaling

PI 3-激酶/Akt 信号转导的转录调节

基本信息

  • 批准号:
    6693182
  • 负责人:
  • 金额:
    $ 4.64万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2003
  • 资助国家:
    美国
  • 起止时间:
    2003-09-01 至 2005-08-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): The regulation of programmed cell death, or apoptosis, plays a critical role in both normal development and in the maintenance of adult tissues. Survival factors that prevent apoptosis act in the normal course of development, or, when inappropriately applied, contribute to pathologies such as cancer or neurodegeneration. Many extracellular survival signals, such as growth factors, stimulate receptor tyrosine kinases at the cell surface. These signals then propagate to intracellular second messenger targets. The PI 3-kinase pathway regulates a variety of transcription factors via the phosphorylation of its downstream effectors Akt and GSK-3B. Akt and GSK-313 may contribute to the control of programmed cell death by regulating gene expression at the transcriptional level. These transcription factors can initiate programs that are either pro- or anti-apoptotic. Studies have begun to elucidate the genes affected by these pathways, however the gene targets of PI 3-kinase/Akt/GSK-36 signaling remain undefined. DNA microarrays will be employed to profile the transcriptional effects of this pathway in growth factor stimulated cells. Inhibitors of PI 3-kinase/Akt and GSK-36 will identify those genes specific to each pathway. Genes identified as targets of PI 3-kinase/Akt and MEK will be assessed for common cis-elements using computational tools. Predicted cis-elements will then be tested by chromatin immunoprecipitation.
描述(由申请人提供): 程序性细胞死亡或凋亡的调节在正常发育和成体组织的维持中起着关键作用。阻止细胞凋亡的存活因子在正常发育过程中起作用,或者当不适当地应用时,导致诸如癌症或神经变性的病理。 许多细胞外存活信号,如生长因子,刺激细胞表面的受体酪氨酸激酶。然后这些信号传播到细胞内第二信使靶点。PI 3-激酶途径通过其下游效应物Akt和GSK-3B的磷酸化来调节多种转录因子。Akt和GSK-313可能通过在转录水平上调节基因表达来控制程序性细胞死亡。这些转录因子可以启动促细胞凋亡或抗细胞凋亡的程序。研究已经开始阐明受这些途径影响的基因,然而PI 3-激酶/Akt/GSK-36信号传导的基因靶点仍然不确定。DNA微阵列将被用来分析该途径在生长因子刺激的细胞中的转录效应。 PI 3-激酶/Akt和GSK-36的抑制剂将识别每种途径特异性的基因。将使用计算工具评估鉴定为PI 3-激酶/Akt和MEK靶标的基因的常见顺式元件。然后通过染色质免疫沉淀法检测预测的顺式元件。

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)

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

JOHN W TULLAI其他文献

JOHN W TULLAI的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('JOHN W TULLAI', 18)}}的其他基金

Transcriptional Regulation by PI 3-kinase/Akt Signaling
PI 3-激酶/Akt 信号转导的转录调节
  • 批准号:
    6798157
  • 财政年份:
    2003
  • 资助金额:
    $ 4.64万
  • 项目类别:

相似海外基金

Bridging the Gap: Next-Gen Tools for Accurate Prediction of Disordered Protein Binding Sites
弥合差距:准确预测无序蛋白质结合位点的下一代工具
  • 批准号:
    24K15172
  • 财政年份:
    2024
  • 资助金额:
    $ 4.64万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Design of protein crystal templates with multiple binding sites for tracking metal complex reactions.
设计具有多个结合位点的蛋白质晶体模板,用于跟踪金属络合物反应。
  • 批准号:
    23K04928
  • 财政年份:
    2023
  • 资助金额:
    $ 4.64万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Dynamic changes in PIP2 binding sites and their impact on axonal targeting and function of epilepsy-associated KCNQ/Kv7 channels
PIP2 结合位点的动态变化及其对癫痫相关 KCNQ/Kv7 通道的轴突靶向和功能的影响
  • 批准号:
    10744934
  • 财政年份:
    2023
  • 资助金额:
    $ 4.64万
  • 项目类别:
Computational methods to identify small molecule RNA binding sites
识别小分子 RNA 结合位点的计算方法
  • 批准号:
    573688-2022
  • 财政年份:
    2022
  • 资助金额:
    $ 4.64万
  • 项目类别:
    University Undergraduate Student Research Awards
Identification of potential drug binding sites within allosteric networks in cyclic nucleotide modulated channels
环核苷酸调节通道变构网络内潜在药物结合位点的鉴定
  • 批准号:
    10704557
  • 财政年份:
    2022
  • 资助金额:
    $ 4.64万
  • 项目类别:
Identification of potential drug binding sites within allosteric networks in cyclic nucleotide modulated channels
环核苷酸调节通道变构网络内潜在药物结合位点的鉴定
  • 批准号:
    10537846
  • 财政年份:
    2022
  • 资助金额:
    $ 4.64万
  • 项目类别:
Identifying new types of inhibitors in quinone binding sites in photosynthetic enzymes
鉴定光合酶醌结合位点的新型抑制剂
  • 批准号:
    2753921
  • 财政年份:
    2022
  • 资助金额:
    $ 4.64万
  • 项目类别:
    Studentship
Development of broad nanovaccines targeting diverse coronavirus receptor-binding sites
开发针对不同冠状病毒受体结合位点的广泛纳米疫苗
  • 批准号:
    10328140
  • 财政年份:
    2022
  • 资助金额:
    $ 4.64万
  • 项目类别:
Exploiting Water Network Perturbations in Protein Binding Sites
利用蛋白质结合位点的水网络扰动
  • 批准号:
    10621368
  • 财政年份:
    2021
  • 资助金额:
    $ 4.64万
  • 项目类别:
SBIR Phase I: Nonlinear optical method for identifying protein-ligand binding sites
SBIR 第一阶段:识别蛋白质-配体结合位点的非线性光学方法
  • 批准号:
    2111821
  • 财政年份:
    2021
  • 资助金额:
    $ 4.64万
  • 项目类别:
    Standard Grant
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了