Novel approaches to identify regulators of Bak1 splicing

识别 Bak1 剪接调节因子的新方法

基本信息

  • 批准号:
    10040977
  • 负责人:
  • 金额:
    $ 45.29万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2020
  • 资助国家:
    美国
  • 起止时间:
    2020-08-01 至 2022-07-31
  • 项目状态:
    已结题

项目摘要

The objective of this application is to unbiasedly identify regulators essential for programming intrinsic neuronal resistance to apoptosis. Apoptosis is a ubiquitous regulated cell death pathway controlling cell turnover and tissue homeostasis in metazoans. A longstanding issue is how neurons suppress apoptosis in favor of longevity. Previous studies on neuronal regulation of apoptosis have focused on why and how extrinsic survival cues help establish and maintain neural circuits through the control of cell death. While these inspiring studies delineate how neurons compete for survival at the time of circuit formation, important questions remain unresolved, i.e., whether neuronal apoptosis sensitivity is genetically determined. In our preliminary studies, we have found that neuronal resistance to apoptosis is intrinsically programmed before circuit formation by depletion of pro-apoptotic mitochondrial protein BAK1. We further found that BAK1 expression is controlled at the RNA level through robust alternative splicing mechanisms. The critical question is: what factors program Bak1 splicing? Identification of these factors will have significant impacts and enable new investigations of neuronal cell death controls in various settings. The proposed study will generate new tools and develop robust cell-based methods to systematically identify regulators of Bak1 splicing. We will integrate experimental and computational approaches to accelerate discoveries that would otherwise be limited and less sensitive. Our team has demonstrated successful collaborations researching cell death, neuronal survival, and RNA molecular genetics in the brain, and expect the proposed research to be fruitful. By revealing novel regulatory mechanisms of apoptosis and associated genetic factors, our findings may inform strategies for enhancing cell survival and tackling neurodegenerative diseases. Completion of the proposed study will also provide proof-of-principle for our broadly applicable strategy to study any alternative exons.
本应用的目的是无偏见地识别内在神经元编程所必需的调节器

项目成果

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会议论文数量(0)
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Liang Chen其他文献

Liang Chen的其他文献

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{{ truncateString('Liang Chen', 18)}}的其他基金

Investigate the immune modulation function of SARS-CoV-2 accessory protein ORF8
研究SARS-CoV-2辅助蛋白ORF8的免疫调节功能
  • 批准号:
    469610
  • 财政年份:
    2022
  • 资助金额:
    $ 45.29万
  • 项目类别:
    Operating Grants
COVID-19 Variant Supplement - Understand the high pathogenicity and zoonotic transmission of the COVID-19 virus: evasion of host innate immune responses
COVID-19 变异补充剂 - 了解 COVID-19 病毒的高致病性和人畜共患传播:逃避宿主先天免疫反应
  • 批准号:
    442863
  • 财政年份:
    2021
  • 资助金额:
    $ 45.29万
  • 项目类别:
    Operating Grants
Understand the high pathogenicity and zoonotic transmission of the COVID-19 virus: evasion of host innate immune responses
了解 COVID-19 病毒的高致病性和人畜共患传播:逃避宿主先天免疫反应
  • 批准号:
    422747
  • 财政年份:
    2020
  • 资助金额:
    $ 45.29万
  • 项目类别:
    Operating Grants
Understanding the NMD regulatory path from genetic variation to phenotypes
了解 NMD 从遗传变异到表型的调控路径
  • 批准号:
    10377405
  • 财政年份:
    2020
  • 资助金额:
    $ 45.29万
  • 项目类别:
Sex as a Biological Variable Supplement - Understand the high pathogenicity and zoonotic transmission of the COVID-19 virus: evasion of host innate immune responses
性别作为生物变量补充 - 了解 COVID-19 病毒的高致病性和人畜共患传播:逃避宿主先天免疫反应
  • 批准号:
    424691
  • 财政年份:
    2020
  • 资助金额:
    $ 45.29万
  • 项目类别:
    Operating Grants
Understanding the NMD regulatory path from genetic variation to phenotypes
了解 NMD 从遗传变异到表型的调控路径
  • 批准号:
    10714885
  • 财政年份:
    2020
  • 资助金额:
    $ 45.29万
  • 项目类别:
Understanding the NMD regulatory path from genetic variation to phenotypes
了解 NMD 从遗传变异到表型的调控路径
  • 批准号:
    10594582
  • 财政年份:
    2020
  • 资助金额:
    $ 45.29万
  • 项目类别:
Study IFITM restriction of HIV-1 entry: cross-talk with adaptive immunity
研究 IFITM 对 HIV-1 进入的限制:与适应性免疫的交叉对话
  • 批准号:
    401410
  • 财政年份:
    2019
  • 资助金额:
    $ 45.29万
  • 项目类别:
    Operating Grants
Overcome HIV-1 Resistance to CRISPR/Cas9 Attack
克服 HIV-1 对 CRISPR/Cas9 攻击的抵抗力
  • 批准号:
    350800
  • 财政年份:
    2016
  • 资助金额:
    $ 45.29万
  • 项目类别:
    Operating Grants
Genomic variation in epidemic carbapenem-resistant K.pneumoniae
流行性耐碳青霉烯类肺炎克雷伯菌的基因组变异
  • 批准号:
    9035583
  • 财政年份:
    2016
  • 资助金额:
    $ 45.29万
  • 项目类别:

相似海外基金

Alternative splicing of Grin1 controls NMDA receptor function in physiological and disease processes
Grin1 的选择性剪接控制生理和疾病过程中的 NMDA 受体功能
  • 批准号:
    488788
  • 财政年份:
    2023
  • 资助金额:
    $ 45.29万
  • 项目类别:
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RBFOX2 失调通过选择性剪接促进胰腺癌进展
  • 批准号:
    10638347
  • 财政年份:
    2023
  • 资助金额:
    $ 45.29万
  • 项目类别:
Long Noncoding RNA H19 Mediating Alternative Splicing in ALD Pathogenesis
长非编码 RNA H19 介导 ALD 发病机制中的选择性剪接
  • 批准号:
    10717440
  • 财政年份:
    2023
  • 资助金额:
    $ 45.29万
  • 项目类别:
Using proteogenomics to assess the functional impact of alternative splicing events in glioblastoma
使用蛋白质基因组学评估选择性剪接事件对胶质母细胞瘤的功能影响
  • 批准号:
    10577186
  • 财政年份:
    2023
  • 资助金额:
    $ 45.29万
  • 项目类别:
Alternative splicing regulation of CLTC in the heart
心脏中 CLTC 的选择性剪接调节
  • 批准号:
    10749474
  • 财政年份:
    2023
  • 资助金额:
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Nitric oxide as a novel regulator of alternative splicing
一氧化氮作为选择性剪接的新型调节剂
  • 批准号:
    10673458
  • 财政年份:
    2023
  • 资助金额:
    $ 45.29万
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Alternative splicing as an evolutionary driver of phenotypic plasticity
选择性剪接作为表型可塑性的进化驱动力
  • 批准号:
    2884151
  • 财政年份:
    2023
  • 资助金额:
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  • 项目类别:
    Studentship
Rescuing SYNGAP1 haploinsufficiency by redirecting alternative splicing
通过重定向选择性剪接挽救 SYNGAP1 单倍体不足
  • 批准号:
    10660668
  • 财政年份:
    2023
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CAREER: Mechanotransduction, transcription, and alternative splicing in cell biology
职业:细胞生物学中的机械转导、转录和选择性剪接
  • 批准号:
    2239056
  • 财政年份:
    2023
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    $ 45.29万
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    Continuing Grant
Investigating the role of alternative splicing in the islets of Langerhans in developing diabetes.
研究朗格汉斯岛中选择性剪接在糖尿病发生中的作用。
  • 批准号:
    468851650
  • 财政年份:
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