Model Studies for FSHD Biomarkers

FSHD 生物标志物的模型研究

基本信息

项目摘要

Project 4: Model Studies for FSHD Biomarkers. Though genetic changes underlying facioscapulohumeral muscular dystrophy (FSHD) have been identified, there is a need to identify downstream pathogenetic mechanisms and to find additional disease biomarkers. Accordingly, the studies under Project 4 will focus on the use of potential mouse models and cultured human FSHD muscle cells to (i) discover or validate FSHD biomarkers, (ii) identify downstream pathogenetic mechanisms, and (iii) test possible therapies. Because affected FSHD muscles show only a small amount of regeneration and repair, it is possible that FSHD pathology could be ameliorated if regeneration and/or muscle hypertrophy were increased. One set of experiments, therefore, will determine if such treatments decrease biomarkers of disease in potential FSHD mouse models. Also, there is considerable indirect evidence to support the idea that apoptosis contributes to FSHD pathogenesis, e.g., activated caspase-3 is found in human FSHD muscle fibers and human FSHD myogenic cells appear to be more susceptible to cell death. No studies have yet directly assessed the contribution of apoptosis to FSHD pathogenesis, and the mechanisms of muscle cell apoptosis are not fully understood. The additional sets of studies are designed to provide a direct assessment of the role of apoptosis in FSHD, to investigate signs of apoptosis as disease biomarkers, and to elucidate apoptotic pathways in diseased muscle cells. The Specific Aims of Project 4 are to: (1) Determine in FSHD mouse models if apoptosis contributes to pathogenesis and if signs of apoptosis are valid disease biomarkers; (2) Determine if treatments that improve regeneration and/or induce hypertrophy will decrease disease biomarkers in FSHD models; and (3) Elucidate mechanisms underlying the increased susceptibility of human FSHD myoblasts and myotubes to cell death upon oxidative stress. Relevance to Public Health. The studies will increase our knowledge of biomarkers for disease progression and how genetic changes lead to disease in FSHD. The experiments could also identify possible new methods to ameliorate FSHD.
项目4:FSHD生物标志物的模型研究。虽然遗传变化的基础面肩肱骨

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 Boone Miller其他文献

Slow and fast myosin heavy chain content defines three types of myotubes in early muscle cell cultures
慢肌球蛋白和快肌球蛋白重链含量定义了早期肌细胞培养物中三种类型的肌管
  • DOI:
  • 发表时间:
    1985
  • 期刊:
  • 影响因子:
    7.8
  • 作者:
    Jeffrey Boone Miller;Michael T. Crow;Frank E. Stockdale
  • 通讯作者:
    Frank E. Stockdale
Membrane fluidity and chemotaxis: Effects of temperature and membrane lipid composition on the swimming behavior of <em>Salmonella typhimurium</em> and <em>Escherichia coli</em>
  • DOI:
    10.1016/s0022-2836(77)80122-8
  • 发表时间:
    1977-04-05
  • 期刊:
  • 影响因子:
  • 作者:
    Jeffrey Boone Miller;D.E. Koshland
  • 通讯作者:
    D.E. Koshland
Developmental regulation of 16S acetylcholinesterase and acetylcholine receptors in a mouse muscle cell line.
小鼠肌肉细胞系中 16S 乙酰胆碱酯酶和乙酰胆碱受体的发育调节。
  • DOI:
    10.1016/0014-4827(83)90221-5
  • 发表时间:
    1983
  • 期刊:
  • 影响因子:
    3.7
  • 作者:
    N. Inestrosa;Jeffrey Boone Miller;Laura Silberstein;Lea Ziskind;Zach W. Hall
  • 通讯作者:
    Zach W. Hall
Evolutionarily conserved sequences of striated muscle myosin heavy chain isoforms. Epitope mapping by cDNA expression.
横纹肌肌球蛋白重链亚型的进化保守序列。
  • DOI:
    10.1016/s0021-9258(18)51604-5
  • 发表时间:
    1989
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Jeffrey Boone Miller;Stephanie B. Teal;F. Stockdale
  • 通讯作者:
    F. Stockdale

Jeffrey Boone Miller的其他文献

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{{ truncateString('Jeffrey Boone Miller', 18)}}的其他基金

Pathogenesis of Muscular Dystrophies
肌营养不良症的发病机制
  • 批准号:
    8603664
  • 财政年份:
    2012
  • 资助金额:
    $ 4.93万
  • 项目类别:
Pathogenesis of Muscular Dystrophies
肌营养不良症的发病机制
  • 批准号:
    8843360
  • 财政年份:
    2012
  • 资助金额:
    $ 4.93万
  • 项目类别:
Pathogenesis of Muscular Dystrophies
肌营养不良症的发病机制
  • 批准号:
    8460485
  • 财政年份:
    2012
  • 资助金额:
    $ 4.93万
  • 项目类别:
Pathogenesis of Muscular Dystrophies
肌营养不良症的发病机制
  • 批准号:
    8297161
  • 财政年份:
    2012
  • 资助金额:
    $ 4.93万
  • 项目类别:
Pathogenesis of Muscular Dystrophies
肌营养不良症的发病机制
  • 批准号:
    8661711
  • 财政年份:
    2012
  • 资助金额:
    $ 4.93万
  • 项目类别:
THE ROLE OF NK CELLS AND THEIR RECEPTORS IN CANCER THERAPY AND TRANSPLANTATION
NK 细胞及其受体在癌症治疗和移植中的作用
  • 批准号:
    7206492
  • 财政年份:
    2005
  • 资助金额:
    $ 4.93万
  • 项目类别:
VACCINATION WITH TETANUS AND KLH TO ASSESS IMMUNE RESPONSES
接种破伤风和 KLH 疫苗以评估免疫反应
  • 批准号:
    7206430
  • 财政年份:
    2005
  • 资助金额:
    $ 4.93万
  • 项目类别:
MT2003-03 CPG 7909 AFTER AUTOLOGOUS TRANSPLANTATION TO ENHANCE RECONSTITUTION
MT2003-03 CPG 7909 自体移植后增强重建
  • 批准号:
    7206500
  • 财政年份:
    2005
  • 资助金额:
    $ 4.93万
  • 项目类别:
VACCINATION WITH TETANUS AND KLH TO ASSESS IMMUNE RESPONSES
接种破伤风和 KLH 疫苗以评估免疫反应
  • 批准号:
    7375861
  • 财政年份:
    2005
  • 资助金额:
    $ 4.93万
  • 项目类别:
MT2004-25: ALLOGENEIC NATURAL KILLER CELLS WITH RELAPSED ACUTE MYELOGENOUS LEUKE
MT2004-25:复发性急性髓性白血病的同种异体自然杀伤细胞
  • 批准号:
    7375901
  • 财政年份:
    2005
  • 资助金额:
    $ 4.93万
  • 项目类别:

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    1995
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Spatial Restriction of Apoptotic Machinery during Neuronal Apoptosis and Pruning
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Examining the contribution of apoptosis repressor with caspase recruitment domain (ARC) to the anti-apoptotic effect of endurance training in skeletal muscle
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