WB | 咨询技术 | Human,Mouse,Rat |
IF | 咨询技术 | Human,Mouse,Rat |
IHC | 1/500-1/1000 | Human,Mouse,Rat |
ICC | 技术咨询 | Human,Mouse,Rat |
FCM | 咨询技术 | Human,Mouse,Rat |
Elisa | 咨询技术 | Human,Mouse,Rat |
Host/Isotype | Mouse IgG2a |
Antibody Type | Primary antibody |
Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
Species Reactivity | Human |
Immunogen | Purified recombinant fragment of human TRIM72 |
Formulation | Purified antibody in PBS with 0.05% sodium azide |
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以下是关于TRIM72抗体的3篇参考文献示例(注:文献信息为模拟示例,实际引用需核实):
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1. **文献名称**: *TRIM72/MG53 is essential for cell membrane repair in skeletal and cardiac muscle*
**作者**: Cai C., et al.
**摘要**: 该研究首次揭示了TRIM72(MG53)在骨骼肌和心肌细胞膜修复中的核心作用,通过生成特异性抗体阻断其功能后,细胞膜损伤修复能力显著下降,表明TRIM72是膜修复复合体的关键成分。
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2. **文献名称**: *Antibody targeting of TRIM72 exacerbates myocardial ischemia-reperfusion injury by disrupting membrane repair*
**作者**: Weisleder N., et al.
**摘要**: 研究利用TRIM72抗体在小鼠心脏缺血再灌注模型中进行干预,发现抗体中和TRIM72功能会加重心肌细胞损伤,提示其在心脏保护中的治疗潜力及抗体使用的潜在风险。
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3. **文献名称**: *TRIM72 antibody-based modulation of skeletal muscle regeneration in a dystrophic model*
**作者**: Zhu H., et al.
**摘要**: 通过TRIM72抗体检测其在肌营养不良模型中的表达动态,发现抗体介导的功能抑制延缓了肌纤维再生,强调TRIM72在肌肉修复中的双向调节作用。
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如需具体文献,建议通过PubMed或Google Scholar以关键词“TRIM72 antibody”“MG53 therapeutic”等检索近年高被引论文。
TRIM72. also known as MG53. is a member of the tripartite motif (TRIM) family of proteins, characterized by conserved RING, B-box, and coiled-coil domains. It is predominantly expressed in striated muscle tissues, including skeletal and cardiac muscle, and plays a critical role in cell membrane repair. TRIM72 facilitates the recruitment of intracellular vesicles to injury sites, promoting membrane resealing and maintaining cellular integrity during mechanical or chemical stress. Its function is particularly vital in muscle cells, where frequent mechanical stress necessitates robust repair mechanisms.
TRIM72 antibodies are essential tools for studying its expression, localization, and molecular interactions. They are widely used in techniques like Western blotting, immunohistochemistry, and immunoprecipitation to investigate TRIM72's involvement in physiological and pathological processes. Research highlights its dual role: while TRIM72 deficiency exacerbates muscle injury and cardiomyopathy, its overexpression is linked to insulin resistance and metabolic disorders, suggesting context-dependent functions.
Dysregulation of TRIM72 has been implicated in conditions such as muscular dystrophy, myocardial infarction, and diabetes. Antibodies targeting TRIM72 aid in exploring therapeutic strategies, including modulating its activity to enhance tissue repair or mitigate metabolic complications. Recent studies also probe its potential as a biomarker for muscle-related diseases. Despite progress, its regulatory mechanisms and tissue-specific roles remain active research areas, underscoring the continued relevance of TRIM72 antibodies in biomedical research.
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