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相关概念视频

mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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相关实验视频

Updated: Jun 2, 2025

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
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通过调节的miR-199b-3p,TSC复合物降低了mTOR的表达.

Na Zhao1,2, Qiuhong Xiong1, Ping Li1

  • 1Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Institutes of Biomedical Sciences, Shanxi University, Taiyuan, 030006, China.

Scientific reports
|January 13, 2025
PubMed
概括
此摘要是机器生成的。

在TSC1或TSC2的遗传变异破坏TSC复合体,导致结核性硬化复合体 (TSC) 疾病. 这项研究确定了miR-199b-3p作为TSC中的mTOR信号传递的新型调节者.

关键词:
在 MTOR 中,我们可以使用 MTOR.在 MiR-199b-3p 中使用.这就是TSC的特点.这就是TSC1的特点.这就是TSC2的特点.

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科学领域:

  • 分子生物学分子生物学
  • 遗传学 遗传学 是一个
  • 细胞信号传输 细胞信号传输

背景情况:

  • 结核性硬化综合体 (TSC) 是一种罕见的遗传疾病,由TSC1或TSC2基因突变引起.
  • TSC复合体 (TSC1/TSC2) 是拉巴胺复合体1 (mTORC1) 的机械性标的关键负调节器.
  • mTOR信号的失调与各种疾病有关,包括TSC.

研究的目的:

  • 研究TSC1和TSC2.2新型遗传变异引起的TSC背后的分子机制.
  • 探索微RNA-199b-3p (miR-199b-3p) 在TSC病原和mTOR信号传递中的作用.
  • 确定TSC的潜在治疗点.

主要方法:

  • 对TSC患者进行基因分析,以确定TSC1和TSC2的变异.
  • 细胞测试以评估已识别的突变对TSC复合体形成和稳定性的影响.
  • 定量实时PCR (qRT-PCR) 用于测量miR-199b-3p表达水平.
  • 西方涂抹用于评估mtor,mtorc1和mtorc2.2的表达和激活.

主要成果:

  • 发现了一种新的TSC2变异 (c.1113delG,p.Q371fs) 与报告的TSC1变异 (c.2509_2512del,p.N837fs) 一起.
  • 观察到TSC复合体形成的减少与受影响细胞中miR-199b-3p表达的减少相关.
  • 证明减少miR-199b-3p表达导致mtOR表达和mtORC1和mtORC2.2.激活的增加.
  • 表明补充miR-199b-3p可以逆转mtor表达和mtorc1/mtorc2激活的增加.

结论:

  • 在TSC1或TSC2的遗传变异破坏TSC复合体的形成,导致TSC疾病.
  • miR-199b-3p在调节mTOR信号通路方面发挥着至关重要的作用.
  • miR-199b-3p代表了管理TSC和相关疾病的潜在治疗标.