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相关概念视频

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Reconstitution Of β-catenin Degradation In Xenopus Egg Extract
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CHIP通过DDX17的蛋白体降解来调节结直肠癌中的Wnt/β-catenin信号

Sunny Kumar1, Sayani Ghosh1, Malini Basu2

  • 1Cancer Biology and Inflammatory Disorder Division, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology (CSIR-IICB), TRUE Campus, CN-6, Sector-V, Salt Lake, Kolkata 700091, India; Academy of Scientific and Innovative Research, Ghaziabad 201002, India.

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Hsc70相互作用蛋白 (CHIP) 的C端通过降解DDX17抑制结肠直肠癌,从而抑制Wnt/β-catenin信号传递,扩散和EMT. 这揭示了CHIP-DDX17-β-catenin轴对CRC调节至关重要.

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芯片 (STUB1)大肠直肠癌 (CRC)没有.一个EMTWnt/β-catenin路径

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科学领域:

  • 分子生物学
  • 癌症学
  • 细胞生物学

背景情况:

  • CHIP (Hsc70交互蛋白的C端) 是一个E3无素连接酶,对蛋白质平衡至关重要.
  • DDX17,一个DEAD-boxRNA酶,调节RNA代谢,并参与癌症过程,如Wnt/β-catenin信号传递和EMT.
  • 这些通路的失调与结直肠癌 (CRC) 的发展有关.

研究的目的:

  • 研究CHIP和DDX17在结直肠癌中的新型调控作用.
  • 阐明CHIP和DDX17相互作用并影响Wnt/β-catenin信号的机制.
  • 确定CHIP-DDX17-β-catenin轴作为CRC的潜在治疗点.

主要方法:

  • 对CPTAC数据库的生物信息分析.
  • 临床CRC样本的免疫组织化学分析.
  • 免疫沉质谱和共免疫沉测试以确认蛋白质相互作用.
  • 域映射,免疫细胞化学和分子对接以确定交互界面.
  • 在CHIP调节时评估细胞循环停止,增殖和EMT标记.

主要成果:

  • 在CRC中观察到CHIP和DDX17表达的显著负相关性.
  • DDX17被确定为CHIP的高可信度相互作用伙伴,CHIP的TPR域对于这种相互作用至关重要.
  • CHIP的过度表达加速了DDX17的降解,抑制了Wnt/β-catenin的信号传递,减少了扩散,并抑制了EMT.
  • 导致DDX17稳定,增强了Wnt/β-catenin信号传递,并促进了致癌的表型.

结论:

  • 通过促进DDX17降解,CHIP作为CRC中的瘤抑制剂.
  • 新的CHIP-DDX17-β-catenin轴是结直肠癌的一个关键调节机制.
  • 针对这一轴可能为CRC治疗提供新的治疗策略.