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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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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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相关实验视频

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The Soft Agar Colony Formation Assay
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通过抑制非正规的Wnt信号,K-Ras促进瘤性

Man-Tzu Wang1, Matthew Holderfield1, Jacqueline Galeas1

  • 1Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, 1450 3(rd) Street, San Francisco, CA 94158, USA.

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概括

与H-Ras不同的是,瘤性K-Ras通过结合calmodulin来抑制非正规的Wnt/ Ca2+信号,从而抑制了CaMKii和Fzd8. 针对这种相互作用提供了一种针对K-Ras驱动的新策略.

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科学领域:

  • 分子生物学
  • 癌症学
  • 细胞信号传输

背景情况:

  • K-Ras和H-Ras突变驱动特定的癌症,尽管它们具有共同的作用,但它们具有独特的致癌作用.
  • 非正规的Wnt/ Ca2+信号与瘤发生有关,但其由Ras异型的特定调节尚不清楚.

研究的目的:

  • 研究瘤性K-Ras和H-Ras在非正规Wnt/Ca2+信号中的差异性作用.
  • 阐明K-Ras影响这种途径的分子机制.
  • 确定K-Ras驱动的癌症的潜在治疗点.

主要方法:

  • 研究K-Ras和H-Ras对癌细胞中的Wnt/Ca2+信号的影响.
  • 使用卡尔莫杜林结合测定和CaMKii活性测量.
  • 评估Fzd8表达及其在瘤发生中的作用.
  • 使用基因操纵和前列腺治疗来破坏K-Ras-calmodulin的相互作用.

主要成果:

  • 瘤性K-Ras,但不是H-Ras,可以抑制非正规的Wnt/ Ca2+信号.
  • 通过结合calmodulin来实现这种抑制,从而降低了CaMKii活性和Fzd8表达.
  • 恢复Fzd8抑制的K-Ras突变胰腺癌恶性.
  • 在H-Ras转化细胞中,减少Fzd8增强了瘤发作.
  • 通过基因或前列腺素破坏K-Ras-calmodulin结合,抑制K-Ras突变胰腺癌的生长.

结论:

  • K-Ras 独特地抑制了非正规的 Wnt/ Ca2+ 信号,从而促进了其致癌潜力.
  • 这种K-Ras-calmodulin相互作用是瘤发生的关键媒介.
  • 针对K-Ras-calmodulin相互作用,例如与前列腺素,为"无法治疗"的K-Ras突变癌症提供了一个有希望的治疗策略.