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首页> 外文期刊>Life sciences >VHL gene methylation contributes to excessive erythrocytosis in chronic mountain sickness rat model by upregulating the HIF-2 alpha/EPO pathway
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VHL gene methylation contributes to excessive erythrocytosis in chronic mountain sickness rat model by upregulating the HIF-2 alpha/EPO pathway

机译:VHL基因甲基化通过上调HIF-2α/ EPO途径有助于慢性山病大鼠模型中过度的红细胞增多

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Aims: Hypoxia-inducible factors (HIFs) play important roles in the pathogenesis of erythrocytosis in chronic mountain sickness (CMS). von Hippel-Lindau (VHL) is a key regulator of hypoxia that can direct the polyubiquitylation and degradation of HIFs. Epigenetic mechanisms are believed to contribute toward adaption to chronic hypoxia. Here, we investigated the contribution and mechanism of VHL methylation in rats with erythrocytosis in CMS.
机译:目的:缺氧诱导因子(HIF)在慢性高原病(CMS)红细胞增多症的发病机制中起重要作用。von Hippel-Lindau(VHL)是缺氧的关键调节因子,可指导HIF的多泛素化和降解。表观遗传学机制被认为有助于适应慢性缺氧。在这里,我们研究了CMS中红细胞增多症大鼠VHL甲基化的贡献和机制。

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