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Blood：揭秘Xga血型！XG/PBDX上游GATA1结合模体可控制Xg（a-）表型

2018-05-13 MedSci MedSci原创

Xg血型GATA1
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中心点：Xg血型蛋白的表达受rs311103调控，其次要等位基因可破坏GATA模体导致Xg（a-）表型。摘要：Xga血型在男、女性红细胞中表达存在差异性。基础基因——PBDX——早在1994年就被发现，但其调控Xga表达的分子机制尚未明确。该基因，现被命名为XG，部分位于伪常染色体1区上，编码X染色体上的一个功能未知的蛋白。通过对比Xga等位基因在不同人群中的频率和XG区域的2612个基因突变发现

中心点：

Xg血型蛋白的表达受rs311103调控，其次要等位基因可破坏GATA模体导致Xg（a-）表型。

摘要：

Xga血型在男、女性红细胞中表达存在差异性。基础基因——PBDX——早在1994年就被发现，但其调控Xga表达的分子机制尚未明确。该基因，现被命名为XG，部分位于伪常染色体1区上，编码X染色体上的一个功能未知的蛋白。

通过对比Xga等位基因在不同人群中的频率和XG区域的2612个基因突变发现，rs311103与预期分布的相关性最强。相同的SNP对全血的XG转录水平影响最显着（p=2.0x10[-22]）。RS311103C等位基因可破坏转录起始点上游3.7kb处的GATA结合模体。沉默红细胞的XG-mRNA的表达，可导致Xg（a-）表型，该结果与119位献血者的SNP分型一致。

通过EMSA可检测到rs311103G的生物素寡核苷酸探针可与GATA1结合，而rs311103C的探针则不能，并通过质朴分析得以证实。

研究人员用荧光素酶报告基因实验发现在HRL细胞中，GATA模体对rs311101G位点较活跃，而对rs311103C则无反应。最后，通过综合性生物信息和分子生物学方法，研究人员阐明了最后一个尚未解决的血型系统的潜在遗传机制，使得Xga分型成为可能。

原始出处：

Mattias Meller，et al.Disruption of a GATA1-binding motif upstream of XG/PBDX abolishes Xga expression and resolves the Xg blood group system.Blood  2018  ：blood-2018-03-842542；  doi： https：//doi.org/10.1182/blood-2018-03-842542

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    2018-05-15 bbjsj_1981

    #ATA#

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    2018-05-15 tastas

    #表型#

    0

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    2018-05-13 1ddf0692m34(暂无匿称)

    学习了.长知识

    0

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    2018-05-13 1e0f8808m18(暂无匿称)

    学习了.谢谢分享.

    0