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通过雌激素调节小鼠kallikrein 1基因表达的一个调节机制

Takumi Iwasaki¹, Megumi Tokumori¹, Misaki Matsubara¹

¹Graduate School of Natural Science and Technology, Okayama University, Okayama, 700-8530, Japan.

Molecular and cellular endocrinology

|August 14, 2023

概括

雌激素通过与特定的AP-1位点结合来调节小鼠子宫中的组织kallikrein 1 (Klk1). 这种由雌激素受体α (ERα) 介导的结合激活了Klk1基因表达.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

组织kallikrein 1 (Klk1) 是一种胺蛋白酶,参与降解细胞外基质和胰岛素样生长因子结合蛋白-3.
已知雌激素,特别是雌激醇-17β (E2),可在小鼠子宫中增加Klk1mRNA的表达.

研究的目的:

阐明雌激素控制小鼠子宫Klk1表达的调节机制.
确定参与雌激素介导的Klk1调节的特定DNA区域和转录因子.

主要方法:

对Klk1 5'-边缘区域的促体分析,以确定最小和雌激素反应的元素.
位点定向突变发生,以调查假定AP-1位点的作用.
染色体免疫沉降 (ChIP) 试验检测雌激素受体α (ERα) 结合.

主要成果:

克尔克1的最小促进物定位在-136/+24区域,在-433/-136.0之间确定了一个对雌激素敏感的区域.
塔莫西芬治疗增加了Klk1mRNA和促进剂活性,涉及AP-1位点.
在-433/-136区域内的两个假定AP-1位点的突变发生证明了它们对Klk1调节的必要性.
ChIP测定证实了ERα与-433/-136区域的结合.

结论:

雌激素受体α (ERα) 直接与Klk1促进体的调节区域中的两个特定的AP-1位点结合.
结合这些AP-1位点的ERα导致小鼠子宫中Klk1基因表达的交换激活.

关键词:

雌二醇是雌二醇的一种.雌激素受体的受体是什么卡利克莱因 1 卡利克莱因 1 在子宫,子宫.

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