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首页> 美国卫生研究院文献>Biochemical Journal >The size of the intracellular beta 1-integrin precursor pool regulates maturation of beta 1-integrin subunit and associated alpha-subunits.
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The size of the intracellular beta 1-integrin precursor pool regulates maturation of beta 1-integrin subunit and associated alpha-subunits.

机译：细胞内β1整合素前体池的大小调节β1整合素亚基和相关的α亚基的成熟。

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A large pool of precursor beta 1-integrin subunits is frequently found intracellularly. During malignant transformation this pool often disappears. Concomitantly, integrin-mediated cell-adhesion functions are disturbed, even though no change in the number of beta 1-integrin receptors on the cell surface can be observed. Here, we have studied the role of an intracellular pre-beta 1-integrin pool by transfecting human MG-63 osteosarcoma cells with plasmid construction producing an antisense RNA for the beta 1-integrin subunit. Stable cell clones expressing beta 1-integrin antisense RNA were shown to have a reduced intracellular pool of pre-beta 1-integrin subunits. In the antisense-transfected cells, the synthesis of the beta 1-integrin chain was reduced by 65% compared with non-transfected or vector-transfected MG-63 cells. The decreased synthesis of the beta 1-integrin chain was associated with accelerated maturation of the beta 1-integrin chain (half-maturation time about 5 h in antisense-transfected cells compared with about 10.5 h in control cells), whereas maturation of the alpha-integrin chain slowed down. The amount of beta 1-integrins on the cell surface, however, remained unaltered. Cell clones with the largest decrease in the relative amount of the pre-beta 1-integrin subunit also showed altered integrin function. They were found to synthesize fibronectin, but were unable to assemble it into a fibronectin matrix on the cell surface. Thus we conclude that the repression of biosynthesis of the beta 1-integrin chain leads to alterations in receptor maturation and may be connected with altered receptor function.
机译：通常在细胞内发现大量的前体β1-整合素亚基。在恶性转化期间，该库经常消失。伴随地，即使没有观察到细胞表面上β1-整合素受体数目的变化，整合素介导的细胞粘附功能也受到干扰。在这里，我们已经研究了转染人MG-63骨肉瘤细胞的质粒内结构，产生了针对β1-整合素亚基的反义RNA，从而研究了细胞内β1-整合素池的作用。表达β1-整合素反义RNA的稳定细胞克隆显示减少的β-1整合素亚基的细胞内池。与未转染或载体转染的MG-63细胞相比，在反义转染的细胞中，β1-整合素链的合成减少了65％。 β1-整合素链的合成减少与β1-整合素链的加速成熟有关（反义转染细胞的半成熟时间约为5小时，而对照细胞为10.5 h）。 -整联蛋白链变慢。然而，细胞表面上的β1-整联蛋白的量保持不变。前β1-整合素亚基相对量减少最大的细胞克隆也显示整合素功能改变。发现它们合成纤连蛋白，但无法将其组装成细胞表面的纤连蛋白基质。因此，我们得出结论，β1整合素链的生物合成的抑制导致受体成熟的改变，并且可能与受体功能的改变有关。

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