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首页> 外文期刊>Molecular and Cellular Biology >Inhibition of phorbol ester-receptor binding by a factor from human serum.
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Inhibition of phorbol ester-receptor binding by a factor from human serum.

机译：来自人血清的一种因子抑制佛波醇酯-受体结合。

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The inhibition of receptor binding of [3H]phorbol-12,13-dibutyrate (PDBu) by a factor from human serum was characterized. The serum factor inhibited [3H]PDBu binding in intact monolayer cultures of the rat embryo cell line CREF N and in a subcellular system containing membranes from these cells. Inhibition occurred at both 37 and 4 degrees C and was rapid and reversible. An analysis of [3H]PDBu binding in the presence of the serum factor indicated that inhibition of [3H]PDBu binding by the serum factor was noncompetitive. Using gel filtration to separate the serum factor from free [3H]PDBu, we obtained evidence that the serum factor does not act by binding or trapping the [3H]PDBu. Unlike the phorbol ester tumor promoters, the serum factor alone did not stimulate the release of choline or arachidonic acid from cellular phospholipids, nor did it inhibit the binding of 125I-labeled epidermal growth factor to cellular receptors. The factor did, however, antagonize the inhibition of epidermal growth factor binding induced by PDBu. Sera from pregnant women were, in general, more inhibitory of [3H]PDBu binding than were those from nonpregnant women, which were more inhibitory than those from men. During these studies we found that CREF N cells responded to being grown in the presence of PDBu by partial down regulation of the phorboid receptor. The 50% effective dose for down regulation was 8 nM PDBu, and the maximum effect occurred after 6 h. Taken together, our results indicate that the serum factor inhibits [3H]PDBu binding by a direct physical effect at the level of the phorboid receptors or their associated membranes. It would appear that if this factor acts in vivo, then it might antagonize certain effects of this class of tumor promoters.
机译：表征了人血清中某因子对[3H] phorbol-12,13-dibutyrate（PDBu）受体结合的抑制作用。在大鼠胚胎细胞系CREF N的完整单层培养物中以及在包含来自这些细胞膜的亚细胞系统中，血清因子抑制[3H] PDBu结合。抑制作用发生在37和4摄氏度，并且迅速且可逆。在血清因子存在下对[3H] PDBu结合的分析表明，血清因子对[3H] PDBu结合的抑制是非竞争性的。使用凝胶过滤将血清因子与游离的[3H] PDBu分离，我们获得了证据表明血清因子不通过结合或捕获[3H] PDBu而起作用。与佛波酯肿瘤启动子不同，仅血清因子不会刺激胆碱或花生四烯酸从细胞磷脂中释放，也不会抑制125I标记的表皮生长因子与细胞受体的结合。然而，该因子确实拮抗了PDBu诱导的表皮生长因子结合的抑制。通常，孕妇的血清对[3H] PDBu结合的抑制作用要比未怀孕的妇女的抑制作用强，而未怀孕的妇女的抑制作用要强于男性。在这些研究中，我们发现CREF N细胞通过局部下调类脉管受体来响应在PDBu存在下的生长。下调的50％有效剂量为8 nM PDBu，最大作用发生在6小时后。两者合计，我们的结果表明，血清因子通过直接物理作用在类蝶形受体或其相关膜的水平上抑制[3H] PDBu结合。看来，如果该因子在体内起作用，那么它可能拮抗这类肿瘤启动子的某些作用。

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