Molecular forms of serum insulin-like growth factor (IGF)-binding proteins in man: relationships with growth hormone and IGFs and physiological significance.

Molecular forms of serum insulin-like growth factor (IGF)-binding proteins in man: relationships with growth hormone and IGFs and physiological significance.
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人类血清胰岛素样生长因子 (IGF) 结合蛋白的分子形式:与生长激素和 IGF 的关系以及生理意义。

DOI:
10.1210/jcem-69-6-1291
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发表时间:
1989
期刊:
The Journal of clinical endocrinology and metabolism
影响因子:
--
通讯作者:
M. Binoux
M. Binoux
中科院分区:
--
文献类型:
--
作者:
Sylvie Hardouin;M. Gourmelen;P. Noguiez;D. Seurin;M. Roghani;Y. Le Bouc;G. Póvoa;T. Merimee;P. Hossenlopp;M. Binoux

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胰岛素样生长因子-I(IGF-I)和IGF-II在血液中与特异性结合蛋白(BP)结合,形成复合物,其在凝胶过滤中聚集,估计分子量约为40和150 kD。后者似乎在GH控制之下。使用125 I标记的IGF通过Western印迹法鉴定了BP的五种分子形式(41.5、38.5、34、30和24 kD)。所有五种形式都存在于较小的复合物中,但只有41.5和38.5 kD的形式存在于较大的复合物中。在这项研究中,免疫印迹显示,41.5-和38.5-kD的形式被识别的抗体直接对GH依赖的BP纯化从人血浆中,和30-kD的形式被识别的抗体直接对BP纯化从羊水中。34-和24-kD形式被证明是免疫无关的其他三个。在含有大量41.5-和38.5-kD形式的血清中,经常在30 kD条带的迁移前沿之前立即观察到额外的条带。这被抗GH依赖性BP抗体识别,可能对应于41.5和38.5 kD BP的降解产物。已发现血清41.5-和38.5-kD BP在肢端肥大症中升高,其中GH分泌过多导致IGF-I水平升高,并且在遗传性或特发性GH缺乏和GH受体缺陷(Laron综合征)的情况下降低,其中IGF-I和IGF-II均降低,以及在患有孤立性IGF-I缺乏症的侏儒成人和儿童中降低。在所有这些条件下,34和30 kD形式的比例与41.5和38.5形式的比例呈负相关。在治疗期间,血压曲线趋于恢复正常。在由肿瘤引起的GH缺乏症的情况下,BP曲线类似于低血糖或正常血清的BP曲线,这取决于IGF水平是否降低或正常。因此,BP的合成似乎与IGF-I的合成相协调,可能不直接依赖GH。中性pH凝胶过滤分析的结果hypopopolysis(特发性和肿瘤)和正常血清点循环IGFs和150 kD IGF-BP复合物的结合单位是41.5-和38.5-kD BP的水平之间的关系。因此,似乎150-kD复合物控制IGF-I和IGF-II的生物利用度。(400字处截断摘要)
Insulin-like growth factor-I (IGF-I) and IGF-II are associated in the blood with specific binding proteins (BPs), forming complexes that elute in gel filtration with estimated mol wt around 40 and 150 kD. The latter appears to be under GH control. Five molecular forms of BP (41.5, 38.5, 34, 30, and 24 kD) have been identified by Western blotting using 125I-labeled IGF. All five forms are present in the smaller complexes, but only the 41.5- and 38.5-kD forms are found in the larger complexes. In this study immunoblotting showed that the 41.5- and 38.5-kD forms were recognized by antibodies directed against the GH-dependent BP purified from human plasma, and the 30-kD form was recognized by antibodies directed against the BP purified from amniotic fluid. The 34- and 24-kD forms proved to be immunologically unrelated to the other three. In sera with large quantities of the 41.5- and 38.5-kD forms, an additional band was often observed immediately ahead of the migration front of the 30 kD band. This was recognized by the anti-GH-dependent BP antibody and probably corresponds to a degradation product of the 41.5- and 38.5-kD BPs. Serum 41.5- and 38.5-kD BPs have been found to be elevated in acromegaly, where GH hypersecretion causes increased IGF-I levels, and diminished in cases of genetic or idiopathic GH deficiency and defects of the GH receptor (Laron's syndrome), where both IGF-I and IGF-II are decreased, as well as in Pygmy adults and children who have isolated IGF-I deficiency. In all of these conditions, the proportions of the 34- and 30-kD forms were inversely related to those of the 41.5- and 38.5-forms. Under treatment, the BP profiles tended to return to normal. In cases of GH deficiency caused by a tumor, the BP profiles resembled those of hypopituitary or normal serum, depending on whether IGF levels were diminished or normal. It, therefore, seems that BP synthesis is coordinated with IGF-I synthesis and may not be directly GH dependent. The results of neutral pH gel filtration analysis of hypopituitary (idiopathic and tumoral) and normal sera point to a relationship between the levels of circulating IGFs and those of the 150-kD IGF-BP complex whose binding units are the 41.5- and 38.5-kD BPs. It, therefore, seems that the 150-kD complex controls the bioavailability of IGF-I and IGF-II.(ABSTRACT TRUNCATED AT 400 WORDS)
垂体功能减退症中的血浆生长调节素结合蛋白:生长激素治疗期间的变化。
DOI: 10.1210/jcem-53-1-100
发表时间: 1981
期刊: The Journal of clinical endocrinology and metabolism
影响因子: --
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Hintz,RL;Liu,F;Rosenfeld,RG;Kemp,SF
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DOI: 10.1056/nejm198704093161503
发表时间: 1987
期刊: The New England journal of medicine
影响因子: --
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来自人血浆的哇巴因结合蛋白。
DOI: 10.1161/01.hyp.0000027134.14160.1d
发表时间: 2002
期刊: Hypertension (Dallas, Tex. : 1979)
影响因子: --
作者:
Parhami-Seren,Behnaz;Haberly,Richard;Margolies,MichaelN;HaupertJr,GarnerT
通讯作者: HaupertJr,GarnerT
来自人 HEP G2 肝癌细胞的胰岛素样生长因子 (IGF) 结合蛋白互补脱氧核糖核酸:预测的蛋白质序列表明 IGF 结合域不同于 IGF-I 和 IGF-II 受体的结合域。
DOI: 10.1210/mend-2-5-404
发表时间: 1988
期刊: Molecular endocrinology (Baltimore, Md.)
影响因子: --
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