Isoproterenol-mediated parotid gland hypertrophy is inhibited by effectors of 4 beta-galactosyltransferase.
Isoproterenol-mediated parotid gland hypertrophy is inhibited by effectors of 4 beta-galactosyltransferase.
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DOI：
10.1016/s0021-9258(18)60868-3
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发表时间：
1987-08
期刊：
影响因子：
--
通讯作者：
M. Humphreys-Beher;C. Schneyer;V. Kidd;R. Marchase
中科院分区：
文献类型：
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作者：
M. Humphreys-Beher;C. Schneyer;V. Kidd;R. Marchase
长期服用β-肾上腺素能受体激动剂异丙肾上腺素会导致腮腺肥大和增生。最近有报道称，腺体的这种生理变化伴随着酶4β-半乳糖基转移酶的合成和积累速度的急剧增加。在这里，异丙肾上腺素诱导的腮腺肥大被4β-半乳糖基转移酶修饰蛋白α-乳清蛋白和牛4β-半乳糖基转移酶的特异性抗血清所阻断。UDP-半乳糖和竞争性受体糖蛋白卵清蛋白对腺体增大有部分抑制作用。这些药物不影响异丙肾上腺素对富含Pro蛋白的生物合成的诱导，也不影响4β-半乳糖基转移酶的生物合成。这些药物还抑制异丙肾上腺素刺激的腮腺细胞在培养中掺入胸腺嘧啶核苷。
Chronic administration of the beta-adrenergic receptor agonist isoproterenol results in parotid gland hypertrophy and hyperplasia. This physiological change in the gland has recently been reported to be accompanied by a dramatic increase in the rate of synthesis and accumulation of the enzyme 4 beta-galactosyltransferase. Here, isoproterenol-induced hypertrophy of the parotid gland is shown to be blocked by the introduction of the 4 beta-galactosyltransferase modifier protein alpha-lactalbumin and also by specific antiserum to bovine 4 beta-galactosyltransferase. Partial inhibition of gland enlargement was observed stereospecifically with UDP-galactose and with the competitive acceptor glycoprotein, ovalbumin, as well. These agents did not affect the induction by isoproterenol of the biosynthesis of the proline-rich proteins nor of 4 beta-galactosyltransferase. These agents also inhibited the incorporation of thymidine by isoproterenol-stimulated parotid cells in culture.