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唾液黏蛋白对颊黏膜钙通道活性的调节作用。

Salivary mucin modulation of buccal mucosal calcium channel activity.

作者信息

Slomiany B L, Fekete Z, Piotrowski J, Murty V L, Slomiany A

机构信息

Research Center, New Jersey Dental School, University of Medicine and Dentistry of New Jersey, Newark 07103-2400.

出版信息

Biochem Mol Biol Int. 1993 Feb;29(2):221-31.

PMID:8388291
Abstract

The effect of the low and high molecular weight salivary mucins on the activity of calcium channel isolated from buccal epithelial cell membranes was investigated. The 45Ca2+ uptake into the vesicle-reconstituted channels, while only moderately (15%) affected by the intact mucin forms, was significantly inhibited (60%) by the acidic mucin fractions. This effect was associated with the sialic acid and sulfate ester groups of the glycoproteins. The channel complex in the presence of epidermal growth factor (EGF) and ATP responded by an increase in protein tyrosine phosphorylation, and the vesicles containing the phosphorylated channels showed a 46% increase in 45Ca2+ uptake. The phosphorylation process was inhibited by the acidic mucins, which also interfered with the binding of EGF to the channel protein. The inhibitory effect was dependent upon the presence of sulfate ester and sialic acid groups, and the loss of the inhibitory capacity occurred following their removal. The results demonstrate the salivary mucins actively participate in the modulation of buccal mucosal calcium channel activity.

摘要

研究了低分子量和高分子量唾液粘蛋白对从颊上皮细胞膜分离的钙通道活性的影响。45Ca2+进入囊泡重组通道的过程,虽然完整的粘蛋白形式仅产生中度影响(15%),但酸性粘蛋白组分可显著抑制(60%)该过程。这种作用与糖蛋白的唾液酸和硫酸酯基团有关。在表皮生长因子(EGF)和ATP存在的情况下,通道复合物的蛋白质酪氨酸磷酸化增加,含有磷酸化通道的囊泡中45Ca2+摄取增加了46%。酸性粘蛋白抑制了磷酸化过程,同时也干扰了EGF与通道蛋白的结合。抑制作用取决于硫酸酯和唾液酸基团的存在,去除这些基团后抑制能力丧失。结果表明唾液粘蛋白积极参与颊黏膜钙通道活性的调节。

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