High molecular weight factor in FCS inhibits Helicobacter pylori VacA-binding to its receptor, RPTPbeta, on AZ-521.
High molecular weight factor in FCS inhibits Helicobacter pylori VacA-binding to its receptor, RPTPbeta, on AZ-521.
复制标题
FCS 中的高分子量因子可抑制幽门螺杆菌 VacA 与其 AZ-521 上的受体 RPTPbeta 的结合。
DOI：
10.1111/j.1348-0421.2003.tb02792.x
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发表时间：
2003
影响因子：
2.6
通讯作者：
Hirayama,Toshiya
中科院分区：
文献类型：
--
作者：
Kimura,Takahiro;Wada,Akihiro;Nakayama,Masaaki;Ogushi,Ken-ichi;Nishi,Yoshito;DeGuzman,BlanquitaB;Moss,Joel;Hirayama,Toshiya
VacA是幽门螺杆菌的一种分泌产物，与其细胞表面受体酪氨酸磷酸酶β结合，导致胃上皮细胞AZ-521细胞胞浆空泡化。含胎牛血清(FCS)的细胞培养液可抑制VacA与细胞表面的结合和VacA依赖的空泡化。经Superose 12凝胶过滤层析分离得到的高相对分子质量组分对VacA结合有抑制作用，而对其他组分的抑制作用较弱。这些数据表明，高相对分子质量的FCS通过阻断AZ-521细胞上毒素与其受体RPTPβ的结合而抑制VacA的作用。
VacA, a secretory product ofHelicobacter pylori, binds to its cell surface receptor, receptor tyrosine phosphatase (RPTP) β, leading to cytoplasmic vacuolization of gastric epithelial AZ‐521 cells. VacA binding to the cell surface and VacA‐dependent vacuolization were inhibited by cell culture media containing fetal calf serum (FCS). The high molecular weight fraction of FCS isolated by Superose 12 gel filtration chromatography inhibited VacA binding, whereas only weak effects were observed with other fractions. These data show that the high molecular weight fraction of FCS inhibits VacA action though its ability to block toxin binding to its receptor, RPTPβ, on AZ‐521 cells.