Mammalian Sly1 regulates syntaxin 5 function in endoplasmic reticulum to Golgi transport
Mammalian Sly1 regulates syntaxin 5 function in endoplasmic reticulum to Golgi transport
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DOI：
10.1074/jbc.271.27.15866
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发表时间：
1996-07-05
影响因子：
4.8
通讯作者：
Balch, WE
中科院分区：
文献类型：
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作者：
Dascher, C;Balch, WE
突触融合蛋白基因家族的成员是蛋白质复合物的组分，所述蛋白质复合物在通过真核细胞的分泌途径运输货物期间调节囊泡对接和/或融合。我们先前已经证明突触融合蛋白5是内质网至高尔基体运输所特异性需要的（Dascher，C.，Matteson，J.，Balch，W. E，（1994）J. Biol. Chem，269，29363-29366）。为了扩展这些观察，我们现在已经从大鼠肝膜中克隆了一种蛋白质，它与突触融合蛋白5形成天然复合物。我们证明，这种蛋白质是哺乳动物的同源酵母Sly 1 p，以前确定为一种蛋白质的遗传和生物化学相互作用的小GTALYpt 1 p和Sed 5 p，蛋白质参与对接/融合在酵母的早期分泌途径。使用瞬时表达，我们发现，大鼠肝脏Sly 1（rSly 1）的过度表达可以中和显性的负面影响过剩syntaxin 5对内质网高尔基体运输。这些结果表明，rSly 1的功能，积极调节syntaxin 5的功能。
Members of the syntaxin gene family are components of protein complexes which regulate vesicle docking and/or fusion during transport of cargo through the secretory pathway of eukaryotic cells, We have previously demonstrated that syntaxin 5 is specifically required for endoplasmic reticulum to Golgi transport (Dascher, C., Matteson, J., and Balch, W. E, (1994) J. Biol. Chem, 269, 29363-29366). To extend these observations we have now cloned a protein from rat liver membranes which forms a native complex with syntaxin 5. We demonstrate that this protein is the mammalian homologue to yeast Sly1p, previously identified as a protein which genetically and biochemically interacts with the small GTPase Ypt1p and Sed5p, proteins involved in docking/fusion in the early secretory pathway of yeast. Using transient expression we find that overexpression of rat liver Sly1 (rSly1) can neutralize the dominant negative effects of excess syntaxin 5 on endoplasmic reticulum to Golgi transport. These results suggest that rSly1 functions to positively regulate syntaxin 5 function.