cTAGE5 acts as a Sar1 GTPase regulator for collagen export
cTAGE5 acts as a Sar1 GTPase regulator for collagen export
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DOI：
10.1101/452904
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发表时间：
2018-10
期刊：
影响因子：
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通讯作者：
N. Sasaki;Masano Shiraiwa;Miharu Maeda;Tomohiro Yorimitsu;Ken Sato;T. Katada;Kota Saito
中科院分区：
文献类型：
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作者：
N. Sasaki;Masano Shiraiwa;Miharu Maeda;Tomohiro Yorimitsu;Ken Sato;T. Katada;Kota Saito
在内质网（ER）内合成的分泌蛋白通过外壳蛋白复合物II（COPII）包被的囊泡输出。COPII包被囊泡的形成是由小GTdR，Sar1的激活启动的。cTAGE 5直接与鸟嘌呤核苷酸交换因子（GEF）Sec12和GTP酶激活蛋白（GAP）Sar 1 Sec23相互作用。我们先前已经证明，cTAGE5招募Sec12到ER出口位点，以有效产生活化的Sar1，用于胶原蛋白分泌。然而，cTAGE 5和Sec23之间相互作用的功能意义尚未完全阐明。在这项研究中，我们发现cTAGE 5增强了Sec23对Sar1差距活性。此外，cTAGE 5与Sec23的相互作用对于胶原从ER退出是必需的。我们的数据表明，cTAGE 5作为一个胶原分泌的Sar1 GTP酶调节剂。
Secretory proteins synthesized within the endoplasmic reticulum (ER) are exported via coat protein complex II (COPII)-coated vesicles. The formation of the COPII-coated vesicles is initiated by activation of the small GTPase, Sar1. cTAGE5 directly interacts with a guanine-nucleotide exchange factor (GEF), Sec12, and a GTPase-activating protein (GAP) of Sar1, Sec23. We have previously shown that cTAGE5 recruits Sec12 to the ER exit sites for efficient production of activated Sar1 for collagen secretion. However, the functional significance of the interaction between cTAGE5 and Sec23 has not been fully elucidated. In this study, we showed that cTAGE5 enhances the GAP activity of Sec23 toward Sar1. In addition, the interaction of cTAGE5 with Sec23 is necessary for collagen exit from the ER. Our data suggests that cTAGE5 acts as a Sar1 GTPase regulator for collagen secretion.