Scaffolding protein GOPC regulates tight junction structure.
Scaffolding protein GOPC regulates tight junction structure.
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DOI：
10.1007/s00441-014-2088-1
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发表时间：
2015-05
影响因子：
3.6
通讯作者：
Wilson, Jean M.
中科院分区：
文献类型：
--
作者：
Lu, Ruifeng;Stewart, Lorraine;Wilson, Jean M.
GOPC（FIG/PIST/CAL）是一种PDZ结构域支架蛋白，可调节多种蛋白质的运输，包括小GTP酶、受体和细胞表面分子，如钙粘蛋白23和CFTR。在Madin-Darby犬肾（MDCK）细胞中，我们发现GOPC定位于反式高尔基体网络（TGN），而不是顺式或反式高尔基体池。也有共定位与早期内体Rab GTNAR Rab 5和TGN/内体标记Rab 14，但不与Rab 11，再循环内体的标记。GOPC不定位于侧膜或紧密连接。我们发现MDCK细胞中GOPC的敲低导致跨上皮阻力降低和细胞旁流量增加。这可能是由于来自TGN的紧密连接组分的运输受损，因为GOPC敲低细胞具有减少的紧密连接蛋白claudin-1的侧向标记和减少的claudin-2的蛋白水平。GOPC可能介导新合成的紧密连接蛋白从TGN运输到细胞表面或这些蛋白从专门的内体隔室再循环。
GOPC (FIG/PIST/CAL) is a PDZ-domain scaffolding protein that regulates the trafficking of a wide array of proteins, including small GTPases, receptors, and cell surface molecules such as cadherin 23 and CFTR. In Madin-Darby Canine Kidney (MDCK) cells, we find that GOPC localizes to the Trans-Golgi Network (TGN), but not the cis or trans Golgi cisternae. There is also colocalization with the early endosome Rab GTPase Rab5 and a TGN/endosome marker Rab14, but not with Rab11, a marker of recycling endosomes. There is no localization of GOPC to the lateral membranes or tight junctions. We find that knockdown of GOPC in MDCK cells results in decreased transepithelial resistance and increased paracellular flux. This may be due to compromised trafficking of tight junction components from the TGN, as GOPC knockdown cells have decreased lateral labeling of the tight junction protein claudin-1 and decreased protein levels of claudin-2. GOPC may mediate trafficking of newly synthesized tight junction proteins from the TGN to the cell surface or recycling of these proteins from specialized endosomal compartments.
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