Peters plus syndrome mutations disrupt a noncanonical ER quality-control mechanism.

Deepika Vasudevan,Hideyuki Takeuchi,Sumreet Singh Johar,Elaine Majerus,Robert S Haltiwanger

Current Biology（2015）

引用 86|浏览21

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摘要

•B3GLCT is required for the secretion of only a subset of POFUT2 targets•O-fucosylation is cotranslational•Addition of fucose and glucose stabilizes properly folded TSRs in the ER•POFUT2 and B3GLCT define a noncanonical ER quality-control mechanism for TSRs

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关键词

syndrome mutations,quality-control

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