Cause and Consequence
Cause and Consequence
复制标题
原因和后果
DOI：
10.1126/stke.2001.78.tw9
复制
发表时间：
2001
期刊：
影响因子：
--
通讯作者：
F. Zhou
中科院分区：
文献类型：
--
作者：
Lin Zhang;Gargey Yagnik;Yong Peng;Jianxiu Wang;H. H. Xu;Yuanqiang Hao;You;F. Zhou
Belden和Barlowe发现，酵母缺乏通过分泌途径运输货物的p24蛋白家族，也分泌酵母内质网（ER）伴侣蛋白Kar2p（在哺乳动物中称为BiP）。p24的缺失，识别具有HDEL一致序列的管腔蛋白的ER检索受体的缺失，或Kar2p的过表达激活了未折叠蛋白反应（UPR）。此外，所有激活UPR的条件也引起Kar2p的分泌，这表明常驻ER蛋白的分泌是UPR的一个指标。UPR的激活可能会上调常驻内质网蛋白的表达，使其恢复和保留机制饱和，导致过量上调蛋白的分泌，通过分泌途径参与运输的蛋白受到干扰会激活UPR。W. J. Belden， C. Barlowe，酵母p24基因缺失激活未折叠蛋白反应。摩尔。杂志。Cell 12, 957-969（2001）。【摘要】【全文】
Belden and Barlowe found that yeast deficient for the family of p24 proteins involved in trafficking cargo through the secretory pathway also secreted the yeast endoplasmic reticulum (ER) chaperone Kar2p (known as BiP in mammals). Loss of p24, loss of the ER retrieval receptor that recognizes luminal proteins with the HDEL consensus sequence, or overexpression of Kar2p activated the unfolded protein response (UPR). Furthermore, all conditions that activated the UPR also caused the secretion of Kar2p, suggesting that secretion of resident ER proteins is an indicator of the UPR. Activation of the UPR may up-regulate the expression of resident ER proteins to a point that saturates that retrieval and retention machinery, leading to the secretion of the excess up-regulated proteins, and interference with proteins involved in trafficking through the secretory pathway activates UPR. W. J. Belden, C. Barlowe, Deletion of yeast p24 genes activates the unfolded protein response. Mol. Biol. Cell 12, 957-969 (2001). [Abstract] [Full Text]