Muresan Z, Arvan P
Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, Massachusetts 02215, USA.
J Biol Chem. 1997 Oct 17;272(42):26095-102. doi: 10.1074/jbc.272.42.26095.
GRP94 serves as a molecular chaperone in the endoplasmic reticulum (ER). In normal thyrocytes, GRP94 interacts transiently with thyroglobulin (Tg), and in thyrocytes of animals suffering from congenital hypothyroid goiter with defective thyroglobulin, GRP94 and thyroglobulin associate in a protracted fashion. In order explore possible consequences of GRP94 binding, we have studied recombinant nonmutant thyroglobulin expressed in control Chinese hamster ovary (CHO) cells in comparison to that produced in CHO cells genetically manipulated for selectively increased GRP94 expression. Levels of ER chaperones other than GRP94 did not detectably differ, and thyroglobulin achieved transport competence in both kinds of CHO cells. However, increased availability of GRP94 caused the residence time of Tg in the ER to be remarkably prolonged. This was accompanied by a major increase in Tg directly associated with GRP94 and an increase in the ER pool size of Tg. Importantly, co-immunoprecipitation analysis revealed disulfide-linked Tg complexes (previously reported as an early Tg-folding intermediate) especially associated with GRP94. Indeed, non-native Tg, GRP94, and a 78-kDa protein likely to be BiP, appeared in ternary complexes. Under these conditions, GRP94 association appears directly involved in prolongation of Tg folding and export, consistent with a role in quality control in the ER.
GRP94作为内质网(ER)中的分子伴侣。在正常甲状腺细胞中,GRP94与甲状腺球蛋白(Tg)短暂相互作用,而在患有先天性甲状腺功能减退性甲状腺肿且甲状腺球蛋白有缺陷的动物的甲状腺细胞中,GRP94和甲状腺球蛋白以持久的方式结合。为了探究GRP94结合可能产生的后果,我们研究了在对照中国仓鼠卵巢(CHO)细胞中表达的重组非突变甲状腺球蛋白,并将其与在经过基因操作以选择性增加GRP94表达的CHO细胞中产生的甲状腺球蛋白进行比较。除GRP94外的内质网伴侣蛋白水平没有明显差异,并且甲状腺球蛋白在两种CHO细胞中都获得了转运能力。然而,GRP94可用性的增加导致Tg在内质网中的停留时间显著延长。这伴随着与GRP94直接相关的Tg大量增加以及内质网中Tg池大小的增加。重要的是,免疫共沉淀分析揭示了特别是与GRP94相关的二硫键连接的Tg复合物(先前报道为早期Tg折叠中间体)。实际上,非天然Tg、GRP94和一种可能是BiP的78 kDa蛋白出现在三元复合物中。在这些条件下,GRP94的结合似乎直接参与了Tg折叠和输出的延长,这与内质网质量控制中的作用一致。