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细胞ATP水平的耗尽会阻止蛋白质从GRP78上解离以及分泌。

Protein dissociation from GRP78 and secretion are blocked by depletion of cellular ATP levels.

作者信息

Dorner A J, Wasley L C, Kaufman R J

机构信息

Genetics Institute, Cambridge, MA 02140.

出版信息

Proc Natl Acad Sci U S A. 1990 Oct;87(19):7429-32. doi: 10.1073/pnas.87.19.7429.

Abstract

Secretory proteins expressed in Chinese hamster ovary (CHO) cells interact to various degrees with glucose-regulated protein 78 (GRP78), a resident protein of the endoplasmic reticulum. von Willebrand factor (vWF) and wild-type tissue plasminogen activator (tPA) are efficiently secreted and exhibit a slight transient association with GRP78. Factor VIII and unglycosylated tPA are inefficiently secreted and display a more stable association with GRP78. We have studied the effect of ATP depletion mediated by carbonyl cyanide 3-chlorophenylhydrazone (CCCP) treatment on GRP78 association and secretion of factor VIII and vWF that are coexpressed in CHO cells. Low concentrations of CCCP in the medium prevented disassociation of factor VIII from GRP78 and blocked its secretion. In the same cells, higher concentrations of CCCP were required to block secretion of vWF. Thus, the block to factor VIII secretion at low CCCP concentrations did not result from a general defect in secretion. Secretion of unglycosylated tPA but not wild-type tPA from CHO cells was also blocked by low concentrations of CCCP. The increased sensitivity to CCCP concentration observed for secretion of factor VIII and unglycosylated tPA compared to wild-type tPA and vWF correlates with their degree of interaction with GRP78. In vivo, dissociation from GRP78 may be a primary ATP-dependent step in transport from the endoplasmic reticulum. ATP requirements for secretion of various proteins may vary.

摘要

在中国仓鼠卵巢(CHO)细胞中表达的分泌蛋白与葡萄糖调节蛋白78(GRP78)存在不同程度的相互作用,GRP78是内质网的一种驻留蛋白。血管性血友病因子(vWF)和野生型组织纤溶酶原激活剂(tPA)能有效分泌,并与GRP78呈现轻微的瞬时结合。凝血因子VIII和未糖基化的tPA分泌效率低下,并与GRP78表现出更稳定的结合。我们研究了用羰基氰3-氯苯腙(CCCP)处理介导的ATP耗竭对CHO细胞中共表达的凝血因子VIII和vWF的GRP78结合及分泌的影响。培养基中低浓度的CCCP可阻止凝血因子VIII与GRP78解离并阻断其分泌。在相同细胞中,需要更高浓度的CCCP才能阻断vWF的分泌。因此,低浓度CCCP时凝血因子VIII分泌受阻并非源于普遍的分泌缺陷。低浓度的CCCP也会阻断CHO细胞中未糖基化tPA的分泌,但不会阻断野生型tPA的分泌。与野生型tPA和vWF相比,凝血因子VIII和未糖基化tPA分泌对CCCP浓度的敏感性增加,这与其与GRP78的相互作用程度相关。在体内,从GRP78解离可能是内质网转运过程中主要的ATP依赖步骤。不同蛋白质分泌所需的ATP可能不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d23/54760/7ba48d51338d/pnas01044-0093-a.jpg

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