病毒糖蛋白分选缺陷的肝癌细胞变体的糖皮质激素依赖性互补作用

Glucocorticoid-dependent complementation of a hepatoma cell variant defective in viral glycoprotein sorting.

作者信息

John N J, Bravo D A, Haffar O K, Firestone G L

机构信息

Department of Physiology-Anatomy, University of California, Berkeley 94720.

出版信息

Proc Natl Acad Sci U S A. 1988 Feb;85(3):797-801. doi: 10.1073/pnas.85.3.797.

DOI:10.1073/pnas.85.3.797

PMID:2829203

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC279642/

Abstract

We have utilized the rat hepatoma (HTC) cell sorting variant CR4 to examine the glucocorticoid-regulated pathways that localize mouse mammary tumor virus glycoproteins to the cell surface. The defective sorting of cell surface mouse mammary tumor virus glycoproteins in CR4 cells was complemented after fusion with either normal rat hepatocytes or uninfected HTC cells. Indirect immunofluorescence of transient heterokaryons revealed that the regulated localization of mouse mammary tumor virus glycoproteins was dependent upon glucocorticoid treatment and required de novo RNA and protein synthesis. Thus, a glucocorticoid-regulated trafficking activity, unrelated to mouse mammary tumor virus sequences, which is induced in both adult rat liver and cultured hepatoma cells, can act in trans to mediate an intracellular sorting pathway for membrane glycoproteins.

摘要

我们利用大鼠肝癌（HTC）细胞分选变体CR4来研究将小鼠乳腺肿瘤病毒糖蛋白定位到细胞表面的糖皮质激素调节途径。CR4细胞中细胞表面小鼠乳腺肿瘤病毒糖蛋白的分选缺陷在与正常大鼠肝细胞或未感染的HTC细胞融合后得到了弥补。瞬时异核体的间接免疫荧光显示，小鼠乳腺肿瘤病毒糖蛋白的调节定位依赖于糖皮质激素处理，并且需要从头合成RNA和蛋白质。因此，一种与小鼠乳腺肿瘤病毒序列无关的糖皮质激素调节的运输活性，在成年大鼠肝脏和培养的肝癌细胞中均被诱导，它可以通过反式作用来介导膜糖蛋白的细胞内分选途径。