Suppr超能文献

微管在转铁蛋白受体从细胞表面转运至内体和高尔基体复合物过程中的作用。

Role of microtubules in transferrin receptor transport from the cell surface to endosomes and the Golgi complex.

作者信息

Jin M, Snider M D

机构信息

Department of Biochemistry, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4935.

出版信息

J Biol Chem. 1993 Aug 25;268(24):18390-7.

PMID:8349714
Abstract

Transferrin receptor (TfR) follows complex pathways of transport after endocytosis from the cell surface. Most TfR is transported to endosomes and returns rapidly to the cell surface. In addition, approximately 10% of the internalized receptor recycles through the Golgi complex. To examine the role of microtubules in TfR traffic, K562 cultured human leukemia cells treated with nocodazole to depolymerize microtubules were studied. Nocodazole caused a 50% increase in the level of surface TfR, which was due to a change in receptor dynamics. The endocytosis rate in treated cells was 20% of control, indicating that TfR endocytosis via clathrin-coated vesicles was slowed, whereas the recycling of internalized receptors to the cell surface was unaffected. In contrast, nocodazole had little effect on the transport of TfR from the cell surface to the Golgi complex. Thus, the fragmentation and dispersal of the Golgi complex caused by microtubule depolymerization, which does not interrupt secretory traffic through this organelle, also does not block recycling through the Golgi. The decreased TfR endocytosis via coated vesicles and the increased TfR transport to the Golgi caused by nocodazole suggest that either (i) endocytosis via coated vesicles is not the rate-limiting step in transport to the Golgi or (ii) coated vesicles are not a part of this pathway. Finally, because nocodazole inhibits traffic from endosomes to lysosomes, surface-to-Golgi transport probably does not involve a lysosomal intermediate.

摘要

转铁蛋白受体(TfR)从细胞表面内吞后遵循复杂的运输途径。大多数TfR被转运至内体并迅速返回细胞表面。此外,约10%内化的受体通过高尔基体复合体进行再循环。为了研究微管在TfR运输中的作用,对用诺考达唑处理使微管解聚的K562培养人白血病细胞进行了研究。诺考达唑使表面TfR水平增加了50%,这是由于受体动力学的改变。处理过的细胞内吞率为对照的20%,表明通过网格蛋白包被小泡的TfR内吞作用减慢,而内化受体向细胞表面的再循环未受影响。相反,诺考达唑对TfR从细胞表面向高尔基体复合体的运输影响很小。因此,由微管解聚引起的高尔基体复合体的碎片化和分散,虽然不中断通过该细胞器的分泌运输,但也不阻断通过高尔基体的再循环。诺考达唑导致通过包被小泡的TfR内吞作用减少以及TfR向高尔基体的运输增加,这表明要么(i)通过包被小泡的内吞作用不是向高尔基体运输的限速步骤,要么(ii)包被小泡不是该途径的一部分。最后,由于诺考达唑抑制从内体到溶酶体的运输,从表面到高尔基体的运输可能不涉及溶酶体中间体。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验