一种新型的ADP核糖基化样因子（ARL-6）与蛋白质传导通道SEC61β亚基相互作用。

A novel ADP-ribosylation like factor (ARL-6), interacts with the protein-conducting channel SEC61beta subunit.

作者信息

Ingley E, Williams J H, Walker C E, Tsai S, Colley S, Sayer M S, Tilbrook P A, Sarna M, Beaumont J G, Klinken S P

机构信息

Laboratory for Cancer Medicine, Department of Biochemistry, The University of Western Australia and Royal Perth Hospital, Perth, W.A., Australia.

出版信息

FEBS Lett. 1999 Oct 1;459(1):69-74. doi: 10.1016/s0014-5793(99)01188-6.

DOI:10.1016/s0014-5793(99)01188-6

PMID:10508919

Abstract

We report here the isolation of a new member of the ADP-ribosylation factor (ARF)-like family (ARL-6) present in the J2E erythroleukemic cell line, but not its myeloid variants. Consistent with this lineage-restricted expression, ARL-6 mRNA increased with erythropoietin-induced maturation of J2E cells, and decreased with interleukin 6-induced differentiation of M1 monoblastoid cells. In tissues, ARL-6 mRNA was most abundant in brain and kidney. While ARL-6 protein was predominantly cytosolic, its membrane association increased following exposure to GTP-gammaS, like many members of the ARF/ARL family. Using the yeast two-hybrid system, six molecules which interact with ARL-6 were identified including SEC61beta, a subunit of the heterotrimeric protein conducting channel SEC61p. Co-immunoprecipitation of ARL-6 confirmed a stable association between ARL-6 and SEC61beta in COS cells. These results demonstrate that ARL-6, a novel member of the ADP-ribosylation factor-like family, interacts with the SEC61beta subunit.

摘要

我们在此报告在J2E红白血病细胞系中存在的ADP核糖基化因子（ARF）样家族的一个新成员（ARL-6）的分离情况，但其髓系变体中不存在该成员。与这种谱系限制表达一致，ARL-6 mRNA随着促红细胞生成素诱导的J2E细胞成熟而增加，随着白细胞介素6诱导的M1单核母细胞分化而减少。在组织中，ARL-6 mRNA在脑和肾中最为丰富。虽然ARL-6蛋白主要位于胞质中，但与ARF/ARL家族的许多成员一样，其膜结合在暴露于GTP-γS后增加。使用酵母双杂交系统，鉴定出六个与ARL-6相互作用的分子，包括异源三聚体蛋白传导通道SEC61p的一个亚基SEC61β。ARL-6的共免疫沉淀证实了在COS细胞中ARL-6与SEC61β之间存在稳定的结合。这些结果表明，ARL-6是ADP核糖基化因子样家族中的一个新成员，与SEC61β亚基相互作用。