Anomalies in the translocation and processing of glycophorin precursors in murine erythroleukemia cells.
Anomalies in the translocation and processing of glycophorin precursors in murine erythroleukemia cells.
复制标题
DOI：
--
复制
发表时间：
1989-01
期刊：
影响因子：
--
通讯作者：
J. Ulmer;G. Palade
中科院分区：
文献类型：
--
作者：
J. Ulmer;G. Palade
人血型糖蛋白的类似物已在许多物种中鉴定，包括小鼠。在小鼠红白血病细胞中，表达三种成熟血型糖蛋白（gp-2，gp-3，34K）和四种推定的前体（21K，23K，26K和27K）。脉冲追踪标记实验表明，21 K和23 K是蛋白质29 K和30 K的gp-3双联体的前体。未发现26K、27K、34K和gp-2的前体-产物关系。两种实验方法，即无细胞翻译和亚细胞分布，已确定处理异常的血型糖蛋白。第一，信号序列，如果存在的话，显然不会被切割后易位跨内质网膜;第二，26 K和27 K推定的前体是无效易位。大多数在胞质溶胶中积累或与内质网膜结合，而不获得对V8蛋白酶的保护。只有少数（约10%）是正确的。
Analogues of human glycophorins have been identified in many species, including mouse. In murine erythroleukemia cells three mature glycophorins (gp-2, gp-3, 34K) and four putative precursors (21K, 23K, 26K, and 27K) are expressed. Pulse-chase labeling experiments suggest that 21K and 23K are the precursors of the gp-3 doublet of proteins 29K and 30K. Precursor-product relationships were not found for 26K, 27K, 34K, and gp-2. Two experimental approaches, i.e. cell-free translation and subcellular distribution, have identified processing anomalies in the glycophorins. First, signal sequences, if present, are apparently not cleaved upon translocation across the endoplasmic reticulum membrane; second, the 26K and 27K putative precursors are inefficiently translocated. The majority accumulates in the cytosol or associates with the endoplasmic reticulum membrane without acquiring protection against V8 protease. Only a minority (approximately 10%) is properly translocated.