COMPLEMENTATION OF MUTATIONS IN THE LDL PATHWAY OF RECEPTOR-MEDIATED ENDOCYTOSIS BY CO-CULTIVATION OF LDL RECEPTOR-DEFECTIVE HAMSTER-CELL MUTANTS
COMPLEMENTATION OF MUTATIONS IN THE LDL PATHWAY OF RECEPTOR-MEDIATED ENDOCYTOSIS BY CO-CULTIVATION OF LDL RECEPTOR-DEFECTIVE HAMSTER-CELL MUTANTS
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DOI：
10.1016/0092-8674(83)90423-3
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发表时间：
1983-01-01
期刊：
影响因子：
64.5
通讯作者：
KRIEGER, M
中科院分区：
文献类型：
--
作者：
KRIEGER, M
分离了不表达低密度脂蛋白受体的中国仓鼠卵巢（CHO）细胞突变体。当一个突变克隆与其他有受体缺陷的克隆共培养时，它被诱导表达能介导正常内吞作用的受体。这些LDL受体缺陷克隆定义了两类突变：cbc（共培养补充）和icc（共培养诱导细胞）。低密度脂蛋白受体在cbc细胞中的诱导和短期（18 h）稳定性不需要icc细胞合成蛋白质。DMSO[二甲亚砜]、5-氮胞苷、磷脂酰胆碱脂质体、二丁基cAMP、紧实蛋白、大豆胰蛋白酶抑制剂、低温（30℃）均不能诱导受体活性。C)，或条件培养基，但可以通过与亲代CHO细胞和正常和LDL受体阴性的人成纤维细胞共培养诱导。只有当cbc和诱导细胞接近时，共培养的互补才会发生，这表明互补需要一个不稳定的扩散因子或密切的细胞间联系。
Chinese hamster ovary (CHO) cell mutants were isolated that do not express low density lipoprotein (LDL) receptors. When one mutant clone was cocultivated with other receptor-defective clones, it was induced to express receptors that could mediate normal endocytosis. These LDL receptor-defective clones defined 2 classes of mutations: cbc (complemented by cocultivation) and icc (inducer cells in cocultivation). The induction and short-term (18 h) stability of LDL receptors in cbc cells did not require protein synthesis by icc cells. Receptor activity could not be induced by DMSO [dimethyl sulfoxide], 5-azacytidine, phosphatidylcholine liposomes, dibutyryl cAMP, compactin, soybean trypsin inhibitor, low temperature (30.degree. C), or conditioned medium, but could be induced by cocultivation with parental CHO cells and normal and LDL receptor-negative human fibroblasts. Complementation by cocultivation only occurred when the cbc and inducing cells were in close proximity, suggesting that an unstable diffusible factor or intimate cell-to-cell association was required for complementation.