CELL LINES FROM MICE MUTANTS IN IRON METABOLISM

描述(部分摘自应用程序的摘要) 这个项目是专门为了克隆有缺陷的基因 造成两种近交系小鼠无法吸收铁的原因， 称为小细胞性贫血(MK)和性连锁贫血(SLA)。该项目涉及 肠道来源细胞系的建立及特性研究 MK和SLA小鼠的细胞和MK小鼠的红系细胞。铁 这些细胞系的新陈代谢将通过检查 已知对细胞内铁有反应的基因的表达 浓度(铁蛋白和转铁蛋白受体)和报告 其表达依赖于特征良好的铁的构造 调节元件结合蛋白。克隆缺陷基因的方法 MK和SLA基因是异常的功能互补之一 利用cDNA文库转染法进行细胞表型的筛选 利用铁依赖表达与正常基因互补 抗生素耐药基因。这些细菌的分离和鉴定 基因应该为哺乳动物细胞如何调控铁的运输提供线索 和摄取，并可能导致新的候选基因座的发展 人类铁代谢紊乱的数量。

DESCRIPTION (taken in part from the application's abstract) This project is specifically intended to clone the defective genes that are responsible for the inability to absorb iron in two inbred strains of mice, called microcytic (mk) and sex-linked anemia (sla). The project involves the development and characterization of cell lines derived from intestinal cells of the mk and sla mice and erythroid cells of the mk mouse. Iron metabolism in these cell lines will be characterized by examining the expression of genes known to be responsive to intracellular iron concentration (ferritin and the transferrin receptor) and reporter constructs whose expression depends upon the well-characterized iron regulatory element binding protein. The approach to cloning the defective mk and sla genes is one of functional complementation of the abnormal phenotype using cDNA library transfection and selection of cells complemented with the normal gene by use of iron-dependent expression of antibiotic resistance genes. The isolation and characterization of these genes should provide clues to how mammalian cells regulate iron transport and uptake, and might result in the development of new candidate loci for a number of human disorders of iron metabolism.