CELL LINES FROM MICE MUTANTS IN IRON METABOLISM

小鼠铁代谢突变体的细胞系

• 批准号: 2518590
• 负责人: DAVID J HAILE
• 金额: $ 7.08万
• 依托单位: UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-09-30 至 1999-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2518590
• 关键词: clone cells; gastrointestinal absorption /transport; gene complementation; gene mutation; immunocytochemistry; iron metabolism; laboratory mouse; light microscopy; molecular cloning; nucleic acid sequence; phenotype; receptor expression; tissue /cell culture; transfection

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.

描述（部分摘自应用程序摘要） 该项目专门旨在克隆有缺陷的基因 负责无法在两只小鼠近交菌株中吸收铁， 称为微细胞（MK）和性链接贫血（SLA）。 该项目涉及 源自肠道的细胞系的发展和表征 MK小鼠的MK和SLA小鼠和红细胞细胞的细胞。 铁 这些细胞系中的代谢将通过检查 已知对细胞内铁反应的基因的表达 浓度（铁蛋白和转铁蛋白受体）和记者 表达取决于特征良好的铁的结构 调节元件结合蛋白。 克隆有缺陷的方法 MK和SLA基因是异常的功能互补之一 使用cDNA文库转染和细胞选择的表型 通过使用铁依赖性表达的正常基因 抗生素抗性基因。 这些的隔离和表征 基因应提供有关哺乳动物细胞如何调节铁转运的线索 和吸收，可能导致开发新的候选基因座 铁代谢的人类疾病数量。