IRON METABOLISM IN ERYTHROID CELLS

红细胞中的铁代谢

• 批准号: 2140170
• 负责人: Jonathan David Glass
• 金额: $ 16.54万
• 依托单位: LOUISIANA STATE UNIV HSC SHREVEPORT
• 依托单位国家: 美国
• 财政年份: 1986
• 资助国家: 美国
• 起止时间: 1986-02-01 至 1998-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2140170
• 关键词: acidity /alkalinity; adenosinetriphosphatase; disease /disorder model; electrical conductance; endocytosis; enzyme activity; erythroid stem cell; fluorescent dye /probe; guanine nucleotide binding protein; iron metabolism; laboratory rabbit; laboratory rat; lactoferrin; membrane transport proteins; metabolism disorder; organelles; receptor binding; reticulocytes; tissue /cell culture; transferrin; transferrin receptor

This is a revised proposal that aims to examine the mechanisms by which iron is taken up into cells from transferrin. Very little is known about this important aspect of iron metabolism. The Applicant will use rabbit reticulocytes as a model system, but his findings should be generally applicable to transferrin mediated iron uptake in all cells. In addition, he will examine the mechanism responsible for defective iron uptake into the erythroid cells of the Belgrade rat. This animal carries a spontaneous recessive mutation that impairs iron uptake into cells, leading to iron-deficient erythropoiesis. The investigator has greatly sharpened the focus of the proposal and has built a logical sequence of experiments. The Investigator has also provided new preliminary data that strengthen several of the hypotheses that he plans to test.

这是一项修订的建议，旨在检查 铁被从转铁蛋白中吸入细胞。 对 铁代谢的这一重要方面。 申请人将使用兔子 网状细胞作为模型系统，但他的发现通常应该是 适用于所有细胞中转铁蛋白介导的铁吸收。 此外， 他将检查导致铁吸收缺陷的机制 贝尔格莱大鼠的红细胞细胞。 这只动物带有 自发隐性突变会损害铁吸收细胞， 导致铁缺乏的红细胞生成。 调查员有很大的 提出了提案的重点，并建立了逻辑序列 实验。 研究人员还提供了新的初步数据 加强了他计划检验的几个假设。