Murine mutants in the study of systemic iron metabolism and its disorders: An update on recent advances

被引:4
作者
Bartnikas, Thomas B. [1 ]
Fleming, Mark D. [1 ]
Schmidt, Paul J. [1 ]
机构
[1] Childrens Hosp, Dept Pathol, Boston, MA 02115 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2012年 / 1823卷 / 09期
关键词
Mouse; Iron; Model; Dietary iron absorption; Hepcidin; Cellular iron metabolism; MICROCYTIC HYPOCHROMIC-ANEMIA; PROTEASE MATRIPTASE-2 TMPRSS6; TRANSFERRIN RECEPTOR 2; DUODENAL CYTOCHROME-B; HEPCIDIN EXPRESSION; DEFICIENCY ANEMIA; DEPENDENT REGULATION; REGULATORY PROTEINS; MOUSE MODEL; MICE LEADS;
D O I
10.1016/j.bbamcr.2012.01.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Many past and recent advances in the field of iron metabolism have relied upon the use of mouse models of disease. These models have arisen spontaneously in breeder colonies or have been engineered for global or conditional ablation or overexpression of select genes. Full phenotypic characterization of these models typically involves maintenance on iron-loaded or -deficient diets, treatment with oxidative or hemolytic agents, breeding to other mutant lines or other stresses. In this review, we focus on systemic iron biology and the contributions that mouse model-based studies have made to the field. We have divided the field into three broad areas of research: dietary iron absorption, regulation of hepcidin expression and cellular iron metabolism. For each area, we begin with an overview of the current understanding of key molecular and cellular determinants then discuss recent advances. Finally, we conclude with brief comments on prospects for future study. This article is part of a Special Issue entitled: Cell Biology of Metals. (C) 2012 Elsevier ay. All rights reserved.
引用
收藏
页码:1444 / 1450
页数:7
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