期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 474, 期 1, 页码 193-197出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2008.02.041
关键词
endocytosis; ferritin; hemochromatosis; hepcidin; TRVb cells
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK040163, R01DK053405, R01DK063016] Funding Source: NIH RePORTER
- NIDDK NIH HHS [R01 DK053405, DK40163, DK063016] Funding Source: Medline
Mutations in either HFE or transferrin receptor 2 (TfR2) cause decreased expression of the iron regulatory hormone hepcidin and hemochromatosis. HFE and TfR2 were recently discovered to form a stable complex at the cell membrane when co-expressed in heterologous cell lines. We analyzed the functional consequences of the co-expression of these proteins using transfected TRVb cells, a Chinese hamster ovary derived cell line without endogenous HFE or transferrin receptor. The co-expression of TfR2 in TRVb cells expressing HFE led to accelerated HFE biosynthesis and late-Golgi maturation, suggesting interaction prior to cell surface localization. The co-expression of HFE in cells expressing TfR2 led to increased affinity for diferric transferrin, increased transferrin-dependent iron uptake, and relative resistance to iron chelation. These observations indicate that HFE influences the functional properties of TfR2, and suggests a model in which the interaction of these proteins might influence signal transduction to hepcidin. (C) 2008 Published by Elsevier Inc.
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