Interactions of the ectodomain of HFE with the transferrin receptor are critical for iron homeostasis in cells

Cindy N. Roy; Eric J. Carlson; Emily L. Anderson; Alivelu Basava; Steven M. Starnes; John N. Feder; Caroline A. Enns

doi:10.1016/S0014-5793(00)02173-6

Interactions of the ectodomain of HFE with the transferrin receptor are critical for iron homeostasis in cells

Cindy N. Roy, Eric J. Carlson, Emily L. Anderson, Alivelu Basava, Steven M. Starnes, John N. Feder, Caroline A. Enns

Cell Developmental and Cancer Biology

Research output: Contribution to journal › Article › peer-review

30 Scopus citations

Abstract

Expression of wild type HFE reduces the ferritin levels of cells in culture. In this report we demonstrate that the predominant hereditary hemochromatosis mutation, C282Y² HFE, does not reduce ferritin expression. However, the second mutation, H63D HFE, reduces ferritin expression to a level indistinguishable from cells expressing wild type HFE. Further, two HFE cytoplasmic domain mutations engineered to disrupt potential signal transduction, S335M and Y342C, were functionally indistinguishable from wild type HFE in this assay, as was soluble HFE. These results implicate a role for the interaction of HFE with the transferrin receptor in lowering cellular ferritin levels. Copyright (C) 2000 Federation of European Biochemical Societies.

Original language	English (US)
Pages (from-to)	271-274
Number of pages	4
Journal	FEBS Letters
Volume	484
Issue number	3
DOIs	https://doi.org/10.1016/S0014-5793(00)02173-6
State	Published - Nov 10 2000

Keywords

Ferritin
HFE
Hemochromatosis
Iron metabolism
Transferrin receptor

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/S0014-5793(00)02173-6

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title = "Interactions of the ectodomain of HFE with the transferrin receptor are critical for iron homeostasis in cells",

abstract = "Expression of wild type HFE reduces the ferritin levels of cells in culture. In this report we demonstrate that the predominant hereditary hemochromatosis mutation, C282Y2 HFE, does not reduce ferritin expression. However, the second mutation, H63D HFE, reduces ferritin expression to a level indistinguishable from cells expressing wild type HFE. Further, two HFE cytoplasmic domain mutations engineered to disrupt potential signal transduction, S335M and Y342C, were functionally indistinguishable from wild type HFE in this assay, as was soluble HFE. These results implicate a role for the interaction of HFE with the transferrin receptor in lowering cellular ferritin levels. Copyright (C) 2000 Federation of European Biochemical Societies.",

keywords = "Ferritin, HFE, Hemochromatosis, Iron metabolism, Transferrin receptor",

author = "Roy, {Cindy N.} and Carlson, {Eric J.} and Anderson, {Emily L.} and Alivelu Basava and Starnes, {Steven M.} and Feder, {John N.} and Enns, {Caroline A.}",

note = "Funding Information: This work was supported by NIH DK 54488. C.N.R. was partially supported by the Training Program in Molecular Hematology, T32-HL00781, National Institutes of Health, National Heart, Lung and Blood Institute.",

year = "2000",

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doi = "10.1016/S0014-5793(00)02173-6",

language = "English (US)",

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pages = "271--274",

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T1 - Interactions of the ectodomain of HFE with the transferrin receptor are critical for iron homeostasis in cells

AU - Roy, Cindy N.

AU - Carlson, Eric J.

AU - Anderson, Emily L.

AU - Basava, Alivelu

AU - Starnes, Steven M.

AU - Feder, John N.

AU - Enns, Caroline A.

N1 - Funding Information: This work was supported by NIH DK 54488. C.N.R. was partially supported by the Training Program in Molecular Hematology, T32-HL00781, National Institutes of Health, National Heart, Lung and Blood Institute.

PY - 2000/11/10

Y1 - 2000/11/10

N2 - Expression of wild type HFE reduces the ferritin levels of cells in culture. In this report we demonstrate that the predominant hereditary hemochromatosis mutation, C282Y2 HFE, does not reduce ferritin expression. However, the second mutation, H63D HFE, reduces ferritin expression to a level indistinguishable from cells expressing wild type HFE. Further, two HFE cytoplasmic domain mutations engineered to disrupt potential signal transduction, S335M and Y342C, were functionally indistinguishable from wild type HFE in this assay, as was soluble HFE. These results implicate a role for the interaction of HFE with the transferrin receptor in lowering cellular ferritin levels. Copyright (C) 2000 Federation of European Biochemical Societies.

AB - Expression of wild type HFE reduces the ferritin levels of cells in culture. In this report we demonstrate that the predominant hereditary hemochromatosis mutation, C282Y2 HFE, does not reduce ferritin expression. However, the second mutation, H63D HFE, reduces ferritin expression to a level indistinguishable from cells expressing wild type HFE. Further, two HFE cytoplasmic domain mutations engineered to disrupt potential signal transduction, S335M and Y342C, were functionally indistinguishable from wild type HFE in this assay, as was soluble HFE. These results implicate a role for the interaction of HFE with the transferrin receptor in lowering cellular ferritin levels. Copyright (C) 2000 Federation of European Biochemical Societies.

KW - Ferritin

KW - HFE

KW - Hemochromatosis

KW - Iron metabolism

KW - Transferrin receptor

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ER -

Interactions of the ectodomain of HFE with the transferrin receptor are critical for iron homeostasis in cells

Abstract

Keywords

ASJC Scopus subject areas

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