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JCI early table of contents for Nov. 26, 2012
Date:11/26/2012

is a tightly regulated process that is sensitive to the balance of the proteins that form hemoglobin, heme and globin. The protein FLVCR1a is responsible for removing excess heme from cells and is essential for erythropoiesis. In this issue of the Journal of Clinical Investigation, researchers led by Emanuela Tolosano at the University of Torino in Italy identified another form of FLVCR1, FLVCR1b, that is responsible for exporting heme from the mitochondria of the cell, the location of heme production. By manipulating the expression of the FLVCR1 proteins in mice, Tolosano and colleagues found that FLVCR1b was required for erythropoiesis. FLVCR1a was not required for erythropoiesis, but was necessary to prevent excess bleeding, swelling, and skeletal abnormalities in the developing mouse embryo. These results indicate that mutations in the Flvcr1 gene may underlie diseases characterized by abnormal heme levels, such as Sideroblastic anemia. In a companion commentary, Mark Fleming of Children's Hospital Boston discusses the role of heme transport in human physiology and disease.

TITLE:
The mitochondrial heme exporter FLVCR1b mediates erythroid differentiation

AUTHOR CONTACT:
Emanuela Tolosano
University of Torino, Torino, UNK, ITA
Phone: 39-011-670-6423; Fax: 39-011-670-6432; E-mail: emanuela.tolosano@unito.it

View this article at: http://www.jci.org/articles/view/62422?key=da4e860633582101d3cb

ACCOMPANYING COMMENTARY

TITLE:
Mitochondrial heme: an exit strategy at last

AUTHOR CONTACT:
Mark Fleming
Children's Hospital Boston, Boston, MA, USA
Phone: 617-919-2664; E-mail: mark.fleming@childrens.harvard.edu

View this article at:

Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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