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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Canonne-Hergaux, F. Articles by Gros, P. Search for Related Content PubMed PubMed Citation Articles by Canonne-Hergaux, F. Articles by Gros, P. Related Collections Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 December 2000, Vol. 96, No. 12, pp. 3964-3970 RED CELLS The Nramp2/DMT1 iron transporter is induced in the duodenum of microcytic anemia mk mice but is not properly targeted to the intestinal brush border François Canonne-Hergaux, Mark D. Fleming, Joanne E. Levy, Susan Gauthier, Trevor Ralph, Virginie Picard, Nancy C. Andrews, and Philippe Gros From the Department of Biochemistry, McGill University, Montreal, Canada; Division of Hematology/Oncology, Children's Hospital, Boston, MA; Howard Hughes Medical Institute, Boston, MA; Division of Hematology and Department of Pathology, Brigham and Women's Hospital, Boston, MA; and Department of Pediatrics, Harvard Medical School, Boston, MA. Microcytic anemia (mk) mice and Belgrade (b) rats are severely iron deficient because of impaired intestinal iron absorption and defective iron metabolism in peripheral tissues. Both animals carry a glycine to arginine substitution at position 185 in the iron transporter known as Nramp2/DMT1 (divalent metal transporter 1). DMT1 messenger RNA (mRNA) and protein expression has been examined in the gastrointestinal tract of mk mice. Northern blot analysis indicates that, by comparison to mk/+ heterozygotes, mk/mk homozygotes show a dramatic increase in the level of DMT1 mRNA in the duodenum. This increase in RNA expression is paralleled by a concomitant increase of the 100-kd DMT1 isoform I protein expression in the duodenum. Immunohistochemical analyses show that, as for normal mice on a low-iron diet, DMT1 expression in enterocytes of mk/mk mice is restricted to the duodenum. However, and in contrast to normal enterocytes, little if any expression of DMT1 is seen at the apical membrane in mk/mk mice. These results suggest that the G185R mutation, which was shown to impair the transport properties of DMT1, also affects the membrane targeting of the protein in mk/mk enterocytes. This loss of function of DMT1 is paralleled by a dramatic increase in expression of the defective protein in mk/mk mice. This is consistent with a feedback regulation of DMT1 expression by iron stores. © 2000 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Thompson, R. M. Molina, J. D. Brain, and M. Wessling-Resnick Belgrade Rats Display Liver Iron Loading J. Nutr., December 1, 2006; 136(12): 3010 - 3014. [Abstract] [Full Text] [PDF] F. Canonne-Hergaux, A. Donovan, C. Delaby, H.-j. Wang, and P. Gros Comparative studies of duodenal and macrophage ferroportin proteins Am J Physiol Gastrointest Liver Physiol, January 1, 2006; 290(1): G156 - G163. [Abstract] [Full Text] [PDF] W.S. Chong, P.C. Kwan, L.Y. Chan, P.Y. Chiu, T.K. Cheung, and T.K. Lau Expression of divalent metal transporter 1 (DMT1) isoforms in first trimester human placenta and embryonic tissues Hum. Reprod., December 1, 2005; 20(12): 3532 - 3538. [Abstract] [Full Text] [PDF] R. E. 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