Disease relevance of Trfr2

• Targeted disruption of the hepatic transferrin receptor 2 gene in mice leads to iron overload [1].
• We found decreased expression of hepcidin and TfR2 and increased expression of TfR1 and NGAL in the beta-thalassemia mouse models, compared with the control mice [2].

High impact information on Trfr2

• To determine the contribution of liver expressed TfR2 in iron homeostasis, we have generated and characterized a liver-specific TfR2-knockout (KO) mouse [1].
• In situ hybridization demonstrated abundant TfR2 expression in hepatocytes [3].
• RESULTS: Ferroportin1, transferrin receptor 2 and HAMP mRNA levels displayed no significant strain differences [4].
• Duodenal Fe absorption and hepatic Fe uptake were measured in vivo by (59)Fe-labeled ascorbate in TfR2 mutant mice, wild-type mice, and Fe-loaded wild-type mice (2% dietary carbonyl Fe) [5].
• Even when compared with Fe-loaded wild-type mice, TfR2 mutant mice had increased Fe absorption, increased duodenal Fe transport gene expression, increased liver Fe uptake, and decreased liver hepcidin expression [5].

Chemical compound and disease context of Trfr2

• In parenteral iron overload, Tfr2 gene and protein expression decreased concomitant to the increase in Hepc, while Hfe RNA remained constant [6].

Anatomical context of Trfr2

• The function of hepcidin in regulating iron absorption is modeled through an inverse relationship between hepatocyte transferrin receptor 2 (TfR2) levels and the rate of iron export processes mediated by ferroportin (Fpn) [7].

Other interactions of Trfr2

• Hfe, Rgmc and Tfr2 expression was not influenced by phlebotomy [6].
• Expression of liver hepcidin, Tfr2, Hjv, Fpn and Hfe RNA was assessed by real-time polymerase chain reaction [8].

Analytical, diagnostic and therapeutic context of Trfr2

• Levels of the iron-related proteins TfR1, TfR2, ferritin, and prohepcidin were analyzed by immunoblotting [1].

References