Mammalian iron metabolism
Iron is essential for a wide array of physiological functions, including oxygen transport, cell proliferation and respiration. On the other hand, iron is also a potential biohazard due to its ability to catalyze the generation of free radicals and to thereby promote oxidative stress. Thus, balanced iron homeostasis is critical for health. While iron deficiency eventually leads to anemia, excessive iron overload (hemochromatosis) results in tissue damage and organ failure.
Our lab is studying mechanisms that control mammalian iron homeostasis at the cellular and systemic level. Specific areas of research are described below:
- Post-transcriptional regulation of cellular iron metabolism by the IRE/IRP regulatory system. Emphasis is given on the molecular mechanisms by which “iron regulatory proteins”, IRP1 and IRP2, sense intracellular iron levels and control the fate of target mRNAs. We are also investigating the responses of IRP1 and IRP2 to iron-independent signals, such as nitric oxide, hypoxia and oxidative stress.
- Regulation of iron transport by hepcidin and hemojuvelin. Our goal is to characterize molecular mechanisms that control systemic iron homeostasis via the hepcidin-hemojuvelin axis.
- Iron metabolism and tumor growth. Cell culture and animal models are developed to investigate how misregulation of iron metabolism affects carcinogenesis and tumor growth.
- Iron metabolism and hepatitis C virus (HCV) . HCV replicon models are utilized to study the role of iron on viral replication and to understand how the virus modulates cellular iron metabolism