Micromanaging Iron Homeostasis

Micromanaging senescence

Normal somatic cells have a limited capacity for division in culture and eventually enter a state of terminal growth arrest termed replicative senescence [1]. Cells that fail to undergo senescence divide indefinitely and develop chromosomal aberrations resulting in neoplastic transformation. Senescence is believed to be a tumor suppressor mechanism that ensures that cells permanently exit the c...

microManaging Mitochondrial Translation

Regulation of gene expression in mammalian mitochondria by microRNAs is reported by Zhang et al. During muscle cell differentiation, localization of a miRNA is increased within mitochondria, where it interacts with Ago2 to selectively activate translation of mtDNA-encoded mRNAs. The findings represent a new mitochondrial regulatory pathway and a potentially powerful means to purposefully manipu...

Orchestration of iron homeostasis.

Systemic iron homeostasis.

The iron hormone hepcidin and its receptor and cellular iron exporter ferroportin control the major fluxes of iron into blood plasma: intestinal iron absorption, the delivery of recycled iron from macrophages, and the release of stored iron from hepatocytes. Because iron losses are comparatively very small, iron absorption and its regulation by hepcidin and ferroportin determine total body iron...

Iron homeostasis and nutritional iron deficiency.

Nonheme food ferritin (FTN) iron minerals, nonheme iron complexes, and heme iron contribute to the balance between food iron absorption and body iron homeostasis. Iron absorption depends on membrane transporter proteins DMT1, PCP/HCP1, ferroportin (FPN), TRF2, and matriptase 2. Mutations in DMT1 and matriptase-2 cause iron deficiency; mutations in FPN, HFE, and TRF2 cause iron excess. Intracell...