Belgrade (b) rats have an autosomal recessive, microcytic, hypochromic anemia. Transferrin (Tf)-dependent iron uptake is defective because of a mutation in DMT1 (Nramp2), blocking endosomal iron efflux. This experiment of nature permits the present study to address whether the mutation also affects
Transferrin and transferrin receptor gene expression and iron uptake in hepatocellular carcinoma in the rat
β Scribed by Rosa Maria Pascale; Maria Rosaria De Miglio; Maria Rosaria Muroni; Maria Maddalena Simile; Lucia Daino; Maria Antonietta Seddaiu; Stefano Pusceddu; Leonardo Gaspa; Diego Calvisi; Giacomo Manenti; Francesco Feo
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 283 KB
- Volume
- 27
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
We have previously shown by immunocytochemistry in rat primary glial cultures that transferrin (Tf) is an early developmental marker for oligodendrocytes. The present work addresses the issue of Tf gene expression and synthesis by neural cells in vitro. For this purpose, we used rat embryonic neuron
HFE-related hereditary hemochromatosis results in hepatic iron overload. Hepatocytes acquire transferrin-bound iron via transferrin receptor (Tfr) 1 and Tfr1-independent pathways (possibly Tfr2-mediated). In this study, the role of Hfe in the regulation of hepatic transferrin-bound iron uptake by th
The versatile chemistry of iron and the noxious reactions this essential metal may promote have compelled iron-dependent organisms to form specific iron-binding proteins to maintain iron in soluble, nontoxic, and accessible form for cellular needs. A variety of pathways can be traversed by iron to g
## Abstract The impact of actinides on living organisms has been the subject of numerous studies since the 1950s. From a general point of view, these studies show that actinides are chemical poisons as well as radiological hazards. Actinides in plasma are assumed to be mainly complexed to transferr