๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Transferrin receptors and the uptake and release of iron by isolated hepatocytes

โœ Scribed by Stephen P. Young; Philip Aisen


Publisher
John Wiley and Sons
Year
1981
Tongue
English
Weight
683 KB
Volume
1
Category
Article
ISSN
0270-9139

No coin nor oath required. For personal study only.

โœฆ Synopsis


Isolated rat hepatocytes accumulate iron from iron-transferrin by a process which is dependent on the temperature and on the transferrin concentration, and which is diminished by treatment of the cells with a proteolytic enzyme. These observations are consistent with a mechanism for iron uptake into hepatocytes involving the binding of iron-transferrin to a specific cell-surface receptor.

Apotransferrin is also able to bind to the hepatocyte but the apparent binding constant is about 35 times lower than that observed fvr the binding of iron-transferrin. The binding of apotransferrin to the cells is completely abolished by a low concentration of iron-transferrin. This suggests that the apotransferrin is binding weakly to the same receptor to which iron-transferrin binds and that there are no receptors on the surface of the hepatocyte specific for apotransferrin. In the absence of such specific-binding sites, apotransferrin may act as a passive acceptor of iron released from the hepatocyte.


๐Ÿ“œ SIMILAR VOLUMES


The role of Hfe in transferrin-bound iro
โœ Anita C.G. Chua; Carly E. Herbison; Sarah F. Drake; Ross M. Graham; John K. Olyn ๐Ÿ“‚ Article ๐Ÿ“… 2008 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 372 KB ๐Ÿ‘ 1 views

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

Increase of transferrin receptors and ir
โœ M. B. Graeber; G. Raivich; Dr. G. W. Kreutzberg ๐Ÿ“‚ Article ๐Ÿ“… 1989 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 799 KB

After injury, motor neurons exhibit a number of metabolic and protein changes that are assumed to be part of an inherent neuronal regeneration program, which, when activated, eventually leads to functional restitution. The mechanisms underlying this regeneration are unclear, but it may be expected t