Lack of hepcidin gene expression and severe tissue iron overload in upstream stimulatory factor 2 (USF2) knockout mice
By G. Nicolas, M. Bennoun, I. Devaux, C. Beaumont, B. Grandchamp, A. Kahn, S. Vaulont. Proceedings of the National Academy of Sciences of the United States of America, 2001
1,320 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/e216785aa8071e18d0e506fb17b109fe5116b9d3
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Citations in the corpus
- BMP-6 is a key endogenous regulator of hepcidin expression and iron metabolism (2009, neutral): “The Bmp6 -null mice contain a neomycin cassette, raising the possibility that expression of neighboring genes might also be affected, as described in other mouse model”
- The Evolution of Iron Chelators for the Treatment of Iron Overload Disease and Cancer (2005, background): “More recently, a peptide hormone secreted by the liver known as hepcidin has been identified to be critical in iron homeostasis by acting as an iron-regulatory hormone (Nicolas et al., 2001; for review, see Ganz, 2003), regulating enterocyte ferroportin 1 expression (Nemeth et al., 2004).”
- Regulation of iron homeostasis by the hypoxia-inducible transcription factors (HIFs). (2007, background): “Genetic studies in mice lacking or overexpressing hepcidin suggest that this peptide inhibits both iron absorption in the small intestine and the release of recycled iron from macrophages (2, 3).”
- Targeted Drug Delivery via the Transferrin Receptor-Mediated Endocytosis Pathway (2002, background): “In addition, a possibility has recently been suggested that TfR2 might play an important role in modulation of hepcifin expression, thus involving the regulation of dietary iron absorption (Nicolas et al., 2001; Fleming and Sly, 2001, 2002).”
- Hepcidin and iron regulation, 10 years later. (2011, background): “32 On the basis of the work by many groups, a model of hepcidin regulation by iron has emerged (Figure 2) in which (1) the BMP receptor and its signaling components are at the core of the regulatory mechanism and control the transcription of hepcidin thorough the Smad pathway; (2) HJV is an iron-spe”
- The iron exporter ferroportin/Slc40a1 is essential for iron homeostasis. (2005, background): “An important clue came from the discovery of hepcidin, a circulating peptide that has profound effects on iron absorption and distribution (Nicolas et al., 2001, 2002).”
- Homeostasis and toxicology of essential metals (2012, background): “Hepcidin controls Fe levels by regulating the absorption of dietary Fe from the intestine, the release of recycled Fe from macrophages, and the movement of stored Fe from hepatocytes (Nicolas et al., 2001; Nemeth et al., 2004).”
- Systemic iron homeostasis. (2013, background): “At the other extreme, hepcidin deficiency in mice or humans causes hyperabsorption of iron and iron overload in parenchymal organs including the liver, pancreas, and the heart, coupled with the paradoxical loss of macrophage iron stores (137, 166, 204).”
- A role of SMAD4 in iron metabolism through the positive regulation of hepcidin expression. (2005, background): “This phenotype may not be explained by the down regulation of hepcidin as no such abnormality was reported in mice carrying targeted disruption of hepcidin (Nicolas et al., 2001).”
- Iron, brain ageing and neurodegenerative disorders (2004, background): “Recent investigations into the role of humoral factors in programming the enterocyte indicated that the main molecules involved are the antimicrobial peptide hepcidi”