High levels of GDF15 in thalassemia suppress expression of the iron regulatory protein hepcidin

By T. Tanno, N. Bhanu, Patricia A. Oneal, S. Goh, Pamela Staker, Y. Lee, J. Moroney, Christopher Reed, N. Luban, Ruihong Wang and 6 more. Nature Medicine, 2007

869 citations recorded by the source corpus.

Subfields: Cancer Research, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/99da2390f56d61251b888612ca6096ddcb488549

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. T. Ganz
2. V. Haase

In Hematology

1. E. Nemeth
2. T. Ganz
3. V. Haase

In Rheumatology

1. T. Ganz

Citations in the corpus

• Systemic iron homeostasis. (2013, background): “GDF-15, a BMP family member whose serum concentrations are greatly increased in iron-loading anemias (32, 125, 236, 237), has been proposed as a hepcidin suppressor in -thalassemia and in congenital dyserythropoietic anemias, but its contribution to hepcidin suppression and iron overload in these co”
• The Role of Hepcidin in Iron Metabolism (2009, background): “Two proteins produced by erythroid precursors, growth differentiation factor 15 (GDF15) and twisted gastrulation protein (TWSG1), have been proposed to mediate hepcidin suppression in anemias with ineffective erythropoiesis [”
• Regulation of erythropoiesis by hypoxia-inducible factors (2013, background): “doses of GDF15 were needed to achieve hepcidin suppression in human HuH-7 hepatoma cells and in primary hepatocytes, while low dose GDF15 treatment increased hepcidin.(213) While demonstrated in mice, studies in humans receiving recombinant EPO have not yet shown a sig-”