Regulation of iron homeostasis by the hypoxia-inducible transcription factors (HIFs).

By C. Peyssonnaux, A. Zinkernagel, R. Schuepbach, Erinn B. Rankin, S. Vaulont, V. Haase, V. Nizet, Richard J. Johnson. Journal of Clinical Investigation, 2007

660 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/f27b17b3aea785f749036251f3d2d8082894dbd7

How researchers see this paper

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

In Genetics

1. E. Nemeth
2. T. Ganz
3. N. Prabhakar
4. G. Semenza
5. C. V. Dang
6. Navdeep S. Chandel
7. V. Haase

In Hematology

1. E. Nemeth
2. T. Ganz
3. G. Semenza

In Rheumatology

1. T. Ganz

Citations in the corpus

• ADAPTIVE AND MALADAPTIVE CARDIORESPIRATORY RESPONSES TO CONTINUOUS AND INTERMITTENT HYPOXIA MEDIATED BY HYPOXIA-INDUCIBLE FACTORS 1 AND 2 (2012, background): “Thus HIFs repress transcription of the gene encoding hepcidin (260) and activate transcription of the genes encoding transferrin (281), transferrin receptor (199, 322), and divalent metal transporter 1 (217).”
• The Role of Hepcidin in Iron Metabolism (2009, background): “GDF15 is a member of the TGF-β superfamily, and although GDF15 knockout or transgenic mice do not have obvious iron abnormalities, larger doses of GDF15 do suppress hepcidin mRNA in vitro. Such doses are comparable to the levels of GDF15 observed in β-thalassemia and congenital dyserythropoietic ane”
• Systemic iron homeostasis. (2013, result): “Hypoxia or erythropoietin were initially thought to regulate hepcidin directly (168, 181, 189), but the preponderance of data now supports a model in which the bone marrow produces a hepcidin suppressor, in response to erythropoietin (141, 148, 176, 257).”