The role of Matriptase-2 during the early postnatal development in humans Article Swipe

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Hepcidin TMPRSS6 Ferroportin Internalization Hemochromatosis DMT1 Erythropoiesis Endocrinology Regulator Repressor Inflammation Downregulation and upregulation Erythropoietin Internal medicine Cell biology Homeostasis Serine protease Biology Gene expression Immunology Anemia Medicine Protease Gene Transporter Biochemistry Receptor Enzyme

Luigia De Falco , Mariasole Bruno , Ebru Yılmaz-Keskin , Ertan Sal , Mustafa Büyükavcı , Zühre Kaya , Domenico Girelli , Achille Iolascon ·

YOU? · · 2016 · Open Access · · DOI: https://doi.org/10.3324/haematol.2015.139808 · OA: W2289926736

The hepatic hormone hepcidin is a key regulator of systemic iron homeostasis. It limits both iron absorption from the intestine and iron release from macrophage stores by binding to ferroportin and triggering its internalization and degradation. Hepcidin expression is modulated in response to several physiologic and pathologic stimuli, which include systemic iron loading, erythropoietic activity and inflammation.1 A type II transmembrane serine protease matriptase-2 (MT-2, encoded by TMPRSS6) was identified as a repressor of hepcidin expression acting through the interruption of BMP6/HJV/SMAD signaling.2–4 Thus, by downregulating hepcidin gene expression, MT-2 controls iron availability to avoid systemic iron deficiency.5,6