Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Guillem Casanovas"'
Publikováno v:
PLoS Computational Biology, Vol 10, Iss 1, p e1003421 (2014)
Systemic iron homeostasis involves a negative feedback circuit in which the expression level of the peptide hormone hepcidin depends on and controls the iron blood levels. Hepcidin expression is regulated by the BMP6/SMAD and IL6/STAT signaling casca
Externí odkaz:
https://doaj.org/article/01d4fa0c77d1458d927b551e10bdb096
Autor:
Guillem Casanovas, Maja Vujić Spasić, Carla Casu, Stefano Rivella, Jens Strelau, Klaus Unsicker, Martina U. Muckenthaler
Publikováno v:
Haematologica, Vol 98, Iss 3 (2013)
In conditions of increased erythropoiesis, expression of hepcidin, the master regulator of systemic iron homeostasis, is decreased to allow for the release of iron into the blood stream from duodenal enterocytes and macrophages. It has been suggested
Externí odkaz:
https://doaj.org/article/40782f4e9dcf44c88eaa0982a15f5f8f
Autor:
Jonathan Beaudoin, Robert A. Levine, Guillem Casanovas, Brittan Morris, Philipp E. Bartko, Margo M. Seybolt, Whitney S. Irvin, Joyce Bischoff, Michael L. Garcia, Elena Aikawa, Dae-Hee Kim, Suzanne Sullivan, Jacob P. Dal-Bianco, Joshua Keegan, Jill Wylie-Sears, J. Luis Guerrero
Rationale : Ischemic mitral regurgitation, a complication after myocardial infarction (MI), induces adaptive mitral valve (MV) responses that may be initially beneficial but eventually lead to leaflet fibrosis and MV dysfunction. We sought to examine
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a0cda9b614482ae0b227090cbcd0a2e9
https://europepmc.org/articles/PMC5215059/
https://europepmc.org/articles/PMC5215059/
Autor:
Martina U. Muckenthaler, Katja Breitkopf-Heinlein, Tobias P. Dick, Guillem Casanovas, Helmut K. Seitz, Teresa Peccerella, Sebastian Mueller, Gunda Millonig, Ingo Ganzleben, Lidia Brodziak-Jarosz
Publikováno v:
Journal of Biological Chemistry. 287:37472-37482
The peptide hormone hepcidin regulates mammalian iron homeostasis by blocking ferroportin-mediated iron export from macrophages and the duodenum. During inflammation, hepcidin is strongly induced by interleukin 6, eventually leading to the anemia of
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c60165a130edde93c42d3f35792a8f38
https://doi.org/10.1074/jbc.m112.358911
https://doi.org/10.1074/jbc.m112.358911
Autor:
Maja Vujić Spasić, Carla Casu, Guillem Casanovas, Martina U. Muckenthaler, Stefano Rivella, Jens Strelau, Klaus Unsicker
Publikováno v:
Haematologica. 98:444-447
In conditions of increased erythropoiesis, expression of hepcidin, the master regulator of systemic iron homeostasis, is decreased to allow for the release of iron into the blood stream from duodenal enterocytes and macrophages. It has been suggested
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::76d92b4ad03b887bc2484e47c9baf8e1
https://doi.org/10.3324/haematol.2012.069807
https://doi.org/10.3324/haematol.2012.069807
Growth differentiation factor 15 in patients with congenital dyserythropoietic anaemia (CDA) type II
Autor:
Hans-Juergen Gross, Martina U. Muckenthaler, Coby M. Laarakkers, M Wiesneth, Hermann Heimpel, Sandro Altamura, Guillem Casanovas, Dorine W. Swinkels, Klaus Schwarz
Publikováno v:
Journal of Molecular Medicine-Jmm, 89, 8, pp. 811-6
Journal of Molecular Medicine-Jmm, 89, 811-6
Journal of Molecular Medicine-Jmm, 89, 811-6
Contains fulltext : 95939.pdf (Publisher’s version ) (Closed access) Congenital dyserythropoietic anaemias (CDAs) are heterogeneous, hereditary disorders hallmarked by ineffective erythropoiesis and tissue iron overload. Growth differentiation fact
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7f84b6428c867d9bbb3e5a41187fbc29
https://doi.org/10.1007/s00109-011-0751-5
https://doi.org/10.1007/s00109-011-0751-5
Autor:
Katarzyna Mleczko-Sanecka, Steven Dooley, A Müller, Guillem Casanovas, Martina U. Muckenthaler, Matthias W. Hentze, Anan Ragab, Michael Boutros, Katja Breitkopf
Publikováno v:
Blood. 115:2657-2665
Hepcidin is the master regulatory hormone of systemic iron metabolism. Hepcidin deficiency causes common iron overload syndromes whereas its overexpression is responsible for microcytic anemias. Hepcidin transcription is activated by the bone morphog
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1bb599b1f5b4a37e44048eae63e60e62
https://doi.org/10.1182/blood-2009-09-238105
https://doi.org/10.1182/blood-2009-09-238105
Autor:
Maria Vittoria Verga Falzacappa, Guillem Casanovas, Georgia G. Braliou, George Simos, Martina U. Muckenthaler, Georgia Chachami
Publikováno v:
Journal of Hepatology. 48:801-810
Background/Aims Hepcidin is a liver-produced hormone that regulates systemic iron homeostasis. Hepcidin expression is stimulated upon iron overload or inflammation while iron deficiency, anemia and tissue hypoxia are negative regulators. We investiga
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bb0b06b7f6b5fd5be16825655822537c
https://doi.org/10.1016/j.jhep.2007.12.021
https://doi.org/10.1016/j.jhep.2007.12.021
Autor:
Sebastian Mueller, Guillem Casanovas, I. Ganzleben, Martina U. Muckenthaler, Gunda Millonig, Teresa Peccerella, Helmut-Karl Seitz
Publikováno v:
Zeitschrift für Gastroenterologie. 48
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::87099bda01a1e886381399ec5f255e86
https://doi.org/10.1055/s-0030-1263852
https://doi.org/10.1055/s-0030-1263852
Autor:
Martina U. Muckenthaler, Guillem Casanovas, Matthias W. Hentze, Katarzyna Mleczko-Sanecka, Sandro Altamura
Publikováno v:
Journal of molecular medicine (Berlin, Germany). 87(5)
The hemochromatosis proteins HFE, transferrin receptor 2 (TfR2) and hemojuvelin (HJV, HFE2) positively control expression of the major iron regulatory hormone hepcidin. HJV is a bone morphogenetic protein (BMP) co-receptor that enhances the cellular
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::faaaa3d85fb0099b1f115d1fc1fc089e
https://pubmed.ncbi.nlm.nih.gov/19238343
https://pubmed.ncbi.nlm.nih.gov/19238343