Martina U. Muckenthaler
Heidelberg University
250 Papers
1.9K Citations
Martina U. Muckenthaler is an academic researcher from Heidelberg University. The author has contributed to research in topics: Hepcidin & Medicine. The author has an hindex of 63, co-authored 219 publications. Previous affiliations of Martina U. Muckenthaler include University of Pennsylvania & Boston Children's Hospital.
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Papers
SLN124, a GalNAc conjugated 19‐mer siRNA targeting tmprss6, reduces plasma iron and increases hepcidin levels of healthy volunteers
John B. Porter,Alison Scrimgeour,Alberto Martinez,Leo James,M Aleku,Rosamund Wilson,Martina U. Muckenthaler,Malcolm Boyce,D. Wilkes,Ute Schaeper,G. Campion +10 more
TL;DR: Results suggest duration of action lasting up to 56 days after a single SLN124 dose, on hepcidin and hematological parameters of iron metabolism (serum iron and TSAT).
13
Cellular Iron Physiology
Martina U. Muckenthaler,Roland Lill +1 more
- 01 Jan 2012
TL;DR: This chapter discusses mechanisms of cellular iron uptake and release, follow iron through the cell to the places of storage and utilization, and elaborate on the mechanisms involved in two major iron-utilizing processes, heme and Fe/S protein biogenesis.
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MAP3K7 is recurrently deleted in pediatric T-lymphoblastic leukemia and affects cell proliferation independently of NF-κB
David M. Cordas dos Santos,David M. Cordas dos Santos,Juliane Eilers,Juliane Eilers,Alfonso Sosa Vizcaino,Elena Orlova,Martin Zimmermann,Martin Stanulla,Martin Schrappe,Kathleen Börner,Kathleen Börner,Dirk Grimm,Martina U. Muckenthaler,Martina U. Muckenthaler,Andreas E. Kulozik,Andreas E. Kulozik,Joachim B. Kunz,Joachim B. Kunz +17 more
TL;DR: This study revealed that the recurrent deletion of MAP3K7/CASP8AP2 is associated with SIL-TAL1 fusions and a mature immunophenotype, but not with response to treatment and risk of relapse, indicating that a residual expression of MAP 3K7 is indispensable for T-lymphoblasts.
Pediatric T-ALL type-1 and type-2 relapses develop along distinct pathways of clonal evolution
Paulina Richter-Pechanska,Joachim B. Kunz,Tobias Rausch,Büşra Erarslan-Uysal,Beat Bornhauser,Viktoras Frismantas,Yassen Assenov,Martin Zimmermann,Margit Happich,C. Von Knebel-Doeberitz,Nils von Neuhoff,Rolf Köhler,Martin Stanulla,Martin Schrappe,Gunnar Cario,Gabriele Escherich,Renate Kirschner-Schwabe,Cornelia Eckert,Smadar Avigad,Stefan M. Pfister,Martina U. Muckenthaler,Jean-Pierre Bourquin,Jan O. Korbel,Andreas E. Kulozik +23 more
TL;DR: In this article , multilevel-omics in 38 matched pairs of initial and relapsed T-ALL revealed 18 (47%) type-1 (defined by being derived from the major ancestral clone) and 20 (53%) type 2 relapses (derived from a minor ancestral clone).
Hemochromatosis proteins are dispensable for the acute hepcidin response to BMP2
Alessia Pagani,Mariateresa Pettinato,Silvia Colucci,Alessandro Dulja,Martina Rauner,Antonella Nai,Clara Camaschella,Sandro Altamura,Martina U. Muckenthaler,Laura Silvestri +9 more
TL;DR: The current model suggests that ALK2 is mainly involved in BMP6-dependent hepcidin upregulation in conditions of iron overload and is inhibited by FKBP12, whereas ALK3 maintains basal hePCidin expression and signals preferentially in response to BMP2.