M
M. Lienhard Schmitz
Researcher at University of Giessen
Publications - 142
Citations - 10172
M. Lienhard Schmitz is an academic researcher from University of Giessen. The author has contributed to research in topics: Transcription factor & Phosphorylation. The author has an hindex of 48, co-authored 130 publications receiving 9354 citations. Previous affiliations of M. Lienhard Schmitz include University of Freiburg & German Cancer Research Center.
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Journal ArticleDOI
p38 and Extracellular Signal-regulated Kinase Mitogen-activated Protein Kinase Pathways Are Required for Nuclear Factor-κB p65 Transactivation Mediated by Tumor Necrosis Factor
Wim Vanden Berghe,Stéphane Plaisance,Elke Boone,Karolien De Bosscher,M. Lienhard Schmitz,Walter Fiers,Guy Haegeman +6 more
TL;DR: It is concluded that, in addition to cytoplasmic activation and DNA binding of NF-κB, the p38 and extracellular signal-regulated kinase MAPK pathways act as necessary cooperative mechanisms to regulate TNF-induced IL-6 gene expression by modulating the transactivation machinery.
Journal ArticleDOI
Regulation of p53 activity by its interaction with homeodomain-interacting protein kinase-2
Thomas G. Hofmann,Andreas Möller,Hüseyin Sirma,Hanswalter Zentgraf,Yoichi Taya,Wulf Dröge,Hans Will,M. Lienhard Schmitz +7 more
TL;DR: It is demonstrated that the human serine/threonine kinase homeodomain-interacting protein kinase-2 colocalizes and interacts with p53 and CREB-binding protein (CBP) within promyelocytic leukaemia (PML) nuclear bodies and implies that HIPK2 is a novel regulator of p53 effector functions involved in cell growth, proliferation and apoptosis.
Journal Article
The Antiinflammatory Sesquiterpene Lactone Parthenolide Inhibits NF-κB by Targeting the IκB Kinase Complex
TL;DR: The sesquiterpene lactone parthenolide could serve as a lead compound for the development of antiinflammatory remedies and is suitable as a molecular tool, allowing the dissection of TNF-α-derived signaling pathways leading to the activation of NF-κB, c-Jun N-terminal kinase, and p38.
Journal ArticleDOI
Glucocorticoid-mediated repression of nuclear factor-κBdependent transcription involves direct interference with transactivation
Karolien De Bosscher,M. Lienhard Schmitz,Wim Vanden Berghe,Stéphane Plaisance,Walter Fiers,Guy Haegeman +5 more
TL;DR: Upon investigating DEX-mediated repression of interleukin-6 expression induced by tumor necrosis factor, DEX treatment was found to act directly on NF-kappaB-dependent transcription, without changing the expression level of IkappaB.
PatentDOI
SESQUITERPENE LACTONES SPECIFICALLY INHIBIT ACTIVATION OF NF-λB BY PREVENTING THE DEGRADATION OF IλB-α AND IλB-$g(b)
TL;DR: Inhibition of NF-κB by SLs resulted in an enhanced cell killing of murine fibroblast cells by tumor necrosis factor-α and the analysis of the cellular redox state by fluorescence-activated cell sorter showed that the SLs had no direct or indirect anti-oxidant properties.