T
Thomas Simmet
Researcher at University of Ulm
Publications - 211
Citations - 15559
Thomas Simmet is an academic researcher from University of Ulm. The author has contributed to research in topics: Proinflammatory cytokine & Monocyte. The author has an hindex of 54, co-authored 202 publications receiving 13691 citations. Previous affiliations of Thomas Simmet include University of Freiburg & French Institute of Health and Medical Research.
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Journal ArticleDOI
Differential expression and regulation of protease-activated receptors in human peripheral monocytes and monocyte-derived antigen-presenting cells
Renato Colognato,Joseph R. Slupsky,Marina Jendrach,Ladislav Burysek,Tatiana Syrovets,Thomas Simmet +5 more
TL;DR: It is demonstrated that differentiation of human monocytes is associated with differential expression of functionally active PARs that mediate distinct regulatory functions in inflammation and atherogenesis.
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Amino-Functionalized Polystyrene Nanoparticles Activate the NLRP3 Inflammasome in Human Macrophages
Oleg Lunov,Tatiana Syrovets,Cornelia Loos,G. Ulrich Nienhaus,G. Ulrich Nienhaus,Volker Mailänder,Katharina Landfester,Mustapha Rouis,Thomas Simmet +8 more
TL;DR: The molecular mechanism of NLRP3 inflammasome activation by amino-functionalized nanoparticles is revealed and a strategy as to how such adverse effects could be antagonized is suggested.
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PKM2 promotes tumor angiogenesis by regulating HIF-1α through NF-κB activation.
Ninel Azoitei,Alexander Becher,Konrad Steinestel,Arefeh Rouhi,Kristina Diepold,Felicitas Genze,Thomas Simmet,Thomas Seufferlein +7 more
TL;DR: This study suggests that in hypoxic pancreatic tumors PKM2 interferes both with NF-κB/p65 and HIF-1α activation that ultimately triggers VEGF-A secretion and subsequent blood vessel formation.
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Skin Levels of Arachidonic Acid-Derived Inflammatory Mediators and Histamine in Atopic Dermatitis and Psoriasis
TL;DR: The elevated levels of the potent proinflammatory and immunomodulating mediator LTB4 could be involved in the pathogenesis of cutaneous inflammation in atopic dermatitis and psoriasis and might explain the therapeutic efficiency of glucocorticosteroids.
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Acetyl-boswellic acids are novel catalytic inhibitors of human topoisomerases I and IIalpha.
TL;DR: This work proposes that acetyl-BA inhibit topoisomerases I and IIalpha through competition with DNA for binding to the enzyme, and demonstrates that these compounds are a unique class of dual catalytic inhibitors of human topoisomersases I or IIalpha.