Thomas Wirth
University of Ulm
244 Papers
1.9K Citations
Thomas Wirth is an academic researcher from University of Ulm. The author has contributed to research in topics: Transcription factor & Medicine. The author has an hindex of 61, co-authored 191 publications. Previous affiliations of Thomas Wirth include Technion – Israel Institute of Technology & Walter and Eliza Hall Institute of Medical Research.
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Papers
NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression
M. Huber,Ninel Azoitei,Bernd Baumann,Stefan Grünert,Andreas Sommer,Hubert Pehamberger,Norbert Kraut,Hartmut Beug,Thomas Wirth +8 more
TL;DR: Evidence of an essential role for NF-κB during distinct steps of breast cancer progression is provided and the cooperation of Ras- and TGF-β–dependent signaling pathways in late-stage tumorigenesis depends critically on NF-σB activity is suggested.
Hodgkin and Reed-Sternberg cells represent an expansion of a single clone originating from a germinal center B-cell with functional immunoglobulin gene rearrangements but defective immunoglobulin transcription
Theresa Marafioti,Michael Hummel,Michael Hummel,Hans-Dieter Foss,Hans-Dieter Foss,Helmut Laumen,Helmut Laumen,Korbjuhn P,Korbjuhn P,Ioannis Anagnostopoulos,Ioannis Anagnostopoulos,Hetty Lammert,Hetty Lammert,Gudrun Demel,Gudrun Demel,Jan Theil,Jan Theil,Thomas Wirth,Thomas Wirth,Harald Stein,Harald Stein +20 more
TL;DR: In this paper, a single-cell study was performed on 25 patients with Hodgkin and Reed-Sternberg (HRS) disease, with and without Epstein-Barr virus infection, for the presence of gene rearrangements.
522
Bruton's Tyrosine Kinase Is a Toll/Interleukin-1 Receptor Domain-binding Protein That Participates in Nuclear Factor κB Activation by Toll-like Receptor 4
Caroline A. Jefferies,Sarah L. Doyle,Cornelia Brunner,Aisling Dunne,Elizabeth Brint,Claudia Wietek,Eva Walch,Thomas Wirth,Luke A. J. O'Neill +8 more
TL;DR: Investigation revealed that the Btk-specific inhibitor, LFM-A13, inhibited the activation of NFκB by LPS in THP-1 cells, implicate Btk as a Toll/interleukin-1 receptor domain-binding protein that is important for NFκBs activation by TLR4.
321
Suppression of NF-κB activity by sulfasalazine is mediated by direct inhibition of IκB kinases α and β
TL;DR: Sulfasalazine is identified as a direct inhibitor of IKK-α and -β by antagonizing adenosine triphosphate binding and contributes to the well-known anti-inflammatory and immunosuppressive effects of sulfasalazines.
299