T
Thomas Stamminger
Researcher at University of Erlangen-Nuremberg
Publications - 156
Citations - 8534
Thomas Stamminger is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Human cytomegalovirus & Viral replication. The author has an hindex of 52, co-authored 144 publications receiving 7844 citations.
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Journal ArticleDOI
The Antiviral Activities of Artemisinin and Artesunate
Thomas Efferth,Marta R. Romero,Marta R. Romero,Dana G. Wolf,Thomas Stamminger,Jose J.G. Marin,Manfred Marschall +6 more
TL;DR: Analysis of the complete profile of the pharmacological activities and molecular modes of action of artemisinin and artesunate and their performance in clinical trials will further elucidate the full antimicrobial potential of these versatile pharmacological tools from nature.
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PML Contributes to a Cellular Mechanism of Repression of Herpes Simplex Virus Type 1 Infection That Is Inactivated by ICP0
TL;DR: PML contributes to a cellular antiviral repression mechanism that is countered by the activity of ICP0, and it is demonstrated that depletion of PML increases both gene expression and plaque formation by an I CP0-negative HSV-1 mutant, while having no effect on wild-type HSVs.
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Enhancement of cytotoxicity of artemisinins toward cancer cells by ferrous iron.
Thomas Efferth,A. Benakis,Marta R. Romero,Maja T. Tomicic,Rolf Rauh,Daniel Steinbach,Ralf Häfer,Thomas Stamminger,Franz Oesch,Bernd Kaina,Manfred Marschall +10 more
TL;DR: Treatment of p53 wild-type TK6 and p53 mutated WTK1 lymphoblastic cells showed that mutational status of the tumor suppressor p53 did not influence sensitivity to artesunate, indicating that artemisinins plus ferrous iron may affect tumor cells more than normal cells.
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The nuclear domain 10 (nd10) is disrupted by the human cytomegalovirus gene product ie1
TL;DR: The disruption of ND10 by HCMV IE1 is very similar to that described for HSV-1 ICP0, and although there is no sequence similarity between proteins, this observation might suggest similar functions in virus-host interactions.
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Evidence for a Role of the Cellular ND10 Protein PML in Mediating Intrinsic Immunity against Human Cytomegalovirus Infections
TL;DR: Results strongly suggest that PML functions as part of an intrinsic immune mechanism against cytomegalovirus infections, and that the depletion of PML augments the initiation of viral IE gene expression.