D
Dirk Kuck
Researcher at German Cancer Research Center
Publications - 18
Citations - 1699
Dirk Kuck is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Helicobacter pylori & CagA. The author has an hindex of 14, co-authored 18 publications receiving 1578 citations. Previous affiliations of Dirk Kuck include Stanford University & Heidelberg University.
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Journal ArticleDOI
Involvement of the CD95 (APO-1/Fas) receptor and ligand system in Helicobacter pylori-induced gastric epithelial apoptosis.
Jochen Rudi,Dirk Kuck,S Strand,S Strand,A. von Herbay,Sara M. Mariani,Peter H. Krammer,Peter R. Galle,Peter R. Galle,Wolfgang Stremmel +9 more
TL;DR: Findings suggest that H. pylori-associated chronic gastritis involves apoptosis of gastric epithelial cells by activation of the CD95 receptor and ligand system.
Journal ArticleDOI
Diversity of Helicobacter pylori vacA and cagA Genes and Relationship to VacA and CagA Protein Expression, Cytotoxin Production, and Associated Diseases
Jochen Rudi,Christof Kolb,Matthias Maiwald,Dirk Kuck,Andreas Sieg,Peter R. Galle,Wolfgang Stremmel +6 more
TL;DR: H. pylori strains of vacA type s1 are associated with the occurrence of peptic ulceration and the presence of cagA, cytotoxin activity, and VacA expression.
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Vacuolating cytotoxin of Helicobacter pylori induces apoptosis in the human gastric epithelial cell line AGS.
Dirk Kuck,Bernhard Kolmerer,Christof Iking-Konert,Peter H. Krammer,Wolfgang Stremmel,Jochen Rudi +5 more
TL;DR: It is demonstrated that the vacuolating cytototoxin of H. pylori is a bacterial factor capable of inducing apoptosis in gastric epithelial cells.
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Novel and selective DNA methyltransferase inhibitors: Docking-based virtual screening and experimental evaluation.
TL;DR: These are the first small molecules reported with biochemical selectivity towards an individual DNMT enzyme capable of binding in the same pocket as the native substrate cytosine, and are promising candidates for further rational optimization and development as anticancer drugs.
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Nanaomycin A Selectively Inhibits DNMT3B and Reactivates Silenced Tumor Suppressor Genes in Human Cancer Cells
TL;DR: This work presents nanaomycin A, initially identified by a virtual screening for inhibitors against DNMT1, as a compound inducing antiproliferative effects in three different tumor cell lines originating from different tissues, establishing the possibility of selectively inhibiting individual DNMT enzymes.