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Dominik Schmiedel
Researcher at Hebrew University of Jerusalem
Publications - 22
Citations - 521
Dominik Schmiedel is an academic researcher from Hebrew University of Jerusalem. The author has contributed to research in topics: Immune system & NKG2D. The author has an hindex of 10, co-authored 15 publications receiving 351 citations. Previous affiliations of Dominik Schmiedel include Fraunhofer Society.
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Journal ArticleDOI
NKG2D Ligands-Critical Targets for Cancer Immune Escape and Therapy.
TL;DR: The post-transcriptional and post- translational mechanisms by which NKG2D ligands are modulated in cancer cells and their impact on patient prognosis are reviewed and controversies and approaches are discussed to apply the understanding of the NKG 2D ligand/NKG2 D-axis for cancer therapy.
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Dynamic Co-evolution of Host and Pathogen: HCMV Downregulates the Prevalent Allele MICA∗008 to Escape Elimination by NK Cells
Einat Seidel,Vu Thuy Khanh Le,Yotam Bar-On,Pinchas Tsukerman,Jonatan Enk,Rachel Yamin,Natan Stein,Dominik Schmiedel,Esther Djian,Yiska Weisblum,Boaz Tirosh,Peter Stastny,Dana G. Wolf,Hartmut Hengel,Ofer Mandelboim +14 more
TL;DR: It is shown that HCMV uses its viral glycoprotein US9 to specifically target MICA*008 and thus escapes NKG2D attack and illustrates the dynamic co-evolution of host and pathogen.
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The RNA binding protein IMP3 facilitates tumor immune escape by downregulating the stress-induced ligands ULPB2 and MICB
TL;DR: It is discovered that IMP3 indirectly targets MICB with a mechanism functionally distinct from that of ULBP2, and IMP3-mediated regulation of stress-ligands leads to impaired NK cell recognition of transformed cells.
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MiR-520d-5p directly targets TWIST1 and downregulates the metastamiR miR-10b
Pinchas Tsukerman,Rachel Yamin,Einat Seidel,Saleh Khawaled,Dominik Schmiedel,Tomer Bar-Mag,Ofer Mandelboim +6 more
TL;DR: It is shown that the miR-520d-5p-mediated decrease of TWIST1 expression results in reduced expression of one of its targets, miB-10b, and in the restoration of E-Cadherin expression, which in turnresults in reduced cellular motility and invasiveness.
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Human cytomegalovirus escapes immune recognition by NK cells through the downregulation of B7-H6 by the viral genes US18 and US20.
Yoav Charpak-Amikam,Tobias Kubsch,Einat Seidel,Esther Oiknine-Djian,Noemi Cavaletto,Rachel Yamin,Rachel Yamin,Dominik Schmiedel,Dana G. Wolf,Giorgio Gribaudo,Martin Messerle,Luka Cicin-Sain,Ofer Mandelboim +12 more
TL;DR: It is demonstrated that the expression of B7-H6 is upregulated following H CMV infection and that HCMV uses two of its genes: US18 and US20, to interfere with B7/H6 surface expression, in a mechanism involving endosomal degradation, in order to evade NK cell recognition.