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Friedrich Koch-Nolte

Researcher at University of Hamburg

Publications -  243
Citations -  11797

Friedrich Koch-Nolte is an academic researcher from University of Hamburg. The author has contributed to research in topics: NAD+ kinase & Gene. The author has an hindex of 51, co-authored 224 publications receiving 9867 citations. Previous affiliations of Friedrich Koch-Nolte include French Institute of Health and Medical Research & University of Rouen.

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CD38 exacerbates focal cytokine production, postischemic inflammation and brain injury after focal cerebral ischemia.

TL;DR: CD38 is differentially regulated following stroke and its deficiency attenuates the postischemic chemokine production, the immune cell infiltration and the cerebral injury after temporary ischemia and reperfusion, and might prove a therapeutic target in ischemic stroke.
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ZBP1 subcellular localization and association with stress granules is controlled by its Z-DNA binding domains

TL;DR: It is shown that both Zα domains can bind Z-DNA independently and that substrate binding is greatly enhanced when both domains are linked, and Polysome stabilization led to the disassembly of ZBP1ΔZα granules, indicating that mRNA are integral components.
Journal Article

A New Monoclonal Antibody Detects a Developmentally Regulated Mouse Ecto-ADP-Ribosyltransferase on T Cells: Subset Distribution, Inbred Strain Variation, and Modulation Upon T Cell Activation

TL;DR: It is shown that ART2.2 is expressed as a GPI-anchored protein on the surface of mature T cells in the mouse, and Nika102 thus defines a new differentiation/activation marker of thymic and postthymic T cellsIn the mouse and should be useful for further elucidating the function of the ART 2.2 cell surface enzyme.
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Rapid Induction of Naive T Cell Apoptosis by Ecto-Nicotinamide Adenine Dinucleotide: Requirement for Mono(ADP-Ribosyl)Transferase 2 and a Downstream Effector

TL;DR: It is reported here that extracellular NAD induces apoptosis in BALB/c splenic T cells with an IC50 of 3–5 μM and it is proposed that one of these is cell surface ART2.2 activity (defective in the NZW parent), the other a downstream effector of ADP-ribosylation (defected in the C57BL/6 parent).
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Emerging functions of extracellular pyridine nucleotides.

TL;DR: Findings have opened the door to a new field of research aimed at elucidating the contribution of extracellular pyridine nucleotides in physiological signaling pathways and pathological conditions.