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Andreas von Knethen
Researcher at Kaiserslautern University of Technology
Publications - 16
Citations - 1322
Andreas von Knethen is an academic researcher from Kaiserslautern University of Technology. The author has contributed to research in topics: Apoptosis & Nitric oxide. The author has an hindex of 15, co-authored 16 publications receiving 1292 citations. Previous affiliations of Andreas von Knethen include University of Erlangen-Nuremberg.
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Nitric oxide and its role in apoptosis
TL;DR: No shares with other toxic molecules such as tumor necrosis factor-alpha the unique ability to initiate and to block apoptosis, depending on multiple variables that are being elucidated, and will determine the role of NO in apoptotic cell death.
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NF-κB and AP-1 Activation by Nitric Oxide Attenuated Apoptotic Cell Death in RAW 264.7 Macrophages
TL;DR: The importance of AP-1 for Cox-2 expression and cell protection by low-level NO was substantiated by using the extracellular signal-regulated kinase inhibitor PD98059, blocking NO-elicited Cox- 2 expression, but leaving the cytokine signal unaltered.
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Activation of the cell death program by nitric oxide involves inhibition of the proteasome.
TL;DR: It is shown that, similar to nitric oxide, treatment of macrophages with specific proteasome inhibitors, including clastolactacystin-β-lactone, induces p53 accumulation and apoptosis, suggesting thatNitric oxide may affect the activity of the proteasomes.
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Activation of Peroxisome Proliferator-Activated Receptor γ by Nitric Oxide in Monocytes/Macrophages Down-Regulates p47phox and Attenuates the Respiratory Burst
TL;DR: It is concluded that NO participates in controlling the pro- vs anti-inflammatory phenotype of macrophages by modulating PPARγ.
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Nitric oxide donors inhibit formation of the Apaf-1/caspase-9 apoptosome and activation of caspases.
TL;DR: It is suggested that NO or a metabolite acts directly at the level of the apoptosome and inhibits the sequential activation of caspases-9, -3 and -8, which are required for both stress- and receptor-induced death in cells that use the mitochondrial subroute of cell demise.