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Nobuhiko Kayagaki

Researcher at Juntendo University

Publications -  69
Citations -  9921

Nobuhiko Kayagaki is an academic researcher from Juntendo University. The author has contributed to research in topics: Fas ligand & Apoptosis. The author has an hindex of 44, co-authored 68 publications receiving 9682 citations. Previous affiliations of Nobuhiko Kayagaki include University of Yamanashi.

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Metalloproteinase-mediated release of human Fas ligand.

TL;DR: Results indicate that human FasL is efficiently released from the cell surface by metalloproteinases like TNF.
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Involvement of tumor necrosis factor-related apoptosis-inducing ligand in surveillance of tumor metastasis by liver natural killer cells.

TL;DR: It is reported that TRAIL is constitutively expressed on murine natural killer cells in the liver and plays a substantial role in suppressing tumor metastasis and provides the first evidence for the physiological function of TRAIL as a tumor suppressor.
Journal Article

[Metalloproteinase-mediated release of human fas ligand].

TL;DR: In this article, metalloproteinase-mediated release of Fas ligand and its clinical relevance are discussed, and it has been recently reported that human FasL was released as a 26 kD soluble form from COS cells transfected with human Fasl cDNA and activated human T cells.
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Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand (Trail) Contributes to Interferon γ–Dependent Natural Killer Cell Protection from Tumor Metastasis

TL;DR: The in vivo induction of mouse TRAIL expression on various tissue NK cells is demonstrated and correlated NK cell activation with TRAIL-mediated antimetastatic function in vivo, indicating that TRAIL induction on NK cells plays a critical role in IFN-γ–mediated antimETastatic effects of IL-12 and α-GalCer.
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Type I Interferons (IFNs) Regulate Tumor Necrosis Factor–related Apoptosis-inducing Ligand (TRAIL) Expression on Human T Cells: A Novel Mechanism for the Antitumor Effects of Type I IFNs

TL;DR: Type I IFNs substantially augmented cytotoxic activity of anti-CD3–stimulated PBT cells against RCC cell lines in a TRAIL-dependent manner, which may be involved in the antitumor effects of type IIFNs against various tumors.