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Shizuo Akira

Researcher at Osaka University

Publications -  1330
Citations -  344469

Shizuo Akira is an academic researcher from Osaka University. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 261, co-authored 1308 publications receiving 320561 citations. Previous affiliations of Shizuo Akira include University of California, Berkeley & Wakayama Medical University.

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Deletion of the Kinase Domain in Death-Associated Protein Kinase Attenuates Tubular Cell Apoptosis in Renal Ischemia-Reperfusion Injury

TL;DR: Results indicate that deletion of the kinase domain from DAPK molecule can attenuate tubular cell apoptosis and renal dysfunction after IR injury and are consistent with the theory that D APK activity stabilizes p53 protein.
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Augmentation of haptoglobin production in Hep3B cell line by a nuclear factor NF‐IL6

TL;DR: Evidence is obtained for the involvement of NF‐IL6 in the induction of acute‐phase proteins by introducing the nuclear factor and its truncated mutant gene into a hepatoma cell line Hep3B, which blocked the production of haptoglobin, fibrinogen and albumin.
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Molecular Cloning of the cDNAs for Interleukin‐6/B Cell Stimulatory Factor 2 and Its Receptor

TL;DR: The molecular cloning of the cDNAs encoding human BSF-2, IFN-/32, and 26 kDa proteine revealed that all these molecules were identical; therefore, this molecule is now called IL-6.
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Bacterial endotoxin induces IL-20 expression in the glial cells.

TL;DR: Bacterial lipopolysaccharide induced IL-20 expression in the primary cultured glial cells and RAW264.7 macrophage cell line suggested to play a crucial role in inflammatory conditions in the brain and to be regulated by a negative feedback loop mediated through glucocorticoids.
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Nonredundant roles of TIRAP and MyD88 in airway response to endotoxin, independent of TRIF, IL-1 and IL-18 pathways.

TL;DR: It is demonstrated that endotoxin-induced acute bronchoconstriction, vascular damage resulting in protein leak, Th1 cytokine and chemokine secretion and neutrophil recruitment in the airways are abrogated in mice deficient for either TIRAP or MyD88, but not in TRIF deficient mice.