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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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Bacterial recognition by TLR7 in the lysosomes of conventional dendritic cells

TL;DR: This work shows that phagosomal bacteria such as group B streptococcus, but not cytosolic bacteria, potently induced interferon in conventional dendritic cells by a mechanism that required Toll-like receptor 7, the adaptor MyD88 and the transcription factor IRF1, all of which localized together with bacterial products in degradative vacuoles bearing lysosomal markers.
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Integral role of Noxa in p53-mediated apoptotic response

TL;DR: Noxa(-/-) mice showed resistance to X-ray irradiation-induced gastrointestinal death, accompanied with impaired apoptosis of the epithelial cells of small intestinal crypts, indicating the contribution of Noxa to the p53 response in vivo.
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Toll‐Like Receptors

TL;DR: Mammalian TLRs (TLR1 to 13) that have an essential role in the innate immune recognition of microorganisms are discussed, and TLR‐mediated signaling pathways and antibodies that are available to detect specific TLRs are discussed.
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Toll-like receptor-mediated regulation of zinc homeostasis influences dendritic cell function.

TL;DR: It is shown that stimulation with the Toll-like receptor 4 agonist lipopolysaccharide (LPS) altered the expression of zinc transporters in dendritic cells and thereby decreased intracellular free zinc, establishing a link between Toll- like receptor signaling and zinc homeostasis.
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Ectopic expression of CHOP (GADD153) induces apoptosis in M1 myeloblastic leukemia cells.

TL;DR: The results indicate that CHOP can induce apoptosis in a p53‐independent manner and requires leucine zipper domain but neither intact basic region nor trans‐activation domain.