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Yuichi Kitai

Researcher at Hokkaido University

Publications -  41
Citations -  691

Yuichi Kitai is an academic researcher from Hokkaido University. The author has contributed to research in topics: Signal transducing adaptor protein & Medicine. The author has an hindex of 9, co-authored 31 publications receiving 407 citations. Previous affiliations of Yuichi Kitai include Nara Institute of Science and Technology.

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DNA-Containing Exosomes Derived from Cancer Cells Treated with Topotecan Activate a STING-Dependent Pathway and Reinforce Antitumor Immunity

TL;DR: In this article, the authors show that TPT-treated cancer cells release exosomes that contain DNA that activate dendritic cells via STING signaling, and that a STING-dependent pathway drives antitumor immunity by responding to tumor cell-derived DNA.

DNA-containing exosomes derived from cancer cells treated with Topotecan activate a STING-dependent pathway and reinforce antitumor immunity

TL;DR: It is shown that treatment of breast cancer cells with the antitumor agent topotecan (TPT), an inhibitor of topoisomerase I, induces danger-associated molecular pattern secretion that triggers dendritic cell activation and cytokine production, suggesting that a STING-dependent pathway drives antitumors immunity by responding to tumor cell–derived DNA.
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IL-17A plays a central role in the expression of psoriasis signature genes through the induction of IκB-ζ in keratinocytes

TL;DR: Novel in vitro data from normal human keratinocytes are presented that would help elucidating the IL-17A-driven keratinocyte activation in psoriasis.
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Intravesicular Acidification Regulates Lipopolysaccharide Inflammation and Tolerance through TLR4 Trafficking.

TL;DR: It is suggested that ATP6V0D2-dependent intravesicular acidification is required for TLR4 internalization, which is associated with prevention from excessive LPS-triggered inflammation and induction of tolerance.
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STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization

TL;DR: It is shown that STAP-2 promotes tumorigenesis of prostate cancer cells through up-regulation of EGF receptor (EGFR) signaling and enhances its stability by inhibiting c-CBL–mediated EGFR ubiquitination.