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Articles by Kosuke Watari
Author Correction: Mitochondrial DNA oxidation propagates autoimmunity by enabling plasmacytoid dendritic cells to induce T FH differentiation
Correction to: Nature Immunology https://doi.org/10.1038/s41590-025-02179-7, published online 17 June 2025. In the version of this article initially published, incorrect representative images were presented in the “58 d” and “100 d” rows in Fig. 1a and the “None” row in Fig. 5q (which inadvertently duplicated the PLA (DNA/IgG) negative-control condition in Fig. 5r). The figures have been updated in the HTML and PDF versions of the article.
Self-amplifying NRF2–EZH2 epigenetic loop converts KRAS-initiated progenitors to invasive pancreatic cancer - Nature Cancer
Abstract Pancreatic ductal adenocarcinoma (PDAC) emerges from mutant KRAS-harboring but dormant low-grade pancreatic intraepithelial neoplasia (PanIN). To examine the role of oxidative stress, a putative PDAC risk factor, we established an organoid-based transformation system. Although the prototypic oxidant H2O2 induced organoid transformation, its effect was nonmutational and was mediated by the oxidant-responsive transcription factor NRF2, which induced the histone methyltransferase EZH2.
Mitochondrial DNA oxidation propagates autoimmunity by enabling plasmacytoid dendritic cells to induce TFH differentiation - Nature Immunology
Abstract Stress-induced oxidized mitochondrial DNA (Ox-mtDNA) fragments enter the cytoplasm, activating the NLRP3 inflammasome and caspase-1 and enabling gasdermin-D-mediated circulatory release of mtDNA. Elevated amounts of circulating mtDNA, presumably oxidized, have been detected in older individuals and patients with metabolic or autoimmune disorders.
Author Correction: FBP1 controls liver cancer evolution from senescent MASH hepatocytes - Nature
Correction to: Nature https://doi.org/10.1038/s41586-024-08317-9 Published online 1 January 2025 In the version of the article initially published, Yahui Zhu was wrongly listed as being affiliated with the Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA, USA. Additionally, in Extended Data Fig.
FBP1 is a nonenzymatic safety valve that curtails AKT activation to prevent insulin hyperresponsiveness
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Oxidized DNA fragments exit mitochondria via mPTP- and VDAC-dependent channels to activate NLRP3 inflammasome and interferon signaling
Antibodies IL-1β Cell Signaling Cat#12426; RRID:AB_2313773 ASC Cell Signaling Cat#67824; RRID:AB_2313773 VDAC Cell Signaling Cat#4161; RRID:AB_10557420 Tom20 Cell Signaling Cat#42406; RRID:AB_2687663 COX1/MT-CO1 Cell Signaling Cat#62101; RRID:AB_2313773 Phospho-STING (Ser365) Cell Signaling Cat#62912; RRID:AB_2799635 cGAS Cell Signaling Cat#31659; RRID: AB_2799008 Cleaved Caspase-9 (Asp353) Cell Signaling Cat#9509; RRID: AB_2073476 Cleaved Caspase-3 (Asp175) Cell Signaling Cat#9661; RRID:...
Bidirectional Regulation between NDRG1 and GSK3β Controls Tumor Growth and Is Targeted by Differentiation Inducing Factor-1 in Glioblastoma
Molecular Cell Biology Hiroshi Ito, Kosuke Watari, Tomohiro Shibata, Tomofumi Miyamoto, Yuichi Murakami, Yukiko Nakahara, Hiroto Izumi, Hiroaki Wakimoto, Michihiko Kuwano, Tatsuya Abe and Mayumi Ono DOI: 10.1158/0008-5472.CAN-19-0438 Published January 2020 This article requires a subscription to view the full text. You may purchase access to this article or login to access your subscription using the links below.
Bi-directional regulation between NDRG1 and GSK3β controls tumor growth and is targeted by differentiation inducing factor-1 in glioblastoma
Research Article Hiroshi Ito, Kosuke Watari, Tomohiro Shibata, Tomofumi Miyamoto, Yuichi Murakami, Yukiko Nakahara, Hiroto Izumi, Hiroaki Wakimoto, Michihiko Kuwano, Tatsuya Abe and Mayumi Ono DOI: 10.1158/0008-5472.CAN-19-0438 Abstract The development of potent and selective therapeutic approaches to glioblastoma (GBM), one of the most aggressive primary brain tumors, requires identification of molecular pathways that critically regulate the survival and proliferation of GBM.
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