Minegishi Yoshiyuki

Research field (1)： Immunology

Research theme for competitive and other funds (21)：

2021 - 2024 新規高IgE症候群の病態形成機構の解明と治療法開発
2016 - 2019 Exome analysis identifed a molecular origin of primary immunodeficiency
2016 - 2017 Elucidation of pathophysiology of novel hyper-IgE syndrome
2015 - 2016 Development of a therapeutic genome editing for hyper-IgE syndrome
2013 - 2016 A molecular mechanism of atopic manifestations of hyper-IgE syndrome

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Papers (58)：

Minegishi Yoshiyuki. The signal transducer and activator of transcription 3 (STAT3) at the center of the causative gene network of hyper-IgE syndrome. Current Opinion in Immunology. 2023. Vol.80. No.2. 102264-102264
Yoshinaga Kaoru, Yasue Akihiro, Mitsui Akagi Silvia Naomi, Minegishi Yoshiyuki, Oyadomari Seiichi, Imoto Issei, Tanaka Eiji. Double Mutations on Tooth Development. Genes. 2023. Vol.14. No.2
Ogishi M, Augusto A, Minegishi Yoshiyuki, Boison-Dupuis S, Jean-Laurent Casanova. Impaired IL-23-dependent induction of IFN-γ underlies mycobacterial disease in patients with inherited TYK2 deficiency. The Journal of Experimental Medicine. 2022. Vol.219. No.10. e20220094-e20220094
Ichihara Aki, Yasue Akihiro, Mitsui Akagi Silvia Naomi, Arai Daishi, Minegishi Yoshiyuki, Oyadomari Seiichi, Imoto Issei, Tanaka Eiji. The C-terminal region including the MH6 domain of Msx1 regulates skeletal development. Biochemical and Biophysical Research Communications. 2020. Vol.526. No.1. 62-69
Silvia Naomi Mitsui, Akihiro Yasue, Kiyoshi Masuda, Takuya Naruto, Yoshiyuki Minegishi, Seiichi Oyadomari, Sumihare Noji, Issei Imoto, Eiji Tanaka. Novel human mutation and CRISPR/Cas genome-edited mice reveal the importance of C-terminal domain of MSX1 in tooth and palate development. Scientific Reports. 2016. 6. 38398

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MISC (355)：

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Books (2)：

Lectures and oral presentations (30)：

Exacerbation of oxazolone-induced atopic dermatitis in a mouse model of hyper-IgE syndrome
(Proceedings of the Japanese Society for Immunology, Vol.46, 2017)
Basophils promote oxazolone-induced atopic dermatitis in mouse model of hyper-IgE syndrome
(The 45th Annual Meeting of The Japanese Society for Immunology 2016)
Dysregulated IgE response in a mouse model of hyper-IgE syndrome attributed to B cell-intrincdic abnormality caused by Stat3 mutation
(Proceedings of the Japanese Society for Immunology 2016)
Analysis of a molecular mechanism underlying the susceptibility to Staphylococcus aureus infection in Hyper-IgE syndrome
(International Congress of Immunology 2016 2016)
Hyper-IgE syndrome model mice exhibit the susceptibility to Staphylococcus aureus infection
(The 44th Annual Meeting of the Japanese Society for Immunology 2015)

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