Rchr
J-GLOBAL ID:201801010891654506   Update date: May. 17, 2024

Hirayama Shoshiro

Hirayama Shoshiro
Research field  (1): Cell biology
Research keywords  (5): Proteolysis ,  Genome wide screening ,  proteasome ,  ubiquitin ,  Protein quality control
Research theme for competitive and other funds  (3):
  • 2022 - 2024 Elucidation of an ESCRT complex-dependent microautophagy/proteasome sorting mechanism
  • 2019 - 2022 Elucidation of the nuclear export mechanism of ubiquitinated proteins
  • 2016 - 2018 Nuclear export mechanism of misfolded proteins
Papers (16):
  • Tomohiro Iriki, Hiroaki Iio, Shu Yasuda, Shun Masuta, Masakazu Kato, Hidetaka Kosako, Shoshiro Hirayama, Akinori Endo, Fumiaki Ohtake, Mako Kamiya, et al. Senescent cells form nuclear foci that contain the 26S proteasome. Cell reports. 2023. 112880-112880
  • Natsuki Shinoda, Misuzu Horikoshi, Yusuke Taira, Masaya Muramoto, Shoshiro Hirayama, Shigeo Murata, Masayuki Miura. Caspase cleaves Drosophila BubR1 to modulate spindle assembly checkpoint function and lifespan of the organism. The FEBS journal. 2023
  • Eiichi Hashimoto, Shota Okuno, Shoshiro Hirayama, Yoshiyuki Arata, Tsuyoshi Goto, Hidetaka Kosako, Jun Hamazaki, Shigeo Murata. Enhanced O-GlcNAcylation Mediates Cytoprotection under Proteasome Impairment by Promoting Proteasome Turnover in Cancer Cells. iScience. 2020. 23. 7. 101299-101299
  • Yoshiyuki Arata, Ayaka Watanabe, Ryo Motosugi, Ryuichi Murakami, Tsuyoshi Goto, Shohei Hori, Shoshiro Hirayama, Jun Hamazaki, Shigeo Murata. Defective induction of the proteasome associated with T-cell receptor signaling underlies T-cell senescence. Genes to Cells. 2019. 24. 12. 801-813
  • Arata Y, Watanabe A, Motosugi R, Iemura SI, Natsume T, Mukai K, Taguchi T, Hirayama S, Hamazaki J, Murata S. FAM48A mediates compensatory autophagy induced by proteasome impairment. Genes to cells. 2019. 24. 8. 559-568
more...
MISC (3):
  • Shoshiro Hirayama, Yuji Yamazaki, Akira Kitamura, Yukako Oda, Daisuke Morito, Katsuya Okawa, Hiroshi Kimura, Douglas M. Cyr, Hiroshi Kubota, Kazuhiro Nagata. マックジック-カウフマン病タンパク質は細胞質と中心体を素早く行き来し,その疾患原因変異体タンパク質は品質管理E3 リガーゼCHIP により素早く分解される. 第40 回日本発生生物学会・第59 回日本細胞生物学会合同大会,福岡市,2007.5.28-30. 2007
  • 平山尚志郎, 山崎祐自, 北村朗, 小田祐香子, 森戸大介, 大川克也, 木村宏, 久保田広志, 永田和宏. McKusick-Kaufman syndromeタンパク質の疾患原因変異体はE3リガーゼCHIPを介してユビキチン-プロテアソーム系で素早く分解される. 臨床ストレス応答学会大会抄録集. 2006. 1st
  • Hiroshi Kubota, Yuji Yamazaki, Akira Kitamura, Yukako Oda, Shoshiro Hirayama, Kazuhiro Nagata. Mckusich- Kaufman syndrome gene product is a chaperonin-like molecule abundan in the centrosome and degraded upon disease-causing mutation. 第58 回日本細胞生物学会大会, さいたま市, 2005. 6. 14-17. 2005
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