The Japanese Biochemical Society

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[3T08a-09(3P-168)] Nuclear pores establish TP53 degradation platform through CRM1-mediated proteasome targeting in wild-type p53 glioblastoma

Ikliptikawati Dini Kurnia1, Kei Makiyama2, Masaharu Hazawa1,2,3, Hemragul Sabit4, Shin-ichi Horike5, Yuka Inaba6, Hiroshi Inoue6, Mitsutoshi Nakada4, Richard W. Wong1,2,3 (1.WPI Nano Life Science Institute, Kanazawa University, Kanazawa, Ishikawa, 2.Laboratory of Molecular Cell Biology, School of Natural System, Institute of Science and Engineering, Kanazawa University, Kanazawa, Ishikawa, 3.Cell-Bionomics Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Ishikawa, 4.Department of Neurosurgery, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Ishikawa, 5.Advanced Science Research Center, Institute for Gene Research, Kanazawa University, Kanazawa, Ishikawa, 6.Metabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Ishikawa)

キーテクノロジー:proteomic and imaging

glioblastoma、p53、MDM2、NUP107、CRM1

kdini96@gmail.com

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