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

^〇Ikliptikawati Dini Kurnia¹, Kei Makiyama², Masaharu Hazawa^1,2,3, Hemragul Sabit⁴, Shin-ichi Horike⁵, Yuka Inaba⁶, Hiroshi Inoue⁶, Mitsutoshi Nakada⁴, Richard W. Wong^1,2,3 (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