换一批Spy1 induces de-ubiquitinating of RIP1 arrest and confers glioblastoma's resistance to tumor necrosis factor (TNF-α)-induced apoptosis through suppressing the association of CLIPR-59 and CYLD.
第一作者：
Zongmei,Ding
第一单位：
a Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target; Nantong University ; Nantong , Jiangsu , PR China.
作者：
关键词
CLIPR-59CLIPR-59, CLIP-170-related 59?kDa proteinFADD, Fas-associated protein with death domainGAPDH, glyceraldehyde 3-phosphate dehydrogenaseGBM glioblastoma multiformeGliomaRIP1RIP1, receptor-interacting protein 1Spy1Spy1, speedy inducer of meiotic maturationTNF-αTNFR1, TNF-receptor-type 1TRADD, TNF receptor-associated death domain proteinapoptosis
医学主题词
细胞凋亡(Apoptosis);细胞周期蛋白质类(Cell Cycle Proteins);细胞系, 肿瘤(Cell Line, Tumor);抗药性, 肿瘤(Drug Resistance, Neoplasm);胶质母细胞瘤(Glioblastoma);HEK293细胞(HEK293 Cells);人类(Humans);微管相关蛋白质类(Microtubule-Associated Proteins);核孔复合蛋白质类(Nuclear Pore Complex Proteins);RNA结合蛋白质类(RNA-Binding Proteins);肿瘤坏死因子α(Tumor Necrosis Factor-alpha);肿瘤抑制蛋白质类(Tumor Suppressor Proteins);泛素化(Ubiquitination)
DOI
10.1080/15384101.2015.1041688
PMID
26017671
发布时间
2021-01-14
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Cell cycle (Georgetown, Tex.)
2149-59页
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