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Troglitazone-mediated sensitization to TRAIL-induced apoptosis is regulated by proteasome-dependent degradation of FLIP and ERK1/2-dependent phosphorylation of BAD

机译：Troglitazone介导的致胰腺炎凋亡的敏化是通过蛋白酶体依赖性降解的蛋白酶体依赖性降解的缺陷和ERK1 / 2依赖性磷酸化。

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Kerstin Grund; Rezvan Ahmadi; Fortunata Jung; Verena Funke; Georg Gdynia; Axel Benner; Jaromir Sykora; Henning Walczak; Stefan Joos; Jörg Felsberg; Guido Reifenberger; Otmar D. Wiestler; Christel Herold-Mende; Wilfried Roth;
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1. Troglitazone-mediated sensitization to TRAIL-induced apoptosis is regulated by proteasome-dependent degradation of FLIP and ERK1/2-dependent phosphorylation of BAD. [J] . Grund K, Ahmadi R, Jung F, Cancer biology & therapy . 2008,第12期

机译：曲格列酮介导的对TRAIL诱导的细胞凋亡的敏感性由蛋白酶体依赖的FLIP降解和ERK1 / 2依赖的BAD磷酸化调节。
2. The Third-Generation EGFR Inhibitor, Osimertinib, Promotes c-FLIP Degradation, Enhancing Apoptosis Including TRAIL-Induced Apoptosis in NSCLC Cells with Activating EGFR Mutations [J] . Puyu Shi, Shuo Zhang, Lei Zhu, Translational Oncology . 2019,第5期

机译：第三代EGFR抑制剂Osimertinib促进c-FLIP降解，增强包括TRAIL诱导的激活EGFR突变在内的NSCLC细胞的凋亡。
3. Refining the minimal sequence required for ERK1/2-dependent poly-ubiquitination and proteasome-dependent turnover of BIM [J] . Ceri M. Wiggins, Mark Johnson, Simon J. Cook Cellular Signalling . 2010,第5期

机译：完善BIM的ERK1 / 2依赖性多泛素化和蛋白酶体依赖性转换所需的最小序列
4. c-FLIP and resistance to TRAIL-induced apoptosis in pancreatic cancer. [D] . Zhang, Jing. 2006

机译：c-FLIP与TRAIL诱导的胰腺癌细胞凋亡的抗性。
5. c-FLIP Degradation Mediates Sensitization of Pancreatic Cancer Cells to TRAIL-Induced Apoptosis by the Histone Deacetylase Inhibitor LBH589 [O] . John Kauh, Songqing Fan, Mingjing Xia, 2010

机译：c-FLIP降解介导组蛋白脱乙酰基酶抑制剂LBH589诱导胰腺癌细胞对TRAIL诱导的细胞凋亡。
6. c-FLIP Degradation Mediates Sensitization of Pancreatic Cancer Cells to TRAIL-Induced Apoptosis by the Histone Deacetylase Inhibitor LBH589 [O] . Kauh, John, Fan, Songqing, Xia, Mingjing, 2010

机译：c-FLIP降解介导组蛋白脱乙酰基酶抑制剂LBH589诱导胰腺癌细胞对TRAIL诱导的细胞凋亡。

Troglitazone-mediated sensitization to TRAIL-induced apoptosis is regulated by proteasome-dependent degradation of FLIP and ERK1/2-dependent phosphorylation of BAD

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