Targeting p38 or MK2 Enhances the Anti-Leukemic Activity of Smac-Mimetics
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- 作者：Najoua Lalaoui1 ; 2 ; Kay Hä ; nggi3 ; Gabriela Brumatti1 ; 2 ; Diep Chau1 ; 2 ; Nhu-Y.N. Nguyen4 ; 5 ; Lazaros Vasilikos3 ; Lisanne M. Spilgies3 ; Denise A. Heckmann1 ; 2 ; Chunyan Ma1 ; 2 ; Margherita Ghisi6 ; 7 ; Jessica M. Salmon6 ; 7 ; Geoffrey M. Matthews6 ; 7 ; Elisha de Valle8 ; 9 ; Donia M. Moujalled4 ; 5 ; Manoj B. Menon10 ; Sukhdeep Kaur Spall1 ; 2 ; Stefan P. Glaser1 ; 2 ; Jennifer Richmond11 ; Richard B. Lock11 ; Stephen M. Condon12 ; Raffi Gugasyan8 ; 9 ; Matthias Gaestel10 ; Mark Guthridge4 ; 5 ; Ricky W. Johnstone6 ; 7 ; Lenka Munoz13 ; Andrew Wei4 ; 5 ; Paul G. Ekert1 ; 14 ; 15 ; David L. Vaux1 ; 2 ; W. Wei-Lynn Wong3 ; John Silke1 ; 2 ; silke@wehi.edu.au" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cancer Cell
- 出版年：2016
- 出版时间：8 February 2016
- 年：2016
- 卷：29
- 期：2
- 页码：145-158
- 全文大小：2667 K
文摘
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Genetic loss or chemical inhibition of p38 or MK2 increases SM-induced TNF
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p38 and MK2 inhibit SM-induced phosphorylation of JNK and ERK
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The combination of SM and p38 inhibitor is well tolerated in vivo
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p38 and MK2 inhibitors potentiate SM killing of AML in vivo