The problem of pyridinyl imidazole class inhibitors of MAPK14/p38α and MAPK11/p38β in autophagy research

被引:23
|
作者
Menon, Manoj B. [1 ]
Dhamija, Sonam [1 ]
Kotlyarov, Alexey [1 ]
Gaestel, Matthias [1 ]
机构
[1] Hannover Med Sch, Inst Biochem, Hannover, Germany
关键词
autophagy; LC3; MAPK11-MAPK14/p38; SB202190; SB203580; SQSTM1; vacuoles; P38-ALPHA; MAPK; TRANSCRIPTION; PATHWAY; CELLS;
D O I
10.1080/15548627.2015.1059562
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In addition to its established role in inflammation, the stress-activated p38 MAP kinase pathway plays major roles in the regulation of cell cycle, senescence, and autophagy. Robust studies could establish mechanistic links between MAPK11-MAPK14/p38 signaling and macroautophagy converging at ATG9-trafficking and BECN1 phosphorylation. However, several reports seem to monitor MAPK11-MAPK14/p38-dependence of autophagy exclusively by the use of the SB203580/SB202190 class of MAPK14/MAPK11/p38/ inhibitors. In this Letter to the editor we present data to support our claim that these inhibitors interfere with autophagic flux in a MAPK11-MAPK14/p38-independent manner and hence should no longer be used as pharmacological tools in the analysis of MAPK11-MAPK14/p38-dependence of autophagy. We propose a general guideline from Autophagy with regard to this issue to avoid such misinterpretations in the future.
引用
收藏
页码:1425 / 1427
页数:3
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