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Myc inhibits JNK-mediated cell death in vivo

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Abstract

The proto-oncogene Myc is well known for its roles in promoting cell growth, proliferation and apoptosis. However, in this study, we found from a genetic screen that Myc inhibits, rather than promotes, cell death triggered by c-Jun N-terminal kinase (JNK) signaling in Drosophila. Firstly, expression of Drosophila Myc (dMyc) suppresses, whereas loss of dMyc enhances, ectopically activated JNK signaling-induced cell death. Secondly, dMyc impedes physiologically activated JNK pathway-mediated cell death. Thirdly, loss of dMyc triggers JNK pathway activation and JNK-dependent cell death. Finally, the mammalian cMyc gene, when expressed in Drosophila, impedes activated JNK signaling-induced cell death. Thus, besides its well-studied apoptosis promoting function, Myc also antagonizes JNK-mediated cell death in Drosophila, and this function is likely conserved from fly to human.

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Acknowledgements

We thank Dr. Peter Gallant, the Bloomington Drosophila Stock Center, Vienna Drosophila Research Center and National Institute of Genetics (NIG-FLY) for fly stocks, members of the Xue laboratory for comments and discussion. This work is supported by the National Natural Science Foundation of China (31371490, 31571516) and Shanghai Committee of Science and Technology (09DZ2260100, 14JC1406000).

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Huang, J., Feng, Y., Chen, X. et al. Myc inhibits JNK-mediated cell death in vivo. Apoptosis 22, 479–490 (2017). https://doi.org/10.1007/s10495-016-1340-4

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