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. 2019 Apr 29;294(23):9186–9197. doi: 10.1074/jbc.RA118.007122

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© 2019 Duan et al.

Published under exclusive license by The American Society for Biochemistry and Molecular Biology, Inc.

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Figure 8. — Proposed model. A, in MDM2-nonamplified A549 and U2OS cells, Nutlin activates p53 that up-regulates JMJD2B. JMJD2B demethylates H3K9me3 and H3K36me3 that are promoted by histone methyltransferases (HMT). Histone demethylation leads to transactivation of ULK1 and ATG16L1 genes that are critical for p53-mediated autophagy. B, in MDM2-amplified MHM and SJSA1 cells, Nutlin-induced p53 increases MDM2 to very high levels. High levels of MDM2 lead to degradation of JMJD2B through an unknown mechanism. Loss of JMJD2B results in increased HMT-mediated histone methylation that represses ULK1 and ATG16L1 genes leading to suppression of p53-mediated autophagy.