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. 2020 Aug 17;13:113. doi: 10.1186/s13045-020-00949-4

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — AMPK regulates differentially hyperactive Ras/RAF/MEK/ERK (MAPK) signaling in Ras- versus BRAF(V600E)-mutated cancers. a In Ras-mutated cancers, the C-terminal 14-3-3 binding site of CRAF is phosphorylated by AMPK, which facilitates CRAF dimerization through improving the association of CRAF dimer with 14-3-3 dimer and thus elevates the activity of CRAF, particularly upon RAF inhibitor treatment or metabolic stress. Under these conditions, CRAF forms homodimers with itself or heterodimers with KSR or BRAF. b In BRAF(V600E)-harboring cancers, AMPK phosphorylates the C-terminal 14-3-3 binding site of BRAF(V600E), which prevents BRAF(V600E) dimerization with KSR through enhancing the association of a single BRAF(V600E) molecule with 14-3-3 dimer and thus blocks the activity of BRAF(V600E) upon metabolic stress