Phosphorylation of AMPK by upstream kinases is required for activity in mammalian cells.

As has been suggested previously [ 22 ], the ability of allosteric AMPK activators to stimulate non-pThr 172 complexes could be highly significant in terms of potential therapeutic strategies for activating AMPK, particularly those diseases where there is a lack of upstream AMPK kinase activity, such as loss of LKB1 in certain cancers [ 41 ].

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