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A recently reported crystal structure has illuminated the complex regulatory mechanisms by which\n                    <jats:styled-content style=\"fixed-case\">AMP<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\n                    cause activation of\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    , involving phosphorylation by the upstream kinase\n                    <jats:styled-content style=\"fixed-case\">LKB<\/jats:styled-content>\n                    1. Once activated by falling cellular energy status,\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    activates catabolic pathways that generate\n                    <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n                    whilst inhibiting anabolic pathways and other cellular processes that consume\n                    <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n                    . A role of\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    is implicated in many human diseases. Mutations in the \u03b32 subunit cause heart disease due to excessive glycogen storage in cardiac myocytes, leading to ventricular pre\u2010excitation.\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    \u2010activating drugs reverse many of the metabolic defects associated with insulin resistance, and recent findings suggest that the insulin\u2010sensitizing effects of the widely used antidiabetic drug metformin are mediated by\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    . The upstream kinase\n                    <jats:styled-content style=\"fixed-case\">LKB<\/jats:styled-content>\n                    1 is a tumour suppressor, and\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    may exert many of its antitumour effects.\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    activation promotes the oxidative metabolism typical of quiescent cells, rather than the aerobic glycolysis observed in tumour cells and cells involved in inflammation, explaining in part why\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    activators have both antitumour and anti\u2010inflammatory effects. Salicylate (the major\n                    <jats:italic>in vivo<\/jats:italic>\n                    metabolite of aspirin) activates\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    , and this could be responsible for at least some of the anticancer and anti\u2010inflammatory effects of aspirin. In addition to metformin and salicylates, novel drugs that modulate\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    are likely to enter clinical trials soon. Finally,\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    may be involved in viral infection: downregulation of\n                    <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\n                    during hepatitis C virus infection appears to be essential for efficient viral replication.\n                  <\/jats:p>","DOI":"10.1111\/joim.12268","type":"journal-article","created":{"date-parts":[[2014,5,13]],"date-time":"2014-05-13T12:44:40Z","timestamp":1399985080000},"page":"543-559","source":"Crossref","is-referenced-by-count":265,"title":["<scp>AMP<\/scp>\n                    \u2010activated protein kinase: a key regulator of energy balance with many roles in human disease"],"prefix":"10.1111","volume":"276","author":[{"given":"D.","family":"Grahame Hardie","sequence":"first","affiliation":[{"name":"Division of Cell Signalling and Immunology College of Life Sciences University of Dundee 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