Journal
NATURE CELL BIOLOGY
Volume 20, Issue 7, Pages 740-741Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41556-018-0120-5
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Specific combinations of mutations cause unique signalling and metabolic requirements. Concurrent G-protein a s (GNAS) and KRAS mutations in a subset of pancreatic tumours are now shown to inhibit SIK kinases through aberrant cAMP-PKA activation, triggering a metabolic program defined by lipid metabolism and fatty acid oxidation.
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