FLCN and AMPK modulate resistance to hyperosmotic stress

New research from Possik et al. (2015) has found that flcn-1 loss in C.elegans results in increased AMPK signalling and the accumulation of glycogen reserves. The rapid degradation of these reserves into the organic osmolyte glycerol confers greater resistance to hyperosmotic stress. Increased levels of glycogen have also been identified in the kidneys of Flcn-null mice. This work suggests that increased glycogen production in FLCN-null cells could have dual roles in tumourigenesis acting both as a source of energy and osmolytes.

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