Abstract
The two metabolic sensors AMPK and SIRT1 take center stage as Fulco et al. reveal, in this issue of Developmental Cell, the signaling mechanism by which low glucose prevents the correct development of the myogenic program. These observations may hold some therapeutic promise against muscle wasting.
MeSH terms
-
AMP-Activated Protein Kinases
-
Animals
-
Cytokines / genetics
-
Cytokines / metabolism
-
Enzyme Activation
-
Glucose / metabolism*
-
Longevity*
-
Mice
-
Multienzyme Complexes / metabolism
-
Myoblasts, Skeletal / enzymology
-
Myoblasts, Skeletal / metabolism*
-
Nicotinamide Phosphoribosyltransferase / genetics
-
Nicotinamide Phosphoribosyltransferase / metabolism
-
Protein Serine-Threonine Kinases / metabolism
-
Sirtuins / genetics
-
Sirtuins / metabolism*
Substances
-
Cytokines
-
Multienzyme Complexes
-
Nicotinamide Phosphoribosyltransferase
-
nicotinamide phosphoribosyltransferase, mouse
-
Protein Serine-Threonine Kinases
-
AMP-Activated Protein Kinases
-
Sirtuins
-
Glucose