Activating Compound | Comment | Organism | Structure |
---|---|---|---|
5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside | activates AMPK in BMMs and RAW264.7 cells. While 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside greatly stimulates osteoclast formation, it acts through an AMPK-independent mechanism | Mus musculus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
A134974 | at 1 nM ablates the stimulatory action of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside with no effects on osteoclast formation in the absence of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside | Mus musculus | |
additional information | osteoclasts and macrophages generated from AMPK beta1-/- mice display no detectable AMPK activity | Mus musculus |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
C57BL/6J mice | - |
Mus musculus C57/BL6J | - |
C57BL/6J mice | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
bone | - |
Mus musculus | - |
additional information | present in BMM cells. Osteoclasts and macrophages lack AMPK beta2 subunit expression | Mus musculus | - |
osteoblast | - |
Mus musculus | - |
RAW-264.7 cell | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + acetyl-CoA carboxylase | - |
Mus musculus | ADP + [acetyl-CoA carboxylase]phosphate | - |
? | |
ATP + acetyl-CoA carboxylase | - |
Mus musculus C57/BL6J | ADP + [acetyl-CoA carboxylase]phosphate | - |
? |
Subunits | Comment | Organism |
---|---|---|
heterotrimer | immunoprecipitation | Mus musculus |
Synonyms | Comment | Organism |
---|---|---|
AMP-activated protein kinase | - |
Mus musculus |
AMPK | - |
Mus musculus |
IC50 Value | IC50 Value Maximum | Comment | Organism | Inhibitor | Structure |
---|---|---|---|---|---|
0.048 | - |
- |
Mus musculus | A134974 |
Organism | Comment | Expression |
---|---|---|
Mus musculus | loss of AMPK beta-subunit expression in beta1-/- and beta2-/- mice, leading to a low-bone-mass phenotype | down |
General Information | Comment | Organism |
---|---|---|
malfunction | germline deletion of either AMPK beta1 or beta2 subunit isoforms results in reduced trabecular bone density and mass, but without effects on osteoclast or osteoblast numbers, as compared to wild-type littermate controls | Mus musculus |
physiological function | AMPK is required to maintain normal bone density, but not through bone cell differentiation, and does not mediate powerful osteolytic effects of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside | Mus musculus |