◀ Back to PRKAB1

NSD1 — PRKAB1

Text-mined interactions from Literome

Hawley et al., Cell Metab 2005 : K ( + ) -induced depolarization in rat cerebrocortical slices, which increases intracellular Ca2+ without disturbing cellular adenine nucleotide levels, activates AMPK , and this is blocked by STO-609
Jensen et al., Am J Physiol Endocrinol Metab 2007 : Similar to KN-93, the CaMKK inhibitor STO-609 strongly reduced AMPK phosphorylation and activity at 2 min and less potently at 10 min. Pretreatment with STO-609 inhibited contraction stimulated glucose uptake at 2 min in soleus, but not EDL, and in both muscles after 10 min ... Finally, neither KN-93 nor STO-609 had effects on the reductions in glucose uptake seen in mice overexpressing a kinase-dead AMPK construct, indicating that the effects of KN-93 and STO-609 on glucose uptake require inhibition of AMPK activity
Mount et al., Atherosclerosis 2008 : Activation of AMPK by BK in BAECs was inhibited by STO-609 , an inhibitor of calmodulin dependent kinase kinase ( CaMKK ), which is a known kinase upstream of AMPK
Kim et al., J Agric Food Chem 2009 (Colonic Neoplasms) : STO-609 , CAMKs inhibitor, also attenuated CK-induced AMPK activation and apoptosis
Miranda et al., Biochem Biophys Res Commun 2010 : Indeed, hypertonicity induced AMPK activation was markedly reduced by the STO-609 CaMKKbeta inhibitor, as was the increase in MLC and cofilin phosphorylation
Lee et al., Bone 2010 (Bone Resorption) : STO-609 , an inhibitor of CaMKK, completely blocked the RANKL induced activation of AMPK-a , but KN-93, an inhibitor of CaMK, did not