◀ Back to CALM1
CALM1 — NSD1
Text-mined interactions from Literome
Monteiro et al., Drug Metab Dispos 2008
(Calcium Signaling) :
This study was designed to analyze the effects of the
Ca2+/calmodulin dependent protein kinase kinase ( CaMKK ) inhibitor
STO-609 ( 7-oxo-7H-benzimidazo [ 2,1-a ] benz [ de ] isoquinoline-3-carboxylic acid ) toward the aryl hydrocarbon receptor (AhR) pathway because Ca2+/calmodulin dependent protein kinase ( CaMK) Ialpha, known as a downstream CaMKK effector, has been recently shown to contribute to the AhR cascade
Cook et al., American journal of physiology. Renal physiology 2009
(Necrosis) :
The specific
calcium/calmodulin dependent kinase kinase inhibitor
STO-609 failed to suppress AMPK activation, suggesting that it was not part of the signal pathway
Kou et al., J Biol Chem 2009
:
Importantly, siRNA mediated knockdown of the key AMPK kinase, calcium/calmodulin dependent protein kinase kinase beta, completely blocked simvastatin induced endothelial cell migration and also abrogated statin promoted phosphorylation of AMPK and LKB1, as did pharmacological inhibition with the specific
calcium/calmodulin dependent protein kinase beta inhibitor
STO-609
Li et al., J Surg Res 2011
(Myocardial Infarction...) :
A Ca ( 2+ )
/calmodulin dependent protein kinase kinase inhibitor
STO609 and a chelator of intracellular Ca ( 2+ ) stores BAPTA-AM also abolished the cardioprotection of morphine
Hsu et al., Cell Signal 2011
(Calcium Signaling...) :
CLA induced activation of AMPK and/or induction of apoptosis were inhibited by infection of TM4t cells with an adenovirus expressing a peptide which blocks the interaction between the G protein coupled receptor ( GPCR ) and Ga ( q ), by the phospholipase C (PLC) inhibitor U73122, by the inositol trisphosphate ( IP ( 3 ) ) receptor inhibitor 2-APB, by the
calcium/calmodulin dependent protein kinase kinase a ( CaMKK ) inhibitor
STO-609 and by the intracellular Ca ( 2+ ) chelator BAPTA-AM
Lee et al., J Biol Chem 2012
(Diabetes Mellitus, Type 1...) :
NaHS induction of AMPK phosphorylation was inhibited by siRNA for calmodulin kinase kinase ß, but not LKB1, upstream kinases for AMPK ;
STO-609 , a
calmodulin kinase kinase ß
inhibitor , had the same effect