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PRKAA2 — VEGFA

Text-mined interactions from Literome

Yun et al., J Biol Chem 2005 (Anoxia...) : In the present study, we examined the mechanisms of VEGF gene expression induced by glucose deprivation in cancer cells, a role of AMP activated protein kinase (AMPK) in the process, and the signal transduction pathway ... In conclusion, our results demonstrate a novel and major role of AMPK in the post-transcriptional regulation of VEGF , further implying its potential role in tumor angiogenesis
Neurath et al., Glia 2006 (Brain Neoplasms...) : The AMPK chemical inhibitor, 5-iodotubericidin, effectively repressed the hypoxic induction of VEGF mRNA levels and hypoxia inducible factor-1 dependent transcription
Lee et al., Biochem Pharmacol 2006 (Prostatic Neoplasms) : Recently, we demonstrated that AMP activated protein kinase (AMPK) , which acts as an energy sensor, providing metabolic adaptation effects under ATP deprived conditions, is critical for the expression of VEGF under oxygen- and glucose deprived conditions ... As carcinogenic metals are potent VEGF expression inducers, we hypothesized that AMPK would also play a crucial role in metal induced VEGF expression
Reihill et al., Biochem Biophys Res Commun 2007 : VEGF caused a rapid, dose dependent stimulation of AMPK activity, with a concomitant increase in phosphorylation of eNOS at Ser1177 ... VEGF stimulated AMPK activity was completely inhibited by the Ca ( 2+ ) /calmodulin dependent protein kinase kinase inhibitor, STO-609
Levine et al., J Biol Chem 2007 (Calcium Signaling) : We studied the role of AMPK in VEGF- and S1P mediated eNOS activation and found that both agonists led to a striking increase in AMPK phosphorylation in pathways involving the calcium/calmodulin dependent protein kinase kinase beta ... Taken together, these results suggest that VEGF and S1P differentially regulate AMPK and establish a central role for an agonist modulated AMPK -- > Rac1 -- > Akt axis in the control of eNOS in endothelial cells
Park et al., Int J Obes Relat Metab Disord 2008 (Neovascularization, Pathologic) : The AMPK activator 5-aminoimidazole-4-carboximide ribonucleoside ( AICAR ) induced VEGF-A expression
Webler et al., Am J Physiol Cell Physiol 2008 : Mechanistically, VEGF stimulated the phosphorylation of the AMP activated protein kinase (AMPK), which has also been linked to CYP induction, and the overexpression of a constitutively active AMPK mutant increased CYP2C expression
Zwetsloot et al., J Physiol 2008 (Anoxia...) : AMPK regulates basal skeletal muscle capillarization and VEGF expression, but is not necessary for the angiogenic response to exercise ... These data are to our knowledge the first to demonstrate in skeletal muscle in vivo that : ( 1 ) AMPK is necessary for hypoxia induced VEGF mRNA stabilization, ( 2 ) acute exercise increases VEGF transcription, ( 3 ) inhibition of AMPK augments the VEGF mRNA response to acute exercise, and ( 4 ) AMPK regulates basal VEGF expression and capillarization, but is not necessary for exercise induced angiogenesis
Stahmann et al., J Biol Chem 2010 : Using genetic and pharmacological approaches, we show that vascular endothelial growth factor ( VEGF ) stimulates AMPK in human and mice endothelial cells via CaMKKbeta ... VEGF induced AMPK activation is potentiated under conditions of energy deprivation induced by 2-deoxyglucose ... Taken together, these data indicate that VEGF stimulated AMPK and eNOS pathways act independently of each other
Kato et al., Biochem Biophys Res Commun 2010 : In the present study, we investigated the involvement of AMPK in FGF-2 stimulated VEGF release in these cells ... The AMPK inhibitor also reduced the mRNA expression of VEGF induced by FGF-2 ... These results strongly suggest that AMPK positively regulates the FGF-2 stimulated VEGF synthesis via p44/p42 MAP kinase and SAPK/JNK in osteoblasts
Jang et al., Br J Pharmacol 2013 (Wounds, Penetrating) : Both an AMPK inhibitor ( compound C ) anda HO-1 activity inhibitor ( SnPPIX ) but not inhibitors of MAPKs, PI3K and PKC reduced the production of VEGF by CKD712
Song et al., Cardiovasc Res 2013 : Histone deacetylase 5 (HDAC5) was phosphorylated by AMPK activity induced by VEGF and the AMPK agonist AICAR ( 5-amino-1-ß-d-ribofuranosyl-imidazole-4-carboxamide )