◀ Back to AKT1

AKT1 — PLAT

Text-mined interactions from Literome

Lee et al., J Neurochem 2007 : Consistent with neurotrophic effects, tPA activated Raf-K/ERK, PKC and PI3-K/Akt , 5-60 min after treatment
An et al., Blood 2008 (Brain Ischemia...) : We found that, in the early phases of the ischemic insult, the interaction between tPA and LRP induces Akt phosphorylation ( pAkt ) in perivascular astrocytes and inhibits pAkt in neurons
Echeverry et al., J Clin Invest 2010 (Ischemia) : In contrast, tPA induced delayed IPC required the proteolytic activity of tPA and was mediated by plasmin, the NMDA receptor, and PKB phosphorylation
Pineda et al., Glia 2012 (MAP Kinase Signaling System) : We found that tPA induces a catalytic independent rapid and sustained activation of extracellular signal regulated kinase ( ERK ) 1/2, Jun N-terminal kinase (JNK), Akt , and p38 signaling pathways
Wang et al., Ann Neurol 2013 (Brain Ischemia...) : Furthermore, rADAMTS13 downregulated tPA induced phosphorylation of Akt and activation of RhoA
Cho et al., Life Sci 2013 : Glucose deprivation induced activation of PI3K-Akt-GSK3ß , p38 and AMPK, and inhibition of these pathways using LY294002, SB203580 and compound C significantly inhibited glucose deprivation induced tPA down-regulation, demonstrating the essential role of these pathways in tPA regulation in glucose deprived astrocytes