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AKT2 — RNF19A

Text-mined interactions from Literome

Marushige et al., Anticancer Res 1999 (MAP Kinase Signaling System...) : The p38 inhibitor, PD169316, reduced the activities of ERK and Akt
Bijur et al., J Neurochem 2000 : Akt activation was not blocked by inhibition of p38 or ERK1/2, indicating the independence of these signaling systems
Gratton et al., J Biol Chem 2001 : Conversely, activation-deficient Akt decreases VEGF stimulated MEKK3 phosphorylation and increases MKK/p38 activation
Souza et al., Mol Med 2001 (MAP Kinase Signaling System) : Interestingly, however, SB203580, a known p38 inhibitor, completely inhibited arsenite induced phosphorylation of AKT and eNOS
Kettritz et al., J Am Soc Nephrol 2002 : p38 MAPK inhibition with 10 microM SB202190 that also decreased ANCA induced superoxide generation prevented S473 phosphorylation of Akt in response to TNF-alpha and to ANCA
Baudhuin et al., Mol Pharmacol 2002 : However, epidermal growth factor, thrombin, and endothelin-1 stimulated Akt S473 phosphorylation require p38 but not MEK ... MEK and p38 activation were sufficient for Akt S473 but not T308 phosphorylation in HEY cells
Yuan et al., J Biol Chem 2003 : In conclusion, our data indicate that AKT2 inhibits cisplatin induced JNK/p38 and Bax activation through phosphorylation of ASK1 and thus, plays an important role in chemoresistance
Gonzalez et al., Mol Cell Biol 2004 (MAP Kinase Signaling System) : Inhibition or activation of p38 with SB203580, dominant negative p38, or MKK6EE regulated Akt kinase activity
Taniyama et al., Am J Physiol Cell Physiol 2004 (MAP Kinase Signaling System) : Inhibition of p38 MAPK activity with SB-203580 dose-dependently inhibits Akt phosphorylation on Ser ( 473 ), but not Thr ( 308 )
Grethe et al., Biochem Biophys Res Commun 2006 : Notably, we also found that doxorubicin provoked apoptosis included p38 MAPK mediated inhibition of Akt and Bad phosphorylation
Liu et al., J Biol Chem 2007 (Insulin Resistance) : Our results show that a prolonged treatment of primary hepatocytes with oleate blunted insulin suppression of hepatic gluconeogenesis, and decreased insulin induced phosphorylation of Akt in a p38 dependent manner
Diehl et al., J Surg Res 2007 (Breast Neoplasms...) : We also found that AKT was activated by p38MAPK in these cells, but this activation did not play a role in invasion
Ogunwobi et al., Am J Gastroenterol 2008 (Adenocarcinoma...) : Simvastatin inhibited activation of extracellular signal regulated kinase ( ERK ) and protein kinase B ( Akt ) but not c-Jun NH ( 2 ) -terminal kinase or p38 mitogen activated protein ( MAP ) kinase
Hong et al., J Exp Clin Cancer Res 2009 (Carcinoma, Squamous Cell...) : Inhibition of Akt activity by PIA decreased NF-kappaB signaling, but did not affect phosphorylation of ERK, JNK, and p38 in KB and KOSCC-25B cells
Rane et al., American journal of physiology. Renal physiology 2010 (Diabetes Mellitus, Experimental...) : These results collectively suggest that downregulation of Akt activation during long-term hyperglycemia contributes to enhanced p38 MAPK activation and RPTC apoptosis
Bulzomi et al., IUBMB Life 2010 (Neoplasms, Hormone-Dependent) : In contrast, Nar stimulation prevents E2-induced extracellular regulated kinases ( ERK1/2 ) and AKT activation and still induces the activation of p38 , the proapoptotic member of mitogen activating protein kinase ( MAPK ) family
Aceros et al., Br J Pharmacol 2011 (Fibrosis...) : In vitro, moxonidine inhibited norepinephrine induced neonatal cardiomyocyte mortality but increased fibroblast mortality, through I ( 1 ) -receptor activation and differential effects on downstream Akt and p38 MAPK
Valente et al., Cell Signal 2012 (Fibrosis...) : These results indicate that IL-17A stimulates CF proliferation and migration via Akt/miR-101/MKP-1 dependent p38 MAPK and ERK1/2 activation
Suwanabol et al., Am J Physiol Heart Circ Physiol 2012 (Carotid Artery Injuries) : Furthermore, inhibition of p38 in vivo led to decreased Akt phosphorylation and SMC proliferation
Yamawaki et al., Biochem Biophys Res Commun 2012 (Inflammation) : The effect is mediated via inhibiting activation of NF-?B and p38 through stimulation of Akt/eNOS signaling and NO production