◀ Back to EPHB2

EPHB2 — NA

Text-mined interactions from Literome

Rao et al., J Biol Chem 1999 : NAC inhibited agonist induced ERK2 , JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet derived growth factor BB-induced ERK2 activation ... To understand the role of redox-sensitive mechanisms in vascular smooth muscle cell ( VSMC ) growth, we have studied the effect of N-acetylcysteine (NAC) , a thiol antioxidant, and diphenyleneiodonium ( DPI ), a potent NADH/NADPH oxidase inhibitor, on serum-, platelet derived growth factor BB-, and thrombin induced ERK2 , JNK1, and p38 mitogen activated protein ( MAP ) kinase activation ; c-Fos, c-Jun, and JunB expression ; and DNA synthesis
Ichiki et al., Hypertension 2001 : Ang II-induced ERK activation was inhibited by NAC as well as by PD98059
Usatyuk et al., Antioxid Redox Signal 2003 (MAP Kinase Signaling System) : Also, NAC prevented H ( 2 ) O ( 2 ) - and diamide induced p38 MAPK, but not ERK activation
Li et al., Free Radic Biol Med 2004 : TGF-beta stimulated ERK and JNK phosphorylation was also inhibited by NAC
Yang et al., Ann N Y Acad Sci 2005 (MAP Kinase Signaling System) : We investigated whether H2O2, superoxide, and ERK participate in nerve growth factor (NGF) induced signaling cascades and whether antioxidant N-acetylcysteine (NAC) regulates these NGF induced responses ... These findings demonstrate that NAC blocks the NGF induced H2O2/ERK signaling in PC12 cells
Dasmahapatra et al., Blood 2006 (Leukemia) : Adaphostin/MG-132 lethality as well as mitochondrial damage, down-regulation of Raf/MEK/ERK , and activation of JNK were attenuated by the free-radical scavenger NAC , suggesting that oxidative damage plays a functional role in antileukemic effects
Deshpande et al., Toxicol Appl Pharmacol 2006 : Neither NAC nor DTT blocked the phosphorylation of ERK suggesting that this activation is not related to oxidative stress
Yano et al., Atherosclerosis 2007 : However, troglitazone, NAC and NMPG all inhibited nuclear translocation of ERK1/2
Lin et al., J Neurosci Res 2006 : Farnesyltransferase and MEK inhibitors completely abolished NAC induced p38 phosphorylation whereas p38 inhibitor did not influence NAC induced ERK phosphorylation
Kim et al., J Immunol 2008 (MAP Kinase Signaling System) : NAC blocked the activation of JNK and down-regulation of ERK , but both z-VAD-fmk ( N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone ) and ZB4 did not inhibit JNK activation of B7-H1 stimulation
Thuc et al., Apoptosis 2010 (Disease Models, Animal...) : L-NAME, 5HD, N-acetylcysteine (NAC) and staurosporine inhibited ERK1/2 phosphorylation and also reduced pravastatin induced cardioprotection, suggesting NO, mitochondrial K ( ATP ) ( mitoK ( ATP ) ) channels, ROS and PKC should be involved in the cardioprotective signaling
Zhou et al., Sheng Li Xue Bao 2010 (Reperfusion Injury) : Furthermore, NAC increased the protein expression of p-ERK , while inhibited protein expression of p-JNK, NF-kappaB in gastric mucosa
Rivadeneira et al., Med Chem 2010 : ERK activation was inhibited by PD98059, Wortmanin and the ROS scavenger NAC ( N-acetyl cysteine )
Chang et al., Biol Pharm Bull 2010 (Bone Neoplasms...) : Furthermore, NAC attenuated shikonin induced ERK phosphorylation
Zhang et al., Toxicological sciences : an official journal of the Society of Toxicology 2011 : In contrast, NAC itself markedly increased extracellular regulated kinase1/2 ( ERK1/2 ) activation, and the upstream mitogen activated protein/extracellular signal regulated kinase kinase inhibitor, PD-98059, only partially inhibited this activation, suggesting that NAC can directly activate ERK1/2 activity
Petersen et al., Acta Physiol (Oxf) 2012 : Analysis was conducted on the mitogen activated protein kinase signalling pathways, demonstrating that NAC infusion blocked the exercise induced increase in JNK phosphorylation, but not ERK1/2 , or p38 MAPK
Krifka et al., Biomaterials 2012 : The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA induced cell death, and inhibited the activation of ERK1/2 , p38 and JNK by TEGDMA
Akool et al., Biochem Pharmacol 2012 (MAP Kinase Signaling System) : The MEK inhibitor U0126, the reactive oxygen species ( ROS ) scavenger N-acetyl-cysteine (NAC) , a cell-permeant superoxide dismutase ( SOD ) and stigmatellin, an inhibitor of mitochondrial cytochrome bc1 complex strongly attenuated the increase in ERK1/2 phosphorylation triggered by PPIase inhibitors
Sun et al., PloS one 2012 (Disease Models, Animal...) : In glial C6 cells, NAC promoted phosphorylation of ERK induced by ( s ) -3,5-dihydroxy-phenylglycine ( DHPG ), an agonist of group I mGlus
Chen et al., Cancer prevention research (Philadelphia, Pa.) 2012 (MAP Kinase Signaling System...) : This is evidenced by the findings that CPT induced ROS in a concentration- and time dependent manner ; CPT induction of ROS was inhibited by N-acetyl-L-cysteine (NAC) , a ROS scavenger ; and NAC attenuated CPT activation of p38/JNK, inhibition of Erk1/2 , and induction of cell death
Teng et al., Toxicol Appl Pharmacol 2012 (Astrocytoma...) : In addition, N-acetyl cysteine (NAC) , an ROS scavenger, blocked cell cycle G2/M arrest and phosphorylation of ERK1/2 and Cdc25cSer ( 216 ) in U87 cells
Franchi et al., J Invertebr Pathol 2013 (MAP Kinase Signaling System) : We studied in vitro zymosan phagocytosis in the presence of manumycin A, which inhibit the activation of Ras, PD98059, SP600125 and SB202190, inhibitors of Erk , JNK and p38, respectively, parthenolide, N-acetyl-l-cysteine (NAC) and pyrrolidine dithiocarbamate ( PDTC ), inhibiting NF-kB activation