Gene interactions and pathways from curated databases and text-mining

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AKT3 — EPHB2

Text-mined interactions from Literome

Kurose et al., Nihon Yakurigaku Zasshi 1999 (Myocardial Reperfusion Injury) : Expression of GRK2-ct inhibited the H2O2 induced activation of ERK by 70 % and also inhibited the activation of Akt by 30 %
Mirza et al., Cell Growth Differ 2000 (Cell Transformation, Neoplastic) : Perhaps surprisingly, activation of M+ Akt : ER* or expression of a constitutively active form of Akt led to rapid activation of MAP/ERK Kinase (MEK) and the extracellular signal regulated kinase ( ERK ) /mitogen activated protein ( MAP ) kinases in Rat1 cells
Tudan et al., J Immunol 2000 (MAP Kinase Signaling System) : CPPD crystals were observed to induce a robust and transient activation of ERK1 , ERK2, and Akt, whereas TNF-alpha produced only a modest and delayed activation of 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
Kurihara et al., Endocr J 2000 (Neuroblastoma) : PD98059 inhibited activation of Erk and LY294002 repressed activation of Akt in response to IGF-I, but did not affect tyrosine phosphorylation of the IGF-IR, IRS-1, IRS-2, or Shc
Kang et al., Mol Pharmacol 2001 : These results demonstrated that t-BHQ activated PI3-kinase and Akt , which was responsible for ARE mediated rGSTA2 induction, and that ERK might negatively regulate rGSTA2 expression, whereas activation of p38 MAP kinase or of JNK by t-BHQ was not associated with the enzyme induction
Nomura et al., J Biol Chem 2001 : Furthermore, the expression of a dominant negative mutant of Erk2 or p38 kinase, but not that of c-Jun N-terminal kinase 1 ( JNK1 ), blocked UVB induced Akt activation
Hsu et al., J Pharmacol Exp Ther 2001 : Inhibition of Akt activation required almost complete inhibition of ERK
Mograbi et al., J Biol Chem 2001 : Thus, both PI3K and Akt act in concert to finely regulate the level of ERK
Li et al., J Surg Res 2001 (Arteriosclerosis) : Co-incubation with the reducing agent dithiothreitol or calcium chelators ( EDTA/EGTA ) inhibited partially or completely menadione 's effects on MEK/ERK and Akt pathways, as well as menadione 's effects on PDGF induced ERK and Akt activations
Weber et al., Mol Biol Cell 2001 : Stimulation of Jurkat T cells with the CXC chemokine stromal cell derived factor-1alpha ( SDF-1alpha ) resulted in a rapid increase in the phosphorylation, i.e., activation of extracellular signal receptor activated kinase ( ERK ) but not c-Jun NH ( 2 ) -terminal kinase or p38 kinase, and phosphorylation of Akt , reflecting phosphatidylinositol 3-kinase (PI3-K) activation
Kim et al., Cell Signal 2002 : C ( 2 ) -ceramide induced a delayed activation of ERK ( > 1 h ) and a much later activation of Akt/PKB ( > 3 h ) in human melanocytes
Frost et al., Mol Cancer Ther 2002 : In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib
Gu et al., Biochem Biophys Res Commun 2003 (MAP Kinase Signaling System) : Interestingly, the suppression of ERK-MAP kinase activation in Csk ( - ) /Csk cells was restored by overexpression of a dominant negative Akt
Castaño et al., J Cell Physiol 2003 : Moreover, 15dPGJ ( 2 ) did not induce activation of PKB/AKT or activation of extracellular signal regulated kinase ( ERK )
Fukuda et al., Cancer Res 2003 (Colonic Neoplasms) : In contrast, phosphorylation of AKT is dependent on ERK and C-SRC activity
Kim et al., Cell Signal 2004 : Furthermore, we found that the growth inhibition by S1P was in part abolished by pertussis toxin ( PTX ) treatment, but that ERK activation and Akt/PKB inhibition were not abrogated, suggesting that S1P functions both intracellularly, as a second messenger, and extracellularly, as a ligand for cell surface receptors
Wang et al., J Biol Chem 2004 (Anoxia) : The inhibition of Bid/Bax induced cell death by hepatocyte growth factor primarily involved p38 MAPK and in part Akt dependent pathways but not ERK1/ERK2
Bayle et al., J Biol Chem 2004 : SOCS6 reduced SCF induced activation of ERK1/2 and p38 but not activation of AKT or STATs in Ba/F3, murine embryonic fibroblast (MEF), or COS-7 cells
Wandzioch et al., Blood 2004 (MAP Kinase Signaling System) : Surprisingly, phosphoinositide-3 (PI-3) kinase inhibitors block not only PKB/Akt activation but also activation of Raf and Erk
Taniguchi et al., Mol Reprod Dev 2004 (MAP Kinase Signaling System) : Here, we showed that HGF activated the distinct phosphorylation of Raf-1, MEK1/2, and ERK1/2 , but did not induce phosphorylation of Akt
Campbell et al., Circ Res 2004 (MAP Kinase Signaling System) : ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors ; when PI3K was inhibited, ERK phosphorylation could be induced by microinjected activated Akt , indicating important cross-talk between the PI3K and ERK1/2 pathways
Yamaguchi et al., J Biol Chem 2004 (Polycystic Kidney Diseases) : Inhibition of Akt or phosphatidylinositol 3-kinase also allowed cAMP dependent activation of B-Raf and ERK in normal calcium
Kim et al., Cell Signal 2004 : We have characterized the role of Drosophila PI3K and AKT in ERK pathway activation involving insulin induced proliferation using Drosophila Schneider cells
Choi et al., J Recept Signal Transduct Res 2004 : In these R- cells, PI3K inhibition by LY294002 enhanced insulin stimulation of ERK phosphorylation whereas LY294002 inhibited insulin stimulation of Akt phosphorylation
Maeda et al., Biochem Biophys Res Commun 2004 : Expression of Gab1 PI3K-m in SK-N-MC human primitive neuroectodermal tumor cells expressing wild-type RET markedly impaired Akt phosphorylation, Rac1 activation, and lamellipodia formation that were induced by GDNF whereas expression of Gab1 SHP2-m partially impaired Erk activation
Vormittag et al., Oncol Rep 2005 (Carcinoma, Squamous Cell...) : ERK inhibition had no effect on Akt expression, and combined application of both agents had the same effect as treatment with nimesulide alone
Wollmann et al., Carcinogenesis 2005 (Breast Neoplasms) : These results suggest that AKT/PKB through MIC-1 could regulate the ERK1 activity and the MIC-1 expression levels may serve as a surrogate marker for the AKT activation in tumors
Evangelopoulos et al., Oncogene 2005 (Neuroblastoma) : We found that in Neuro2a neuroblastoma cells, EGFR, ERK1/2 and Akt showed increased phosphorylation after serum withdrawal, and that the activation of EGFR was necessary for the activation of Akt and ERK1/2
Hahn et al., Mol Cancer Ther 2005 (Leukemia) : These events were associated with marked down-regulation of Raf-1, MEK, and ERK phosphorylation, diminished Akt activation , and enhanced phosphorylation of c-Jun NH2-terminal kinase (JNK)
Shiote et al., Neuroscience 2005 (Anoxia...) : In the lumbar segment, we observed that reduced Flk-1 expression and hypoxic challenge for 7 days resulted in approximately 50 % loss of motor neurons, in which the activation of Akt and ERK, that is, increased levels of phosphorylated-Akt and of phosphorylated-ERK by hypoxia, was markedly inhibited
Peng et al., Mol Cancer Res 2005 : Cell signaling analysis with pathway-specific inhibitors reveals that SDF-1alpha induced Akt activation is not required for ERK1/2 activation and vice versa, indicating that activations of Akt and ERK1/2 occur independently
Zhou et al., Toxicological sciences : an official journal of the Society of Toxicology 2005 : Concurrent with p53 activation, DON activated two anti-apoptotic survival pathways as evidenced by both ERK dependent p90 Rsk and AKT activation
Iordanov et al., J Invest Dermatol 2005 (Dermatitis) : Using a variety of inhibitors and blocking antibodies, we demonstrated that : ( i ) apoptosis is required for the generation of the signal ( s ) leading to the activation of EGFR, ERK, and Akt; (ii) the activation of EGFR, ERK , and Akt by FasL is indeed mediated by its bona fide receptor Fas ; ( iii ) the activation of EGFR is essential for the subsequent activation of ERK and Akt ; and ( iv ) apoptotic keratinocytes secrete soluble EGFR ligands ( including amphiregulin ) that are processed from membrane bound proligand forms by metalloproteinase ( s )
El-Assal et al., Gastroenterology 2005 (Colitis, Ischemic...) : HB-EGF enhances restitution after intestinal ischemia/reperfusion via PI3K/Akt and MEK/ERK1/2 activation
Kobayashi et al., Exp Dermatol 2005 : We show ( i ) UV induced up-regulation of TNF-alpha mRNA and protein expression in keratinocytes ; ( ii ) cells treated with KTI before UV irradiation showed a significantly lower accumulation of TNF-alpha protein in a dose dependent manner and a reduced UV-induced up-regulation of TNF-alpha mRNA expression ; ( iii ) KTI inhibited the induction of TNF-alpha target molecules interleukin-1beta (IL-1beta) and IL-6 proteins ; ( iv ) UV irradiation transiently activated c-Jun N-terminal kinase (JNK) and Akt signaling but only weakly activated extracellular signal regulated kinase ( ERK ) and p38 ; ( v ) KTI specifically inhibited UV-induced activation of ERK , JNK, and p38, but not Akt ; ( vi ) treatment of cells with SP600125, a pharmacological inhibitor of JNK, predominantly suppressed UV-induced up-regulation of TNF-alpha expression ; and ( vii ) KTI did not enhance suppression of UV-induced JNK phosphorylation by SP600125
Qiu et al., Int J Oncol 2005 (Ovarian Neoplasms) : Paclitaxel induced ERK and AKT activity was inhibited by the EGFR inhibitor, PD153035 ; ERK inhibitor, U0126 ; and PI3 kinase inhibitor, LY294002, respectively
Botolin et al., J Lipid Res 2006 (MAP Kinase Signaling System) : 22 : 6,n-3 transiently inhibits insulin induced Akt phosphorylation but induces Erk phosphorylation
Liu et al., Dig Liver Dis 2006 (MAP Kinase Signaling System...) : Phospho-ERK1/2 , Akt activity and expression of c-Myc were significantly induced by etoposide in a time dependent manner ; moreover, there was a weak effect on the expression of p53 protein
Hunker et al., Arch Biochem Biophys 2006 : In addition, expression of Rab5 : WT and Rab5 : Q79L enhance both Erk1/2 and Akt activation without affecting JN- and p38-kinase activities, while the expression of Rab5 : S34N blocks both Erk1/2 and Akt activation
Jiang et al., J Ocul Pharmacol Ther 2006 : EGF induced cell migration in a dose dependent manner ; EGF induced EGFR phosphorylation and downstream activation of c-Jun N-terminal protein kinase (JNK), p38 MAP kinase ( p38 ), extracellular signal regulated kinase ( ERK1/2 ) and AKT , were inhibited by PD153035 ( EGFR inhibitor ), JNKi ( JNK inhibitor ), SB203580 ( p38 inhibitor ), U0126 ( MEK/ERK inhibitor ), and LY294002 ( PI3K/AKT inhibitor ), respectively
Zhang et al., Am J Physiol Cell Physiol 2006 : Pertussis toxin ( PTX ) blocks LPA induced activation of p38 and ERK but only slightly inhibits LPA induced activation of Akt
Xie et al., Cancer Biol Ther 2006 (Carcinoma, Hepatocellular...) : Furthermore, SLD dose- and time-dependently inhibited the phosphorylation of Raf-1 on Ser 259, which is an established event by which Akt inhibits ERK1/2 activation
Xu et al., Am J Physiol Lung Cell Mol Physiol 2006 (Hyperoxia...) : Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia induced cell death in lung epithelial cells through reduction of ROS, activation of ERK/MAPK , and PI3K-Akt cell survival signaling pathways
Ceolotto et al., Free Radic Biol Med 2006 : Insulin induced Akt phosphorylation was increased by pravastatin and ERK1/2 phosphorylation attenuated
Hattrup et al., Breast Cancer Res 2006 (Breast Neoplasms...) : Additional changes were seen at the protein level, such as increased expression of c-Myc, heightened phosphorylation of AKT , and decreased activation of MEK1/2 and ERK1/2
Lee et al., Am J Physiol Heart Circ Physiol 2006 (Inflammation...) : However, inhibitors of Raf-1 and MEK or a dominant negative ERK mutant blocked FKN induced ERK, but not Akt and eNOS, phosphorylation
Li et al., J Cell Physiol 2006 (Carcinoma, Non-Small-Cell Lung) : Interestingly, inhibition of ERK1/2 prevented the activation of Akt whereas the suppression of Akt had no effect on ERK1/2, suggesting that Akt was not necessary for TGZ-PPARgamma-ERK pathway
Liu et al., Br J Dermatol 2006 (Lymphatic Metastasis...) : Our study shows that the expression of IGF-1R and the induction of p-AKT and the p-ERK1/2 pathway may play an important role in the pathogenesis of EMPD
Punn et al., Mol Endocrinol 2006 : Furthermore, time course studies and use of selective inhibitors demonstrated that ERK1/2 activation occured within 5 min, was sustained for at least 60 min, and was dependent on both phosphatidylinositol 3-kinase (PI3-K)/Akt activation and epidermoid growth factor receptor transactivation involving matrix metelloproteinases
Byun et al., J Biol Chem 2006 (Breast Neoplasms) : These results suggest that expression of a splice variant of CD99 contributes to the invasive ability of human breast cancer cells by up-regulating AP-1 mediated gene expression through the Akt dependent ERK and JNK signaling pathways
Tortorella et al., J Gerontol A Biol Sci Med Sci 2006 : Whereas Akt inhibition also affected GM-CSF dependent ERK1/2 phosphorylation, ERK1/2 inhibition did not affect GM-CSF induced Akt phosphorylation, suggesting that phosphoinositide 3-kinase (PI3-K)/Akt and ERK1/2 are activated in series and that PI3-K is located upstream of ERK1/2 along the GM-CSF dependent signaling pathway
Li et al., J Biol Chem 2007 (Breast Neoplasms...) : Interestingly, hPEBP4 overexpression in TRAIL-sensitive DU145 cells promoted Akt activation but inhibited ERK1/2 activation
Zecchin et al., Diabetes 2007 (Obesity) : In addition, ACh induces JAK2/IRS-1 and IRS-1/phosphatidylinositol (PI) 3-kinase associations, downstream activation of Akt/protein kinase B, endothelial cell-nitric oxide synthase ( eNOS ), and extracellular signal regulated kinase ( ERK ) -1/2
Nazari et al., J Med Invest 2007 (MAP Kinase Signaling System) : Pretreatment of Ang II increased ERK1/2 phosphorylation and inhibited insulin induced Akt phosphorylation
Cuevas et al., J Hepatol 2007 : Changes in ERK phosphorylation in IRS-4 depleted cells were independent of ras/raf/MEK1/2- and PI3K/Akt-cascades
Zhou et al., J Allergy Clin Immunol 2007 (Asthma...) : MEK-ERK inhibition also significantly increased Akt phosphorylation under all conditions and decreased Smad-3 phosphorylation in the presence of IL-13+TGF-beta1 ... In contrast, phosphoinositide-3 kinase-Akt inhibition increased phosphorylation of ERK and Smads, leading to increased TIMP-1
Xu et al., J Cell Biochem 2008 (MAP Kinase Signaling System) : The activation of ERK1/2 was inhibited by a PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not inhibit phosphorylation of Akt and GSK3 beta
Boisvert et al., Mol Immunol 2007 : Inhibition studies indicated that activation of ERK and JNK MAPKs and PI3K/AKT are necessary for both TCR- and TCR+alpha2 beta1 integrin dependent IFN-gamma production and that Coll I increases TCR dependent activation of ERK and JNK MAPKs, and AKT
Tsokas et al., J Neurosci 2007 (MAP Kinase Signaling System) : The role of ERK in regulating PDK1 and Akt , with their extensive effects on cellular function, has important implications for the coordinated response of the neuron to LTP inducing stimulation
Chuang et al., Endocrinology 2007 (Diabetes Mellitus, Experimental...) : MAPK/ERK inhibitor PD98059 inhibited the PI3K activity, Akt phosphorylation, and lipid accumulation triggered by HG
Merla et al., Am J Physiol Heart Circ Physiol 2007 : We asked if the blockade of adenosine receptors ( A ( 1 ), A ( 2A ), A ( 2B ), or A ( 3 ) receptors ) could attenuate the induction of Akt and eNOS by atorvastatin ( ATV ) and whether ERK1/2 is involved in the ATV regulation of Akt and eNOS
Khundmiri et al., Am J Physiol Cell Physiol 2007 (MAP Kinase Signaling System) : Ouabain mediated Akt phosphorylation was inhibited by U0126, a MEK/ERK inhibitor, suggesting that ouabain mediated Akt phosphorylation is dependent on ERK
Kim et al., Biol Pharm Bull 2007 : Water extract of Korean red ginseng stimulates angiogenesis by activating the PI3K/Akt dependent ERK1/2 and eNOS pathways in human umbilical vein endothelial cells ... This study demonstrated that KRGE stimulates in vitro and in vivo angiogenesis through the activation of the PI3K/Akt dependent ERK1/2 and eNOS signal pathways and their cross talk
Kaomongkolgit et al., Oral Oncol 2008 (Carcinoma, Squamous Cell...) : Studies using specific inhibitors of extracellular signal regulated kinase ( ERK1/2 ) and of Akt ( SH-5 ) demonstrated that iron regulated MMP-9 through ERK1/2 and Akt, and that ERK1/2 was an upstream activator of Akt
Zhao et al., Neurosci Lett 2007 (Anoxia) : Immunoblots revealed that insulin upregulated activation of Akt and inhibited ERK activation through the PI3K pathway ... In summary, our data suggest that insulin prevent apoptosis in ES-NPCs by activating Akt and inhibiting ERK through the PI3K pathway
Anger et al., J Biochem Mol Biol 2007 : The high degree of specificity in RGS proteins depending modulation of G ( q ) - and G ( i/o ) -mediated ERK and Akt activation in the muscarinic network can not merely be attributed exclusively to RGS protein selectivity towards G ( q ) or G ( i/o ) proteins ... Counter-regulatory mechanisms and inter signaling cross-talk may alter the sensitivity of GPCR induced ERK and Akt activation to RGS protein regulation
Unfried et al., Am J Physiol Lung Cell Mol Physiol 2008 : Moreover, overexpression of mutant Akt , as well as pretreatment with an Akt inhibitor, reduced nanoparticle-specific ERK1/2 phosphorylation, which is decisive for nanoparticle induced proliferation
Kim et al., J Cell Biochem 2008 : Epinephrine also induced phosphorylation of ERK1/2 ( p44/42 MAPKs ), while inhibition of PKC or Akt blocked this phosphorylation
Lin et al., Rheumatol Int 2008 (Chondrosarcoma...) : Using chondrosarcoma cells stimulated with IL-1beta, the effects of GLN on the mRNA and protein levels of MMP-3, the activation of JNK, ERK , p38, NF-kappaB, and AP-1, the nuclear translocation of NF-kappaB/Rel family members, and PI3-kinase/Akt activation were studied
Frogne et al., Breast Cancer Res Treat 2009 (Breast Neoplasms) : Treatment with the EGFR inhibitor gefitinib preferentially inhibited growth and reduced the S phase fraction in the resistant cell lines concomitant with inhibition of Erk and unaltered Akt activation
Kang et al., Int J Mol Med 2008 (Cell Transformation, Neoplastic) : ERK and PI3K/AKT inhibitors inhibit ECM induced ERK , AKT activation and cell proliferation
Jovanovic et al., J Invest Dermatol 2008 (Melanoma...) : In a univariate analysis, shorter overall survival was associated with the presence of ulceration ( P=0.001 ) and BRAF exon 15 mutations ( P=0.005 ) as well as the absence of nuclear activation of Akt ( P=0.022 ) and of cytoplasmic activation of ERK ( P=0.003 )
Kato et al., Biochem Biophys Res Commun 2008 : OML induced ERK phosphorylation was inhibited by specific inhibitors of PI3K and SFKs, and OML induced Akt phosphorylation was inhibited by a inhibitor of SFKs
Kim et al., Stem Cells 2008 : Furthermore, mitogen activated protein kinase 1/2 inhibitor or knockdown of Erk1 could restore activation of Akt and downregulate mTOR
Rossi et al., Peptides 2008 : Western blot experiments documented an activation of external receptor activated kinases ( ERK1/2 ) and Akt in a dose dependent fashion, as well as involvement of the cAMP pathway in ERK1/2 phosphorylation
Sun et al., FASEB J 2009 (Inflammation) : Kinetic analysis indicated that PKC isoforms induced early ERK1/2 activation, while PI3K-Akt contributed to the pathway at later time points
Ruhland et al., Exp Parasitol 2009 : Interestingly, activation of PI3K/Akt signaling had differential effects on ERK and p38 activation
Yao et al., J Neurosci 2009 : Blocking TRPC channels and specific downregulation of TRPC channels 1 and 5 resulted in suppression of CCL2 induced ERK/CREB activation but not Akt/NF-kappaB activation
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
Yu et al., Vascul Pharmacol 2009 (MAP Kinase Signaling System) : TNF-alpha induced apoptosis was significantly decreased by SB203580, a p38 MAPK inhibitor or SP600125, a JNK inhibitor, but was enhanced by an ERK1/2 pathway inhibitor, PD98059 or a PI3-kinase/Akt pathway inhibitor , wortmannin
Park et al., Biochem Pharmacol 2009 (Ovarian Neoplasms) : Treatment of SKOV3 cells with PKI-166 ( EGFR1/2 inhibitor ), LY294002 ( AKT inhibitor ), and PD98059 ( ERK inhibitor ) decreased c-FLIP ( L ) expression and co-treatment with TRAIL further reduced the level of c-FLIP ( L, ) respectively, as did TSA
Rodrigues et al., Mol Cell Endocrinol 2009 (MAP Kinase Signaling System) : Also, ERK1/2 activation is not significantly affected by protein kinase A (PKA), protein kinase C ( PKC ) and protein kinase B or Akt ( Akt/PKB ) specific inhibitors
Park et al., Am J Physiol Cell Physiol 2009 : Especially, phosphorylation of caveolin-1 is attenuated by AG1478, herbimycin A ( tyrosine kinase inhibitors ), and pyrazolopyrimidine 2 ( PP2, Src inhibitor ) and EGF induced ERK activation was blocked by PP2, methyl-beta-cyclodextrin ( MbetaCD ), caveolin-1 small interfering RNA ( siRNA ), LY-294002 [ phosphoinositol-3 kinase inhibitor ( PI3K ) ], and Akt inhibitor
Yin et al., J Biol Chem 2009 : In normal human chondrocytes, tBHP triggered strong IRS-1 ( Ser-312 and Ser-616 ) and ERK phosphorylation and inhibited IGF-I induced IRS-1 ( Tyr-612 ) and Akt phosphorylation ... Chemical inhibition of ERK significantly enhanced IGF-I phosphorylation of Akt and alleviated tBHP inhibition of Akt phosphorylation
Ge et al., J Ethnopharmacol 2010 : Pretreatment with ginsenoside Rg1 could increase the Akt phosphorylation and inhibit the ERK1/2 phosphorylation induced by 6-OHDA
Sambade et al., Radiother Oncol 2009 (Breast Neoplasms...) : In SUM102 cells, an EGFR+ basal breast cancer cell line, exposure to ionizing radiation elicited strong activation of ERK1/2 and JNK, which was blocked by lapatinib, and weak/no activation of p38, AKT or STAT3
Lennartsson et al., Cell Signal 2010 : Erk 5 is necessary for sustained PDGF induced Akt phosphorylation and inhibition of apoptosis ... However, reduction of the expression of Erk5 by siRNA resulted in only a transient Akt phosphorylation, and an inability of PDGF-BB to suppress caspase 3 activation and inhibit apoptotic nuclear morphological changes such as condensed or fragmented chromatin under serum-free conditions
Qiu et al., J Biol Chem 2010 (Breast Neoplasms...) : We further demonstrated that IOI-42 could reduce the endogenous association of hPEBP4 with Raf-1/MEK1 and enhance the activation of ERK1/2 and JNK while inhibiting Akt activation
Qu et al., Mol Cell Biochem 2010 (Leukemia, Basophilic, Acute) : These observations indicate that Cbl-b promotes RBL-2H3 apoptosis induced by VP-16 or Ara-c, probably through inhibition of Akt and activation of ERK
Chen et al., Mol Carcinog 2010 (Neoplasms) : We found that low concentrations rapamycin increased Akt and ERK phosphorylation through a mTORC1 dependent mechanism because knockdowned raptor induced the activation of Akt and ERK, but higher doses of rapamycin inhibited Akt and ERK phosphorylation mainly via the mTORC2 signaling pathway because that the silencing of rictor led to the inhibition of Akt and ERK phosphorylation
Ranzato et al., J Cell Biochem 2010 (Calcium Signaling) : Western blot analysis on scratch wounded HuVEC showed that PL induced no activation of p38, a transient activation of AKT , and a sustained activation of ERK1/2
Liu et al., Acta Biochim Biophys Sin (Shanghai) 2010 : The Akt inhibitor 1701-1 significantly diminished the expression of phospho-Akt, phospho-ERK1/2 , and cyclin D1 stimulated by apelin-13
Lu et al., Biol Psychiatry 2010 (Inflammation) : In addition, DHA caused AKT and ERK activation in a time dependent manner, and the DHA induced HO-1 upregulation could be attenuated by PI-3 kinase/AKT and MEK/ERK inhibitors
Ricciardi et al., Chemotherapy 2010 (Pancreatic Neoplasms) : Sorafenib reduced c-Kit, ERK and VEGFR2 activation and on the other hand, gemcitabine inhibited Akt phosphorylation
Basuroy et al., Am J Physiol Cell Physiol 2011 : The ability of CO to inhibit TNF-a induced ERK1/2 and p38 MAPK activities in an Akt dependent manner appears to be the key element in ROS dependent survival of endothelial cells during TNF-a mediated brain inflammatory disease
Khalil et al., Cell cycle (Georgetown, Tex.) 2011 (MAP Kinase Signaling System) : Altogether, our results show that low levels of DSBs trigger ATM- and AKT dependent ERK pro-survival signaling and increased cell proliferation whereas higher levels result in ERK dephosphorylation consistent with a dose dependent switch from pro-survival to anti-survival signaling
Sabri et al., Cell Biochem Funct 2011 (MAP Kinase Signaling System) : Interestingly, inhibition of PI3K/AKT enhanced EGF stimulated ERK1/2 activity, and inhibition of ERK1/2 and JNK reduced AKT phosphorylation
Zhang et al., J Cell Physiol 2012 (Carcinoma, Non-Small-Cell Lung...) : EGF stimulated IL-8 production, phosphorylation of Akt and Erk, and cell proliferation and movement could be inhibited by EGFR inhibitor ( Erlotinib ), PI3K inhibitor ( GDC-0941 BEZ-235 and SHBM1009 ), and ERK1/2 inhibitor ( PD98059 )
Takebayashi et al., Biochem Biophys Res Commun 2011 : RBP4 significantly increased p-Akt and p-eNOS production, and significantly inhibited p-ERK1/2 production
Pu et al., J Lipid Res 2011 : Weakening AMPK activity reduced phosphorylation of Akt but not ERK1/2, and Akt inhibitor could not affect ERK1/2 activation either ... Meanwhile, ERK1/2 inhibitors had no effect on Akt phosphorylation
Pasqualetti et al., Lung Cancer 2011 (Carcinoma, Non-Small-Cell Lung...) : Sorafenib reduced c-Kit and ERK activation and gemcitabine inhibited Akt phosphorylation
Wu et al., Clin Cancer Res 2011 (Carcinoma, Endometrioid...) : AKT inhibition in APC ( - ) /Pten ( - ) tumor cells resulted in compensatory upregulation of ERK signaling
Zhang et al., Neurochem Int 2011 : T2FA was able to inhibit the activation of GSK3ß, but not ERK , in an Akt dependent manner
Gangoiti et al., Biochimie 2012 : The mitogenic action of C1P also involved activation of phosphatidylinositol 3-kinase/Akt , ERK1/2 and the mammalian target of rapamycin
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
Zheng et al., Proc Natl Acad Sci U S A 2012 : By suppressing GRK expression with siRNA, we demonstrated that lowering GRK5/6 abolishes IGF1 mediated ERK and AKT activation, whereas GRK2 inhibition increases ERK activation and partially inhibits AKT signaling
Hong et al., Molecular vision 2012 : Furthermore, NGF affected cell cycle progression of HCECs by regulating cyclin D through Akt and Erk activation upon treatment with the pathway inhibitors, LY294002 for Akt or PD98059 for Erk pathways
Kittilson et al., Frontiers in endocrinology 2011 : Although blockade of the ERK pathway had no effect on the activation of Akt, inhibition of PI3K-Akt partially prevented activation of ERK , suggesting cross-talk between the ERK and PI3K-Akt pathways
Shin et al., Neurochem Res 2012 (Brain Ischemia) : Resveratrol increased expression of SIRT1 and phosphorylation of Akt and p38 but inhibited the increase in phosphorylation of ERK1/2
Leisner et al., Oncogene 2013 (MAP Kinase Signaling System...) : In defining each pathway 's contributions, we found that AKT inhibition alone maximally induced GAPDH nuclear accumulation, whereas MEK/ERK inhibition alone had no effect on GAPDH localization
Auer et al., Frontiers in cellular neuroscience 2012 : When analyzing possible signaling mechanisms we found that extracellular signal regulated kinase ( ERK ) and Akt are activated by C3 ( bot ) and ERK is induced by the C3 ( E174Q ) mutant
Leander et al., PLoS Comput Biol 2012 (Tularemia) : The model confirms that phagocytosis associated changes in the composition of the cell membrane can inhibit ERK activity and predicts that Akt and Ras-GAP synergize to inhibit ERK
Wang et al., PloS one 2012 (Granulosa Cell Tumor...) : Whereas TGFa triggered a transient activation of Akt , it induced a sustained activation of ERK1/2 in KGN cells
Khan et al., Steroids 2013 : Furthermore, E2 rapidly enhanced ERK and Akt activation in cortical neurons, and inhibitors of ERK and Akt activation significantly attenuated E2 induction of excitatory glutamatergic synapses
Marsigliante et al., J Cell Physiol 2013 (Breast Neoplasms) : Although activated by different CCL20 concentrations, these pathways function in parallel and crosstalk to some extent, inasmuch as Akt activation was responsible for ERK1/2 nuclear translocation and enhanced the transcription of of c-fos and c-myc, involved in cell proliferation
Aslan et al., Arterioscler Thromb Vasc Biol 2013 : Stimulation of platelets with the glycoprotein receptor VI agonist, collagen related peptide, rapidly activated PAK in a time course preceding phosphorylation of PAK substrates, LIM domain kinase LIMK1 and the MAPK/ERK kinase MEK, and the subsequent activation of MAPKs and Akt
Hong et al., Exp Cell Res 2013 (MAP Kinase Signaling System...) : AKT upregulates B-Raf Ser445 phosphorylation and ERK1/2 activation in prostate cancer cells in response to androgen depletion ... Using androgen deprived LNCaP cells, in which ERK1/2 activation occurs in strong correlation with AKT activation, we found that AKT mediated B-Raf regulation is necessary for ERK1/2 activation ... In contrast, AKT activity was sufficient to induce not only B-Raf phosphorylation but also MEK/ERK activation in the hormone refractory LNCaP variant, C4-2
Ishiki et al., Endocrinology 2013 (Insulin Resistance) : a-Lipoic acid enhanced Akt phosphorylation and decreased ERK and JNK phosphorylation, whereas a-tocopherol enhanced ERK and JNK phosphorylation but had little effect on Akt phosphorylation
Li et al., Invest Ophthalmol Vis Sci 2013 (MAP Kinase Signaling System) : Inhibitors of EGF stimulated ERK1/2 activity did not inhibit AKT activation but blocked proliferation