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AKT1 — JUN

Pathways - manually collected, often from reviews:

• WikiPathways Insulin Signaling: GSK3B/AKT2/AKT1/SGK3/SGK1/GSK3A/PDPK1/SGK2 → SRF/ELK1/FOXO1/FOS/JUN/FOXO3/EGR1 (activation)
  

Text-mined interactions from Literome

Sarmiere et al., Mol Cell Neurosci 2001 : In contrast to c-Rel, activated PI 3-kinase and Akt inhibit c-Jun phosphorylation but have only a small effect on cytochrome c release
Ivanov et al., J Biol Chem 2002 : Conversely, inhibition of PI3K-AKT signaling via the specific pharmacological inhibitor LY294002 up-regulated AP1/Jun- and STAT dependent transcriptional activities, resulting in suppression of the FasR promoter activities and decreased FasR surface expression
Kim et al., J Gastrointest Surg 2001 (Second Messenger Systems) : Hypoosmotic stress stimulates growth in HepG2 cells via protein kinase B-dependent activation of activator protein-1 ... We hypothesized that cell swelling modulates proliferation in HepG2 cells via the protein kinase B-dependent activation of activator protein-1 ... In HepG2 cells, hypoosmotic stress induced swelling stimulates proliferation via protein kinase B-mediated activation of activator protein-1
Bozinovski et al., J Biol Chem 2002 (MAP Kinase Signaling System) : Granulocyte/macrophage-colony stimulating factor ( GM-CSF ) regulates lung innate immunity to lipopolysaccharide through Akt/Erk activation of NFkappa B and AP-1 in vivo
Karoor et al., J Mol Cell Cardiol 2004 : In contrast, phospho-kinase levels of ERK and Akt were increased at 9-10 months, but phospho-kinase levels of c-Jun N-terminal kinase (JNK) increased only at 15-20 months ( when cardiomyopathy was fully manifest )
Mendoza-Gamboa et al., Oncol Rep 2004 (Breast Neoplasms) : Inhibition of HER2/Grb2/Akt decreased AP-1 binding activity in HER2 transfected cells, but increased AP-1 activity in cells that are naturally HER2 overexpressing
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)
Leaner et al., Mol Cell Biol 2005 : In addition, c-Jun overexpression resulted in an increase in phospho-AKT while phosphorylation of ERK1/2 remained largely unaffected
Chandrasekar et al., J Biol Chem 2005 : Src kinase inhibitors PP1 and PP2, phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, Akt inhibitor, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, antisense JNK and dominant negative MyD88, interleukin-1 receptor associated kinase ( IRAK)-1, IRAK4, and phosphatidylinositol 3-kinase expression all attenuated IL-18 mediated AP-1 binding and reporter activity, CXCL16 promoter-reporter activity, and CXCL16 expression
Hui et al., Brain Res 2005 (Brain Ischemia) : In contrast, insulin, a PI3K agonist, not only obviously activated Akt1 during early and later reperfusion, but also inhibited phosphorylation of JNK1/2, c-Jun , and Bcl-2 and attenuated the activation of caspase-3
Wang et al., Cancer Res 2005 (MAP Kinase Signaling System) : Because PTEN is a well-known phosphatase involved in the regulation of phosphatidylinositol 3-kinase (PI-3K)/Akt signaling pathway, taken together with the evidence that PI-3K/Akt plays an important role in the activation of AP-1 and NF-kappaB during tumor development, we anticipate that inhibition of AP-1 and NF-kappaB by tumor suppressor p53 seems to be mediated via PTEN, which may be a novel mechanism involved in anticancer activity of p53 protein
Gao et al., Blood 2006 (Leukemia) : Synergistic interactions between these agents were associated with inactivation of Akt and activation of c-Jun N-terminal kinase (JNK)
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
Sunters et al., Cancer Res 2006 (Breast Neoplasms) : To further investigate its mechanism of action, we treated MCF-7 cells with paclitaxel and showed a dose dependent increase in nuclear localization of FOXO3a, which coincided with decreased Akt signaling but increased c-Jun NH2-terminal kinase 1/2 (JNK1/2) , p38, and extracellular signal regulated kinase 1/2 ( ERK1/2 ) activity
Liao et al., Neurochem Int 2007 : The inductive action of manganese was accompanied by generation of oxidative stress, activation of mitogen activated protein kinases ( MAPKs ), AKT , and protein kinase C-alpha (PKC-alpha), and increased NF-kappaB and AP-1 DNA binding activities
Kim et al., Biol Pharm Bull 2007 (Atherosclerosis) : Pre-treatment of VSMCs with NQ304 ( 1-10 microM ) was found to significantly inhibit the 5 % FBS induced phosphorylations of ERK1/2 and Akt , the activation of AP-1 and the expression of c-fos
Song et al., Gut 2007 (Adenocarcinoma...) : Unconjugated bile acids induce CREB and AP-1 dependent COX-2 expression in Barrett 's oesophagus and OA through ROS mediated activation of PI3K/AKT and ERK1/2
Kim et al., Carcinogenesis 2008 (Breast Neoplasms) : 15d-PGJ ( 2 ) -induced COX-2 expression was mediated by activation of Akt and subsequently activator protein-1 (AP-1)
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
Choi et al., Stem Cells Dev 2008 (MAP Kinase Signaling System) : As a consequence of PI3K-Akt and ERK1/2, the upregulation of c-Jun in the Sca-1 ( + ) BMMSCs, after stimulation with FGF-2 or FGF-4, was observed after 12 and 24 h
Han et al., Toxicol Appl Pharmacol 2008 : Phosphatidylinositol 3 (PI3)-kinase, its downstream signaling molecule, Akt , and mitogen activated protein kinases ( MAPK ) were also significantly activated by the o, p'-DDT induced AP-1 and CRE activation
Hou et al., J Cell Biochem 2009 : US-increased the binding of c-Fos and c-Jun to the AP-1 element on the BMP-2 promoter and the enhancement of AP-1 luciferase activity was inhibited by Ly294002 and Akt inhibitor ... US-increased the binding of c-Fos and c-Jun to the AP-1 element on the BMP-2 promoter and the enhancement of AP-1 luciferase activity was inhibited by Ly294002 and Akt inhibitor
Wu et al., J Am Soc Nephrol 2009 (Diabetes Mellitus, Experimental...) : PKC is known to mediate glucose induced TGF-beta1 upregulation through the transcription factor AP-1 ; here, inhibitors of phosphoinositide-3-OH kinase, PKC-beta and Akt, and dominant negative Akt all prevented glucose induced activation of AP-1 and upregulation of TGF-beta1
Park et al., Carcinogenesis 2009 (Breast Neoplasms...) : KPS-A decreased PMA induced transcriptional activation of NF-kappaB and AP-1 and inhibited PMA induced phosphorylation of ERK1/2 and Akt
Shin et al., Mol Cancer Res 2009 (Pancreatic Neoplasms) : Our study also uncovered a novel mechanism by which protein kinase Akt controls c-Jun activity in pancreatic cancer cells
Chiu et al., J Immunol 2009 (Arthritis, Rheumatoid) : PGN mediated an increase in the accumulation of phosphorylated c-Jun in the nucleus, AP-1-luciferase activity, and c-Jun binding to AP-1 element was inhibited by Ly294002, Akt inhibitor, and FAK mutant
Shrotriya et al., Cancer Res 2010 (Skin Neoplasms) : Diallyl trisulfide inhibits phorbol ester induced tumor promotion, activation of AP-1 , and expression of COX-2 in mouse skin by blocking JNK and Akt signaling ... Pharmacologic inhibition of JNK or Akt by SP600125 or LY294002, respectively, resulted in diminished AP-1 DNA binding, reduced levels of c-Jun and c-Fos, and inhibition of COX-2 expression in TPA treated mouse skin ... Taken together, the inhibitory effects of DATS on TPA induced AP-1 activation and COX-2 expression through modulation of JNK or Akt signaling may partly account for its antitumor promoting effect on mouse skin carcinogenesis
Vlahos et al., Am J Respir Crit Care Med 2010 (Pneumonia) : We have previously shown that granulocyte/macrophage colony stimulating factor ( GM-CSF ) regulates lung innate immunity to LPS through Akt/Erk activation of nuclear factor-kappaB and activator protein (AP)-1
Gao et al., Cell death & disease 2011 (Leukemia) : These events were accompanied by the caspase independent downregulation of Mcl-1, inactivation of Akt , as well as activation of Jun N-terminal kinase (JNK)
Kim et al., Int J Neurosci 2011 (Disease Models, Animal...) : First, we observed that MPTP induced impairment of Akt activation, but not MPTP induced c-Jun activation , was effectively restored by acupuncture treatment in the substantia nigra
Chung et al., Dig Dis Sci 2012 (Colorectal Neoplasms...) : Knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells ... These results indicate that knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells
Wu et al., Neurobiol Dis 2012 : We found that BDNF dependent c-Jun expression and nuclear translocation required prior phosphorylation of extracellular signal regulated kinase ( ERK ) 1/2, but not Akt
Chen et al., PloS one 2012 : HGF mediated AP-1-luciferase activity and c-Jun binding to the AP-1 element was reduced by c-Met inhibitor, Ly294002, Akt inhibitor, and PP2
Liu et al., Toxicological sciences : an official journal of the Society of Toxicology 2012 : In the present study, we describe a novel signaling axis of the c-Jun NH2 kinase (JNK) and signal transducer and activator of transcription 3 ( Stat3 ) and its involvement in As ( 3+ ) -induced Akt activation in human bronchial epithelial cells
Scullen et al., Leukemia 2013 (MAP Kinase Signaling System...) : Our findings demonstrate that lenalidomide acts directly on bone marrow stromal cells via an Akt mediated increase in Jun N-terminal kinase dependent signaling resulting in activin A secretion, with consequent inhibition of osteoblastogenesis
Scheinman et al., Mol Cell Endocrinol 2013 : Specific inhibition of p-Akt by wortmannin did not affect cholesterol 's stimulation of the expression of c-Jun and Jun-B, however the vanadate effect of increasing p-ERK1/2, inhibited c-Jun expression, specifically, and the MBCD effect of increasing p-ERK and inhibiting p-Akt reduced c-Jun expression