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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