◀ Back to JUN
JUN — VEGFA
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Marumo et al., Diabetes 1999
:
Binding activity of transcription factor
AP-1 , which is suggested to regulate induction of the MCP-1 gene together with NF-kappaB, was also
stimulated by
VEGF ... PD 98059 inhibited the
VEGF induced activation of
AP-1
Hossain et al., J Biol Chem 2000
:
Transfection of cells with a c-jun dominant negative effectively inhibited both
AP-1 activation and
VEGF mRNA
induction by lead
Matsushita et al., J Dent Res 2000
:
VEGF induced the activation of
activator protein 1 (AP-1) and c-fos mRNA expression in human dental pulp cells
Bancroft et al., Clin Cancer Res 2001
(Carcinoma, Squamous Cell...) :
Expression of IL-8 and
VEGF in the cell lines was associated with coactivation of both NF-kappaB and AP-1, and U0126
inhibited both NF-kappaB and
AP-1 reporter activity in UM-SCC-9 and UM-SCC-11B cells
Hu et al., J Natl Cancer Inst 2001
(Ovarian Neoplasms) :
Forced overexpression of
c-Jun and c-Fos in OVCAR-3 cells
stimulated VEGF promoter activity fourfold
Shih et al., Growth Factors 2001
:
Role of
AP-1 and HIF-1 transcription factors in TGF-beta activation of
VEGF expression ... The tyrosine kinase inhibitor genistein and
AP-1 inhibitor curcumin significantly
blocked TGF-beta induction of
VEGF expression while SP-1 and MKK1 inhibitors did not
Pollmann et al., Cancer Res 2001
:
We conclude that CSN directed
c-Jun signaling
mediates high
VEGF production in HeLa and HL-60 cells
Hu et al., Zhonghua Yi Xue Za Zhi 2001
:
Triptolide might
inhibit VEGF expression and production by interfering with transcription factor
AP-1 formation
Hoshi et al., Biochem Biophys Res Commun 2002
:
High glucose and the PKC stimulator, phorbol 12-myristate 13-acetate ( PMA ) induced
activator protein-1 (AP-1) dependent transcriptional activity and expression of
VEGF
Urata et al., Free Radic Biol Med 2002
:
Promoter assay showed that the induction of
VEGF was
dependent on
AP-1 ... The activity of Ras/Raf-1/MEK/ERK1/2 was involved in the CML-BSA stimulated signaling pathways to activate the AP-1 transcription with a peak at 1 h. AGE-BSA also induced
VEGF mediated by
AP-1 , however, there was a difference of effect between AGE-BSA and CML-BSA in the activation of AP-1
Bancroft et al., Int J Cancer 2002
(Carcinoma, Squamous Cell...) :
Recombinant EGF induced EGFR phosphorylation,
activation of NF-kappaB and
AP-1 reporter genes and IL-8 and
VEGF expression, indicating that EGFR can mediate coactivation of both transcription factors and cytokine genes in HNSCC
Cho et al., Arthritis Rheum 2002
:
CSA may exert an antiangiogenic effect by inhibiting
AP-1 mediated
VEGF expression in rheumatoid synovial fibroblasts
Burroughs et al., Mol Cancer Res 2003
(MAP Kinase Signaling System) :
The expression of an
activator protein (AP)-1 dominant negative in an immortalized prostate epithelial cell line PZ-HPV-7
suppressed the IGF-I induced increase in
VEGF promoter activity
Pufe et al., J Pathol 2004
(Osteoarthritis) :
VEGF stimulation
induced receptor phosphorylation, activation of the mitogen activated protein kinases ERK 1/2, and long lasting activation of the transcription factor
AP-1 ( activator protein-1 )
Grau et al., Cancer Res 2004
(Colonic Neoplasms) :
This cyclopentenone was able to inhibit
activator protein1 (AP-1) dependent transcriptional induction of COX-2 and
VEGF promoters induced by phorbol 12-myristate 13-acetate ( PMA ) or c-Jun overexpression
Stanley et al., Biochem Biophys Res Commun 2005
(Neovascularization, Pathologic...) :
These effects are
caused by the inhibition of constitutively active
AP-1 in prostate cancer cells, resulting in the down-regulation of secretion of
VEGF and TGF-beta1 from PC-3 cells
Chang et al., Int J Oncol 2006
(Neoplasms...) :
Extracellular signal regulated kinases and
AP-1 mediate the up-regulation of
vascular endothelial growth factor by PDGF in human vascular smooth muscle cells ... Transient transfection studies using an AP-1 decoy oligonucleotide confirmed that the activation of
AP-1 is
involved in PDGF induced
VEGF upregulation ... The above results suggest that ERK-1/2 and
AP-1 signaling pathways are
involved in the PDGF induced
VEGF expression in human VSMCs and that these paracrine signaling pathways induce endothelial cell proliferation
Lee et al., J Biomed Sci 2006
:
Hyperbaric oxygen
induces VEGF expression through ERK, JNK and
c-Jun/AP-1 activation in human umbilical vein endothelial cells
Kilic et al., FASEB J 2006
(Brain Ischemia) :
Following 90-min episodes of middle cerebral artery occlusion,
VEGF increased phosphorylated ( but not total ) Akt and ERK-1/-2 and
reduced phosphorylated mitogen activated protein kinase/p38 and
c-Jun NH2-terminal kinase (JNK)-1/-2 levels, at the same time decreasing inducible NO synthase expression in ischemic neurons
Tang et al., Mol Cancer Res 2006
(Breast Neoplasms...) :
To explore the underlying signaling pathways used by EMMPRIN, we studied the
involvement of phosphoinositide 3-kinase (PI3K)-Akt, mitogen activated protein kinase ( MAPK ),
JUN , and p38 kinases in EMMPRIN mediated
VEGF regulation
Park et al., Int J Oncol 2006
:
EGCG were found to inhibit dose-dependently the
VEGF expression and
activation of PDGF receptor, Erk-1/2 and
AP-1 induced by PDGF
Bian et al., Exp Eye Res 2007
:
Moreover, TGF-beta2 induced RPE
VEGF secretion was significantly
reduced by inhibitors of mitogen activated protein ( MAP ) kinase ( MEK ) ( U0126 ), p38 ( SB202190 ),
c-Jun NH2-terminal kinase (JNK) , Sp600125, protein tyrosine kinase ( PTK ) ( Genistein ), and phosphatidylinositol 3-kinase (PI3K) ( Ly294002 )
Textor et al., Ann N Y Acad Sci 2006
(Hypoglycemia) :
Using c-jun ( -/- ) and junB ( -/- ) mouse embryonic fibroblasts, we demonstrate that both
c-Jun and JunB are
required for the hypoglycemia mediated induction of
VEGF expression
von Metzler et al., Leukemia 2007
(Bone Resorption...) :
The
AP-1 blockade
contributed to significant reduction of osteoclastic
vascular endothelial growth factor production
Kim et al., Biochem Biophys Res Commun 2008
(Breast Neoplasms) :
VEGF reporter gene activity was significantly
inhibited by either hypoxia-inducible factor-alpha ( HIF-1alpha ) siRNA or
AP-1 decoy ODN
Hu et al., Cell Signal 2008
(Burkitt Lymphoma...) :
The increase in
VEGF expression by LPA is
mediated by the activation of
c-Jun N-terminal Kinase (JNK) and transcription factor NFkappaB since blocking JNK or NFkappaB activation inhibited LPA induced VEGF expression
Guma et al., Proc Natl Acad Sci U S A 2009
(Anoxia...) :
We found that hypoxia induces JNK activation and
regulates VEGF expression by enhancing the binding of
phospho-c-Jun to the VEGF promoter
Matsuo et al., Mol Cancer Res 2009
(Carcinoma, Pancreatic Ductal...) :
Similar results were obtained using another pair of immortalized human pancreatic duct derived cells, E6/E7/st and its oncogenic K-Ras variant, E6/E7/Ras/st. Taken together, our results suggest that angiogenesis is initiated by paracrine epithelial secretion of CXC chemokines and
VEGF downstream of activated oncogenic K-Ras, and that this vascular maturation is in part
dependent on MEK1/2 and
c-Jun signaling
Yin et al., Biomed Pharmacother 2009
(Breast Neoplasms) :
Finally using chromatin immunoprecipitation ( CHIP ) assays, we found that
p-c-Jun bound to the VEGF promoter and
regulated VEGF transcription directly
Kim et al., Mol Cancer Ther 2009
(Breast Neoplasms...) :
Molecular analyses using reporter genes and Western blots supported the
involvement of
c-Jun/activator protein-1 and hypoxia-inducible factor 1alpha in enhanced
VEGF transcription in TAMR-MCF-7 cells ... Pin1, a peptidyl prolyl isomerase, was consistently overexpressed in TAMR-MCF-7 cells, and
c-Jun/activator protein-1
dependent VEGF transcription in TAMR-MCF-7 cells was almost completely inhibited by Pin1 siRNA and by the Pin1 inhibitor juglone
Chuang et al., Chem Biol Interact 2010
:
Thus, the present results indicate that R in combination with VE attenuates
VEGF expression in HL-60 cells and that this effect is
mediated by a decreased binding activity of
AP-1 through down-regulation of protein expression of insulin-like growth factor 1 receptor ( IGF1-R ) /IRS-1, while the antioxidant activity of R+VE appears to play a minor role
Rohr-Udilova et al., Hepatology 2012
(Carcinoma, Hepatocellular...) :
Activation of the
activator protein 1 (AP-1) transcription factor as well as increased serum levels of
vascular endothelial growth factor ( VEGF ) and interleukin (IL)-8 predict poor prognosis of patients with hepatocellular carcinomas (HCCs)
Shen et al., Cell Biochem Biophys 2012
(MAP Kinase Signaling System) :
Furthermore,
VEGFA induced the phosphorylation of ASK1, SEK1/MKK4, MKK7, and
c-Jun , which are upstream or downstream signals of JNK/SAPK
Tripathi et al., Mol Cell Biochem 2012
(MAP Kinase Signaling System...) :
Gel shift assays demonstrated that ANP inhibited
VEGF stimulated
AP-1 and CREB DNA binding ability by 67 and 62 %, respectively ... The addition of the protein kinase G ( PKG ) inhibitor, KT-5823, restored the
VEGF stimulated activation of MAPKs,
AP-1 , and CREB, demonstrating the integral role of cGMP/PKG signaling in NPRA mediated effects
Finkenzeller et al., Biochem Biophys Res Commun 1995
:
In this study, we investigated the functional
role of the transcription factor
AP-1 in hypoxia induced expression of the
vascular endothelial growth factor ( VEGF ) by using dexamethasone as an inhibitor of AP-1 activity ... These results indicate that hypoxia induced
VEGF expression is
independent of
AP-1 mediated transcription
Tsurumi et al., Nat Med 1997
:
In contrast, nitric oxide ( NO ) donors
inhibit PKC induced
VEGF upregulation by interfering with binding of the transcription factor
activator protein-1 (AP-1) to the VEGF promoter