Zinc deficiency
|
0.010 |
Biomarker
|
disease |
BEFREE |
Zinc deficiency increases the susceptibility of human neuroblastoma cells to lead-induced activator protein-1 activation.
|
16484283 |
2006 |
Virus Diseases
|
0.030 |
AlteredExpression
|
group |
BEFREE |
C-Jun N-terminal kinases (JNK) are activated in course of many viral infections.
|
22628315 |
2012 |
Virus Diseases
|
0.030 |
Biomarker
|
group |
BEFREE |
Among the AP-1 factors identified to bind to their cognate DNA element during viral infections of Madin-Darby canine kidney and U937 cells are those that are regulated via phosphorylation by JNKs.
|
11150300 |
2001 |
Virus Diseases
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Activation of AP-1 genes was also observed to occur during infections with other enteroviruses and with Semliki Forest A7(74) virus, suggesting that the phosphorylation of MAPKs and induction of AP-1 gene expression may be important regulators of host cell behavior during viral infections.
|
9770423 |
1998 |
Vascular inflammations
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
AhR mediates indoxyl sulfate-enhanced leukocyte-endothelial interactions through AP-1 transcriptional activity, which may constitute a new mechanism of vascular inflammation in patients with renal disease.
|
26860885 |
2016 |
Vascular Diseases
|
0.020 |
Biomarker
|
group |
BEFREE |
Transcription factor activator protein-1 (AP-1) is activated and upregulated in injured arterial smooth muscle cells in vivo, yet the exact role of the AP-1--related pathway in vascular disease in vivo has remained unclear.
|
11889018 |
2002 |
Vascular Diseases
|
0.020 |
Biomarker
|
group |
BEFREE |
Our findings demonstrate the feasibility, efficacy, and specificity of the anti-AP-1 RNA dON approach for the treatment of allograft vasculopathy in an animal model.
|
31720303 |
2019 |
Varicosity
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In this context, we recently reported that a chronic increase in venous wall stress or biomechanical stretch is sufficient to cause development of varicose veins through the activation of the transcription factor activator protein 1.
|
26908399 |
2016 |
Tumor Promotion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
Although the c-jun oncogene is an integral part of the AP-1 transcriptional complex implicated in the process of tumor promotion, its role in the pathogenesis of human tumors is unknown.
|
8542585 |
1996 |
Tumor Promotion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
Inhibitors of AP-1 have been shown to block tumor promotion, transformation, progression and invasion.
|
16784822 |
2006 |
Tumor Promotion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
We conclude that transactivation of a subset of AP-1-dependent genes is required for tumor promotion and may be targeted for cancer prevention.
|
10449779 |
1999 |
Tumor Promotion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
The net outcome of SAG-mediated inhibition of c-Jun/AP-1 (pro-tumor promotion) and of p27 (antiproliferation) increased skin hyperplasia, with no apparent effect on apoptosis, as evidenced by increased skin thickness, and increased rate of DNA synthesis, but hardly any apoptosis.
|
18258608 |
2008 |
Tumor Promotion
|
0.060 |
AlteredExpression
|
phenotype |
BEFREE |
Activation of activator protein 1 (AP-1) and nuclear factor kappaB (NFkappaB)-dependent transcription is required for tumor promotion in cell culture models and transgenic mice.
|
17363560 |
2007 |
Tumor Promotion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
Overall, these results indicate that MnSOD regulates both cellular redox status and selectively modulates PKCepsilon signaling, thereby delaying AP-1 activation and inhibiting tumor promotion, resulting in reduction of tumors in MnSOD transgenic mice.
|
11507057 |
2001 |
Tumor Progression
|
0.070 |
AlteredExpression
|
phenotype |
BEFREE |
The actin-binding protein Ezrin and the activator protein 1 (AP-1) transcription factor are implicated in cancer progression and metastasis.
|
23752190 |
2014 |
Tumor Progression
|
0.070 |
AlteredExpression
|
phenotype |
BEFREE |
Here we show that at the receiving end of the miR-10b pathway is the proto-oncogene c-Jun, a transcription factor that plays a critical role in stimulation of cell proliferation and tumor progression. c-Jun is known to be translationally activated by loss of cell contacts or restructuring of the cytoskeleton.
|
27494896 |
2016 |
Tumor Progression
|
0.070 |
AlteredExpression
|
phenotype |
BEFREE |
Gefitinib-resistant cells acquired an increased expression and activation of JUN, a known oncogene involved in cancer progression.
|
28566434 |
2017 |
Tumor Progression
|
0.070 |
AlteredExpression
|
phenotype |
BEFREE |
In summary, there are a variety of mechanisms underlying the induction of c-Jun protein expression and activity leading to tumor progression and development, and this diverse regulatory machinery is due to the heterogeneity of different tumor types, particularly in malignant melanoma.
|
24315690 |
2015 |
Tumor Progression
|
0.070 |
Biomarker
|
phenotype |
BEFREE |
Nuclear factor-kappaB (NF-κB) and activator protein 1 (AP-1) is a major transcription factor which regulates many biological and pathological processes such as inflammation and cell proliferation, which are major implicates in cancer progression.
|
29287195 |
2018 |
Tumor Progression
|
0.070 |
Biomarker
|
phenotype |
BEFREE |
Our results show that Jun proteins (pc-Jun and JunD) influence carcinogenesis and tumour progression, suggesting a significant role as prognostic predictors in human ovarian carcinoma.
|
23942796 |
2013 |
Tumor Progression
|
0.070 |
AlteredExpression
|
phenotype |
BEFREE |
The AP-1 factor JUNB was shown to drive ALCL proliferation and the expression of the characteristic ALCL Ki-1 antigen, CD30. cJUN and JUNB target PDGFRB, thereby leading to tumor progression and dissemination.
|
25961698 |
2015 |
Tumor Immunity
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Furthermore, we expose how the misdirected action of the main regulators of these miRNAs, such as nuclear factor κB (NF-κB), activator protein-1 (AP-1), and signal transduction and activators of transcription (STAT) transcription factors, or AKT and transforming growth factor β (TGFβ) signaling pathways, can contribute to decrease anti-tumor immunity and enhance cell proliferation and oncogenesis.
|
23550646 |
2013 |
Tumor Cell Invasion
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Following direct co-culture with MSCs, breast cancer cells expressed elevated levels of oncogenes (NCOA4, FOS), proto-oncogenes (FYN, JUN), genes associated with invasion (MMP11), angiogenesis (VEGF) and anti-apoptosis (IGF1R, BCL2).
|
20087650 |
2010 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Activator protein 1 (AP-1) contributes to EpCAM-dependent breast cancer invasion.
|
22132731 |
2011 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In summary, these results suggest that c-Src, mitogen-activated protein kinase, and a composite activator protein 1 on the uPA promoter are responsible for EGF-induced uPA expression and GBM invasion.
|
20467333 |
2010 |