|
Kidney Failure, Acute
|
0.340 |
Biomarker
|
disease |
BEFREE |
Our study underscores an adaptive mechanism whereby TLR4 regulates SCF<sup>Fbxw7α</sup>-dependent Fn14 stabilization during inflammatory tubular damage and further supports investigation of targeting Fn14 in clinical trials of patients with septic AKI.
|
31017010 |
2019 |
|
Kidney Failure, Acute
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
Additionally, folic acid-induced AKI in mice resulted in increased expression of Fn14 and necroptosis mediators, such as receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage domain-like protein (MLKL).
|
29588419 |
2018 |
|
Kidney Failure, Acute
|
0.340 |
Biomarker
|
disease |
CTD_human |
Repeat oral dose toxicity studies of melamine in rats and monkeys.
|
23052191 |
2013 |
|
Kidney Failure, Acute
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
A transcriptomics analysis of experimental AKI revealed increased kidney expression of Fn14 and transmembrane chemokine CXCL16, as well as a decreased expression of the kidney-secreted anti-ageing hormone Klotho.
|
23093094 |
2012 |
|
Kidney Failure, Acute
|
0.340 |
Biomarker
|
disease |
BEFREE |
The TWEAK/Fn14 pathway contributed to cell death and interstitial inflammation during acute kidney injury, to glomerular injury in lupus nephritis, to hyperlipidemia-associated kidney injury, and to tubular cell hyperplasia following unilateral nephrectomy.
|
21697814 |
2011 |
|
Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
|
Acute Kidney Insufficiency
|
0.300 |
Biomarker
|
disease |
CTD_human |
Repeat oral dose toxicity studies of melamine in rats and monkeys.
|
23052191 |
2013 |
|
Acute kidney injury
|
0.300 |
Biomarker
|
disease |
CTD_human |
Repeat oral dose toxicity studies of melamine in rats and monkeys.
|
23052191 |
2013 |
|
Myocardial Infarction
|
0.300 |
Biomarker
|
disease |
CTD_human |
Likewise, a rapid and sustained elevation of Fn14 mRNA and protein levels in the left ventricle was observed after experimental MI.
|
20082609 |
2010 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Fibroblast growth factor inducible-14 (Fn14) is a receptor protein that plays an important role in the progression of cancer and some other diseases.
|
31580829 |
2019 |
|
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
We have shown previously that FN14 (TNFRSF12A) and downstream NF-κB signaling is required for metastasis in this model.
|
31312026 |
2019 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Moreover, TWEAK/Fn14 activation promoted the proliferation, migration, and invasion of cultured SCC cells.
|
30414907 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Fibroblast growth factor inducible-14 (Fn14) is a receptor protein that plays an important role in the progression of cancer and some other diseases.
|
31580829 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Fn14 mRNA expression levels in nonneoplastic brain, primary (newly diagnosed) GBM, and recurrent GBM (post-chemotherapy and radiation) specimens were obtained from The Cancer Genome Atlas data portal.
|
29897522 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This phase I study evaluates the safety, MTD, pharmacokinetics (PK), pharmacodynamics, and preliminary anticancer activity of enavatuzumab, a humanized IgG1 antibody to the TWEAK receptor, in patients with advanced solid malignancies.
|
29054986 |
2018 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, it is reported that EGFRvIII activates Stat5 and GBM invasion by inducing the expression of a previously established mediator of glioma cell invasion and survival: fibroblast growth factor-inducible 14 (Fn14).
|
29724813 |
2018 |
|
Glioma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These results support a role for Fn14 in the more aggressive and invasive phenotype associated with IDH1 WT tumors and indicate that the low levels of Fn14 gene expression noted in IDH1 R132H mutant gliomas may be due to epigenetic regulation via changes in DNA methylation.
|
29453678 |
2018 |
|
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
CONCLUSIONS The data demonstrated that the Src/Fn14/NF-κB axis plays a critical role in NSCLC metastasis.
|
29500337 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
GBM is notable for a highly infiltrative growth pattern and several groups have reported that high Fn14 expression levels can increase tumor cell invasiveness.
|
29453678 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Fn14 expression is also significantly elevated in GSM tumors.
|
29897522 |
2018 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Overexpression of Fn14 restored the potential of migration and invasion as well as the activation of NF-κB signaling in Src-silenced NSCLC cells.
|
29500337 |
2018 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Here, it is reported that EGFRvIII activates Stat5 and GBM invasion by inducing the expression of a previously established mediator of glioma cell invasion and survival: fibroblast growth factor-inducible 14 (Fn14).
|
29724813 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Fn14 mRNA expression levels in nonneoplastic brain, primary (newly diagnosed) GBM, and recurrent GBM (post-chemotherapy and radiation) specimens were obtained from The Cancer Genome Atlas data portal.
|
29897522 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Because EGFR inhibitors display limited therapeutic efficacy in GBM patients, the EGFRvIII-Stat5-Fn14 signaling pathway represents a node of vulnerability in the invasive GBM cell populations.<b>Implications:</b> Targeting critical effectors in the EGFRvIII-Stat5-Fn14 pathway may limit GBM tumor dispersion, mitigate therapeutic resistance, and increase survival.<i></i>.
|
29724813 |
2018 |
|
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We found that Fn14 is more highly expressed in recurrent GBM tumors than their matched primary GBM counterparts.
|
29897522 |
2018 |