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EGFR inhibitors display limited therapeutic efficacy in Glioblastoma multiforme (GBM) patients, the EGFRvIII-Stat5-Fn14 signaling pathway represents a node of vulnerability in the invasive GBM cell populations.Implications: Targeting critical effectors in the EGFRvIII-Stat5-Fn14 pathway may limit GBM tumor dispersion, mitigate therapeutic resistance, and increase survival.
These results demonstrate that TWEAK/Fn14 signaling contributes to Graves' orbitopathy (GO) pathogenesis. Moreover, serum TWEAK level is a potential diagnostic biomarker for inflammatory GO, and modulating TWEAK activity may be an effective therapeutic strategy for suppressing inflammation and tissue remodeling in GO.
High levels of TNFRSF12A associated with MMP-9 overexpression may be important to explain the progression of breast cancer, and survival could be improved using therapy targeting TNFRSF12A.
PK/PD model suggested a unique bell-shaped relationship between target coverage and antibody affinity for anti-Fn14 monoclonal antibody.
Expression level of Fn14 was significantly associated with overall survival and disease-free survival in low-grade gliomas. Fn14 was an independent predictive biomarker for the progression and prognosis in low-grade gliomas.
TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-kappaB pathway
Data demonstrated that the Src/Fn14/NF-kappaB axis plays a critical role in NSCLC metastasis.
Results show that Fn14 expression is high compared in non-small cell lung cancer compared to normal lung tissues. In addition, high Fn14 expression is associated with poor prognosis in lung adenocarcinoma.
TWEAK/Fn14 contributes to endothelial dysfunction through modulation of reactive oxygen species (ROS), and mitochondrial ROS.
Expression of the TWEAK-Fn14 axis was upregulated in patients with autoimmune thyroid disease and might play a role in the pathogenesis of autoimmune thyroid disease.
Data suggest that expression of Fn14 on a tumor can initiate cachexia; an antibody against Fn14 may be an effective antineoplastic agent. [REVIEW]
The results suggest that TWEAK/Fn14 interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB pathways.
TWEAK upregulated the expression of Fn14.
Fn14.TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK which induces lymphoblast apoptosis.
Data show that aurintricarboxylic acid (ATA) targets the TNF-related WEAK inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling axis, which could potentially be developed as a new therapeutic agent for treatment of glioblastoma (GBM) patients.
TNFRSF12A was knocked down in the SMMC7721 cell line through siRNA. This demonstrated that cells exhibited reduced reproductive and metastatic capacity ex vivo.
In this review article, we summarize studies indicating that (i) Fn14 gene expression is low in normal brain tissue but is upregulated in advanced brain cancers and, in particular, in GB tumors ; TWEAK: Fn14 engagement as well as Fn14 overexpression can stimulate glioma cell migration, invasion and resistance to chemotherapeutic agents in vitro.
Fn14 is a receptor of mitogen TWEAK (tumor necrosis factor-like weak inducer of apoptosis), expressed on the membranes of HPCs and promoting their proliferation.
EGFR Del 19 may promote Fn14 and JAK1/STAT1 expression in NSCLC.
TWEAK/Fn14 activation induces keratinocyte proliferation under psoriatic inflammation
stimulating the TWEAK-Fn14 pathway may elevate the expression of NF-kappaB, thereby slow the function recovery of SCI mice whereas inhibiting the TWEAK-Fn14 pathway may improve the neurogenesis status in mice with spinal cord injuries.
this study shows that Fn14 deficiency effectively protects SCID mice from anti-dsDNA IgG-induced glomerular damage
Fn14 on PMVECs plays an important role in the progress of septic Acute Lung Injury. Fn14 blockade may prove to be an innovative lung-protective strategy for the treatment of septic Acute Lung Injury.
TWEAK/Fn14 signalling is important in the pathogenesis of ultraviolet B-induced cutaneous disease manifestations in the MRL/lpr model of lupus.
Disruption of the TWEAK/Fn14 pathway affects several interconnected pathways, including those associated with IL-13, IL-33, and IL-13Ralpha2, to attenuate 5-fluorouracil-induced intestinal side effects.
TWEAK/Fn14 interactions play an important role in the pathogenesis of neuropsychiatric lupus by increasing the accumulation of inflammatory cells in the choroid plexus, disrupting blood brain barrier integrity, and increasing neuronal damage
TWEAK/Fn14 signaling is strongly implicated in the pathogenesis of the cutaneous manifestations in the MRL/lpr model of spontaneous lupus in mice.
In SOD1 and Neurotomized mice the results of this studysuggest LC3, Fn14, Bcl3 and Gadd45a as candidate genes involved in the maintenance of the severe atrophic state.
Fn14 mediates wound-healing responses that are necessary to survive acute liver injury during alcohol exposure.
Overexpression of Dnmt3a inhibits the gene expression of Fn14 and attenuates skeletal muscle atrophy upon denervation. Denervation also causes the activation of ERK1/2, JNK1/2, and ERK5 MAPKs and AP1 and SP1.
TWEAK-FN14 signaling is necessary for the healthy adult liver to regenerate normally after acute partial hepatectomy.
role in inflammation, fibrosis, and T helper 2-type immunity in colitis
The levels of TWEAK receptor Fn14 are increased in skeletal muscle during aging. Deletion of Fn14 attenuates age-associated skeletal muscle fiber atrophy.
this study showed that the apoptosis signal-regulating kinase 1 (ASK1)-JNK1/2 pathway, which was activated by large magnitude mechanical stretch induced expression of Fn14 gene in osteoblasts.
a model in which constitutive down-regulation of Fn14 facilitates dynamic regulation of Fn14 protein levels and prevents spontaneous or inappropriate receptor signaling.
study demonstrates that TWEAK induces muscle atrophy through repressing the levels of PGC-1alpha
Data show that TWEAK receptor (Fn14) deficiency delays formation of regenerating foci after partial pancreatectomy (Px) and limits their expansion.
We found that the TNF-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor inducible-14 (Fn14) pathway is involved in the development of pathologic retinal neovascularization.
Fn14 ablation attenuates right ventricular hypertrophy after Pulmonary Artery Banding and activation of TWEAK/Fn14 signaling promotes cardiomyocyte growth in vitro.
Manifestations of neuropsychiatric lupus, including depression-like behavior and altered cognition, are normalized in MRL/lpr mice lacking Fn14. Results indicate a role for the TWEAK/Fn14 pathway in the pathogenesis of neuropsychiatric lupus.
The TWEAK-independent Fn14 activation augments TLR4-mediated inflammatory responses in the intestine of piglets.
Receptor for TNFSF12/TWEAK. Weak inducer of apoptosis in some cell types. Promotes angiogenesis and the proliferation of endothelial cells. May modulate cellular adhesion to matrix proteins.
, fibroblast growth factor-inducible immediate-early response protein 14
, tumor necrosis factor receptor superfamily member 12A
, type I transmembrane protein Fn14
, fibroblast growth factor regulated protein 2
, fibroblast growth factor-regulated protein 2
, fibroblast growth factor-inducible 14