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The results suggest that TWEAK (show TNFSF12 Proteins)/Fn14 interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB (show NFKB1 Proteins) pathways.
TWEAK (show TNFSF12 Proteins) upregulated the expression of Fn14.
Fn14.TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK (show TNFSF12 Proteins) which induces lymphoblast apoptosis.
Data show that aurintricarboxylic acid (ATA) targets the TNF-related WEAK inducer of apoptosis (TWEAK (show TNFSF12 Proteins))-fibroblast growth factor-inducible 14 (show DDX3X Proteins) (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 (show TNFSF12 Proteins): 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 (show TNFSF12 Proteins) (tumor necrosis factor (show TNF Proteins)-like weak inducer of apoptosis), expressed on the membranes of HPCs and promoting their proliferation.
EGFR (show EGFR Proteins) Del 19 may promote Fn14 and JAK1 (show JAK1 Proteins)/STAT1 (show STAT1 Proteins) expression in NSCLC.
TWEAK (show TNFSF12 Proteins)/Fn14 activation induces keratinocyte proliferation under psoriatic inflammation
The results demonstrated that vitreous fluid from patients with PDR had higher levels of TWEAK and Fn14 than that from T2DM patients without PDR, thus suggesting an important regulatory role of TWEAK/Fn14 signaling in the pathogenesis of PDR.
TWEAK (show TNFSF12 Proteins)/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 (show TNFSF12 Proteins)/Fn14 signaling is strongly implicated in the pathogenesis of the cutaneous manifestations in the MRL/lpr (show FAS Proteins) model of spontaneous lupus in mice.
In SOD1 (show SOD1 Proteins) and Neurotomized mice the results of this studysuggest LC3 (show MAP1LC3A Proteins), Fn14, Bcl3 (show BCL3 Proteins) and Gadd45a (show GADD45A Proteins) 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 (show DNMT3A Proteins) inhibits the gene expression of Fn14 and attenuates skeletal muscle atrophy upon denervation. Denervation also causes the activation of ERK1/2, JNK1 (show MAPK8 Proteins)/2, and ERK5 (show MAPK7 Proteins) MAPKs and AP1 (show JUN Proteins) and SP1 (show SP1 Proteins).
TWEAK (show TNFSF12 Proteins)-FN14 signaling is necessary for the healthy adult liver to regenerate normally after acute partial hepatectomy.
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 (show MAP3K5 Proteins))-JNK1 (show MAPK8 Proteins)/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
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