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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 (zeige TNFSF12 Proteine)/Fn14 interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB (zeige NFKB1 Proteine) pathways.
TWEAK (zeige TNFSF12 Proteine) upregulated the expression of Fn14.
Fn14.TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK (zeige TNFSF12 Proteine) which induces lymphoblast apoptosis.
Data show that aurintricarboxylic acid (ATA) targets the TNF-related WEAK inducer of apoptosis (TWEAK (zeige TNFSF12 Proteine))-fibroblast growth factor-inducible 14 (zeige DDX3X Proteine) (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 (zeige TNFSF12 Proteine): 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 (zeige TNFSF12 Proteine) (tumor necrosis factor (zeige TNF Proteine)-like weak inducer of apoptosis), expressed on the membranes of HPCs and promoting their proliferation.
EGFR (zeige EGFR Proteine) Del 19 may promote Fn14 and JAK1 (zeige JAK1 Proteine)/STAT1 (zeige STAT1 Proteine) expression in NSCLC.
TWEAK (zeige TNFSF12 Proteine)/Fn14 activation induces keratinocyte proliferation under psoriatic inflammation
TWEAK (zeige TNFSF12 Proteine)/Fn14 signalling is important in the pathogenesis of ultraviolet B-induced cutaneous disease manifestations in the MRL/lpr (zeige FAS Proteine) model of lupus.
Disruption of the TWEAK (zeige TNFSF12 Proteine)/Fn14 pathway affects several interconnected pathways, including those associated with IL-13 (zeige IL13 Proteine), IL-33 (zeige IL33 Proteine), and IL-13Ralpha2, to attenuate 5-fluorouracil-induced intestinal side effects.
TWEAK (zeige TNFSF12 Proteine)/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 (zeige TNFSF12 Proteine)/Fn14 signaling is strongly implicated in the pathogenesis of the cutaneous manifestations in the MRL/lpr (zeige FAS Proteine) model of spontaneous lupus in mice.
In SOD1 (zeige SOD1 Proteine) and Neurotomized mice the results of this studysuggest LC3 (zeige MAP1LC3A Proteine), Fn14, Bcl3 (zeige BCL3 Proteine) and Gadd45a (zeige GADD45A Proteine) 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 (zeige DNMT3A Proteine) inhibits the gene expression of Fn14 and attenuates skeletal muscle atrophy upon denervation. Denervation also causes the activation of ERK1/2, JNK1 (zeige MAPK8 Proteine)/2, and ERK5 (zeige MAPK7 Proteine) MAPKs and AP1 (zeige JUN Proteine) and SP1 (zeige SP1 Proteine).
TWEAK (zeige TNFSF12 Proteine)-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 (zeige MAP3K5 Proteine))-JNK1 (zeige MAPK8 Proteine)/2 pathway, which was activated by large magnitude mechanical stretch induced expression of Fn14 gene in osteoblasts.
The TWEAK (zeige TNFSF12 Proteine)-independent Fn14 activation augments TLR4 (zeige TLR4 Proteine)-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