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Human TNFRSF12A Protein expressed in HEK-293 Cells - ABIN2181851
Wiley, Cassiano, Lofton, Davis-Smith, Winkles, Lindner, Liu, Daniel, Smith, Fanslow: A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis. in Immunity 2001
Show all 2 references for ABIN2181851
Human TNFRSF12A Protein expressed in Human Cells - ABIN2002839
Burkly, Dohi: The TWEAK/Fn14 pathway in tissue remodeling: for better or for worse. in Advances in experimental medicine and biology 2010
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.
Results indicate that FN14 and GRP94 (show HSP90B1 Proteins) are prediction/prognosis markers which open up new possibilities for preventing/treating brain metastasis in breast cancer patients.
Evidence that higher tumor Fn14 expression is required for pharmacodynamic response to the anti-TWEAK (show TNFSF12 Proteins) monoclonal antibody RG7212 in patients with Fn14-positive solid tumors.
Fn14 has multiple roles in tumor metastasis. (Review)
TWEAK (show TNFSF12 Proteins)/Fn14 interaction promotes oxidative stress through NADPH oxidase (show NOX1 Proteins) activation in macrophages.
Activated Fn14 expression increases extracellular matrix synthesis and fibroblast activation. Activation of Fn14 is done by the TGF-beta (show TGFB1 Proteins) signaling pathway through the transcription factor SMAD4 (show SMAD4 Proteins).
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