Recombinant Human Tumor Necrosis Factor Receptor Superfamily Member 12A Protein (TNFRSF12A), Active

Beta LifeScience SKU/CAT #: BLC-06053P

Recombinant Human Tumor Necrosis Factor Receptor Superfamily Member 12A Protein (TNFRSF12A), Active

Beta LifeScience SKU/CAT #: BLC-06053P
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Product Overview

Description Recombinant Human Tumor Necrosis Factor Receptor Superfamily Member 12A Protein (TNFRSF12A), Active is produced by our E.coli expression system. This is a protein fragment.
Purity Greater than 95% as determined by SDS-PAGE and HPLC.
Endotoxin Less than 1.0 EU/μg as determined by LAL method.
Activity Fully biologically active when compared to standard. The ED50 as determined by inhibiting TWEAK- dependent proliferation of human umbilical vein endothelial cells (HUVEC) is less than 30 ng/ml, corresponding to a specific activity of >3.3x10 4 IU/mg, in the presence of 15 ng/ml of rHuTWEAK.
Uniprotkb Q9NP84
Target Symbol TNFRSF12A
Synonyms CD 266; CD266; CD266 antigen; FGF inducible 14; FGF-inducible 14; Fibroblast growth factor inducible immediate early response protein 14; Fibroblast growth factor-inducible immediate-early response protein 14; FN 14; FN14; TNFRSF 12A; TNFRSF12A; TNR12_HUMAN; Tumor necrosis factor receptor superfamily member 12A; TWEAK R; Tweak receptor; Tweak-receptor; TweakR
Species Homo sapiens (Human)
Expression System E.Coli
Tag Tag-Free
Complete Sequence EQAPGTAPCS RGSSWSADLD KCMDCASCRA RPHSDFCLGC AAAPPAPFRL LWP
Expression Range 28-80aa
Protein Length Partial
Mol. Weight 5.6 kDa
Research Area Cancer
Form Liquid or Lyophilized powder
Buffer 0.2 μm filtered PBS, pH 7.4, lyophilized
Storage 1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.

Target Details

Target Function 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.
Subcellular Location Membrane; Single-pass type I membrane protein.
Database References

HGNC: 18152

OMIM: 605914

KEGG: hsa:51330

STRING: 9606.ENSP00000326737

UniGene: PMID: 29741404

  • TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-kappaB pathway PMID: 29143982
  • Data demonstrated that the Src/Fn14/NF-kappaB axis plays a critical role in NSCLC metastasis. PMID: 29500337
  • 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. PMID: 29251323
  • TWEAK/Fn14 contributes to endothelial dysfunction through modulation of reactive oxygen species (ROS), and mitochondrial ROS. PMID: 29257217
  • 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. PMID: 28636775
  • Data suggest that expression of Fn14 on a tumor can initiate cachexia; an antibody against Fn14 may be an effective antineoplastic agent. [REVIEW] PMID: 27254081
  • 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. PMID: 27441657
  • TWEAK upregulated the expression of Fn14. PMID: 28411440
  • Fn14.TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK which induces lymphoblast apoptosis. PMID: 28455246
  • 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. PMID: 28103571
  • TNFRSF12A was knocked down in the SMMC7721 cell line through siRNA. This demonstrated that cells exhibited reduced reproductive and metastatic capacity ex vivo. PMID: 28138696
  • 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. PMID: 26300004
  • 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. PMID: 28180936
  • EGFR Del 19 may promote Fn14 and JAK1/STAT1 expression in NSCLC. PMID: 27350337
  • TWEAK/Fn14 activation induces keratinocyte proliferation under psoriatic inflammation PMID: 26264384
  • 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. PMID: 27051016
  • Results indicate that FN14 and GRP94 are prediction/prognosis markers which open up new possibilities for preventing/treating brain metastasis in breast cancer patients. PMID: 26497551
  • Evidence that higher tumor Fn14 expression is required for pharmacodynamic response to the anti-TWEAK monoclonal antibody RG7212 in patients with Fn14-positive solid tumors. PMID: 26446946
  • Fn14 has multiple roles in tumor metastasis. (Review) PMID: 26592249
  • TWEAK/Fn14 interaction promotes oxidative stress through NADPH oxidase activation in macrophages. PMID: 26224570
  • Activated Fn14 expression increases extracellular matrix synthesis and fibroblast activation. Activation of Fn14 is done by the TGF-beta signaling pathway through the transcription factor SMAD4. PMID: 26625141
  • Fn14 modulates cell growth and drug resistance by upregulating Bcl-xl expression through the NF-kappaB pathway. PMID: 25054270
  • Results indicate that oncogenic Src may contribute to Fn14 overexpression in solid tumors, and that Src mediated cell invasion could potentially be inhibited with Fn14- targeted therapeutics. PMID: 25392346
  • HPV type 16 infections keratinocytes turns from apoptosis to proliferation cycle under FN14 protein influence. PMID: 26016896
  • The first human data to show a transient activation of the TWEAK-Fn14 axis. PMID: 25539934
  • TWEAK-Fn14 axis may be involved in the pathogenesis of polymyositis and dermatomyositis PMID: 24467773
  • TweakR protein was expressed in about half of human breast cancer samples PMID: 25375638
  • abundantly expressed in the dermal vessel wall of lesional skin in patients with urticarial vasculitis but not controls PMID: 23968277
  • Results position TWEAK-Fn14 signaling through Mcl-1 as a significant mechanism for NSCLC tumor cell survival PMID: 24469836
  • results define one upstream mechanism, via FN14 signaling, through which the NFkappaB pathway contributes to prostate cancer metastasis. PMID: 24970477
  • Receptor-targeted therapeutics for both MET and FN14 are in clinical development, the use of which may mitigate the metastatic potential of NSCLC. PMID: 24710956
  • insight into the Fn14 signaling mechanism PMID: 23750247
  • High FN14 expression is associated with resistance to 5-fluorouracil in gastric cancer. PMID: 24337061
  • a model in which constitutive down-regulation of Fn14 facilitates dynamic regulation of Fn14 protein levels and prevents spontaneous or inappropriate receptor signaling. PMID: 24652288
  • 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. PMID: 24408972
  • These new findings of the effect of Fn14 on valvular interstitial cell-like differentiation may provide a novel therapeutic strategy for heart valve disease treatment. PMID: 24122208
  • Increased podocyte Fn14 expression is associated with proteinuric kidney disease. PMID: 23999007
  • Fn14 overexpression is associated with hepatocellular carcinoma. PMID: 23886137
  • Induced overexpression of Fn14 levels in MCF7 cells through HER2 (ERBB2) signaling translated to an improved therapeutic index of hSGZ treatment. PMID: 23722548
  • Fn14 protein may have a role in breast carcinoma progression PMID: 23300011
  • results validate the TWEAK-Fn14 interaction as a chemically tractable target and provide the foundation for further exploration utilizing chemical biology approaches focusing on validating this system as a therapeutic target in invasive cancers. PMID: 24056367
  • The Fn14/TWEAK pathway contributes to the endothelial steps of neuroinflammation. PMID: 23320797
  • The expression of TWEAK and Fn14 in neuroblastoma suggests that TWEAK functions as an important regulator of primary neuroblastoma growth, invasion and survival. PMID: 23443741
  • TWEAK/Fn14, by activating macrophages, could be ovarian tumor suppressors. PMID: 23469193
  • we show that TWEAK/Fn14 can signal through the JAK-STAT pathway to induce interferon-beta, and that the ability of TWEAK to induce tumor cell apoptosis is mediated by JAK-STAT signaling. PMID: 23107828
  • TWEAK binds to hFn14 by surface plasmon resonance (View interaction) xeFn14 binds to TWEAK by enzyme linked immunosorbent assay PMID: 23438059
  • LCN2 and TWEAKR-TWEAK as crucial downstream effectors of NFAT1 that regulate breast cancer cell motility and invasive capacity. PMID: 22767506
  • Fn14, the receptor for TNF-like weak inducer of apoptosis, is selectively upregulated in patients with Alcoholic Hepatitis. PMID: 22637703
  • TWEAK/Fn14 can regulate expression and secretion of HMGB1 in monocytes/macrophages, participating in the inflammatory response associated with atherosclerotic plaque development. PMID: 23288170

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    Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

    Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

    Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

    Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

    To learn more about how to properly dissolve the lyophilized recombinant protein, please visit Lyophilization FAQs.

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