Recombinant Human TWEAKR Protein (Fc Tag)

Beta LifeScience SKU/CAT #: BLPSN-4702

Recombinant Human TWEAKR Protein (Fc Tag)

Beta LifeScience SKU/CAT #: BLPSN-4702
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Product Overview

Tag Fc
Host Species Human
Accession Q9NP84
Synonym CD266, FN14, TWEAKR
Background Fn14 (tumor necrosis factor receptor superfamily, member 12A), also known as TNFRSF12A, is the receptor for TNFSF12/TWEAK. Fn14 shares 82% amino acid identity with the mouse sequence. It contains a signal peptide, an extracellular domain, a membrane-anchoring domain, and a cytoplasmic domain. In response to FGF1, calf serum, or phorbol ester stimulation of human quiescent fibroblasts in vitro, the level of Fn14 is increased. A 1.2-kb FN14 transcript was expressed at high levels in heart, placenta, and kidney, at intermediate levels in lung, skeletal muscle, and pancreas, and at low levels in brain and liver. In addition, elevated FN14 expression was found in human liver cancer cell lines and hepatocellular carcinoma specimens. Expression of mouse Fn14 was upregulated in hepatocellular carcinoma nodules that develop in 2 different transgenic mouse models of hepatocarcinogenesis. TNFRSF12A is the weak inducer of apoptosis in some cell types. It promotes angiogenesis and the proliferation of endothelial cells. TNFRSF12A may modulate cellular adhesion to matrix proteins.
Description A DNA sequence encoding the human TNFRSF12A isoform 1 (Q9NP84-1) extracellular domain (Glu 28-Trp 79) was fused with the Fc region of human IgG1 at the N-terminus.
Source HEK293
Predicted N Terminal Glu
AA Sequence Glu 28-Trp 79
Molecular Weight The recombinant human TNFRSF12A/Fc chimera is a disulfide-linked homodimeric protein. The reduced monomer consists of 313 a.a. and has a calculated molecular mass of 34 kDa. In SDS-PAGE under reducing conditions, the apparent molecular mass of rhTNFRSF12A/Fc monomer is approximately 37 kDa.
Purity >95% as determined by SDS-PAGE
Endotoxin < 1.0 EU per μg of the protein as determined by the LAL method
Bioactivity Immobilized Cynomolgus mFc-TNFSF12 at 10 ug/ml (100 ul/well) can bind human Fc-TNFRSF12A, The ED50 of human Fc-TNFRSF12A is 0.07-0.15 ug/ml.
Formulation Lyophilized from sterile PBS, pH 7.4.
Stability The recombinant proteins are stable for up to 1 year from date of receipt at -70°C.
Usage For Research Use Only
Storage Store the protein under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

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
Tissue Specificity Highly expressed in heart, placenta and kidney. Intermediate expression in lung, skeletal muscle and pancreas.

Gene Functions References

  1. 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. PMID: 29741404
  2. TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-kappaB pathway PMID: 29143982
  3. Data demonstrated that the Src/Fn14/NF-kappaB axis plays a critical role in NSCLC metastasis. PMID: 29500337
  4. 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
  5. TWEAK/Fn14 contributes to endothelial dysfunction through modulation of reactive oxygen species (ROS), and mitochondrial ROS. PMID: 29257217
  6. 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
  7. 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
  8. 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
  9. TWEAK upregulated the expression of Fn14. PMID: 28411440
  10. Fn14.TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK which induces lymphoblast apoptosis. PMID: 28455246
  11. 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
  12. 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
  13. 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
  14. 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
  15. EGFR Del 19 may promote Fn14 and JAK1/STAT1 expression in NSCLC. PMID: 27350337
  16. TWEAK/Fn14 activation induces keratinocyte proliferation under psoriatic inflammation PMID: 26264384
  17. 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
  18. 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
  19. 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
  20. Fn14 has multiple roles in tumor metastasis. (Review) PMID: 26592249
  21. TWEAK/Fn14 interaction promotes oxidative stress through NADPH oxidase activation in macrophages. PMID: 26224570
  22. 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
  23. Fn14 modulates cell growth and drug resistance by upregulating Bcl-xl expression through the NF-kappaB pathway. PMID: 25054270
  24. 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
  25. HPV type 16 infections keratinocytes turns from apoptosis to proliferation cycle under FN14 protein influence. PMID: 26016896
  26. The first human data to show a transient activation of the TWEAK-Fn14 axis. PMID: 25539934
  27. TWEAK-Fn14 axis may be involved in the pathogenesis of polymyositis and dermatomyositis PMID: 24467773
  28. TweakR protein was expressed in about half of human breast cancer samples PMID: 25375638
  29. abundantly expressed in the dermal vessel wall of lesional skin in patients with urticarial vasculitis but not controls PMID: 23968277
  30. Results position TWEAK-Fn14 signaling through Mcl-1 as a significant mechanism for NSCLC tumor cell survival PMID: 24469836
  31. results define one upstream mechanism, via FN14 signaling, through which the NFkappaB pathway contributes to prostate cancer metastasis. PMID: 24970477
  32. 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
  33. insight into the Fn14 signaling mechanism PMID: 23750247
  34. High FN14 expression is associated with resistance to 5-fluorouracil in gastric cancer. PMID: 24337061
  35. 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
  36. 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
  37. 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
  38. Increased podocyte Fn14 expression is associated with proteinuric kidney disease. PMID: 23999007
  39. Fn14 overexpression is associated with hepatocellular carcinoma. PMID: 23886137
  40. Induced overexpression of Fn14 levels in MCF7 cells through HER2 (ERBB2) signaling translated to an improved therapeutic index of hSGZ treatment. PMID: 23722548
  41. Fn14 protein may have a role in breast carcinoma progression PMID: 23300011
  42. 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
  43. The Fn14/TWEAK pathway contributes to the endothelial steps of neuroinflammation. PMID: 23320797
  44. 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
  45. TWEAK/Fn14, by activating macrophages, could be ovarian tumor suppressors. PMID: 23469193
  46. 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
  47. TWEAK binds to hFn14 by surface plasmon resonance (View interaction) xeFn14 binds to TWEAK by enzyme linked immunosorbent assay PMID: 23438059
  48. LCN2 and TWEAKR-TWEAK as crucial downstream effectors of NFAT1 that regulate breast cancer cell motility and invasive capacity. PMID: 22767506
  49. Fn14, the receptor for TNF-like weak inducer of apoptosis, is selectively upregulated in patients with Alcoholic Hepatitis. PMID: 22637703
  50. 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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