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Recombinant Human Tumor necrosis factor receptor superfamily member 12A protein (TNFRSF12A), partial (Active)

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  • 货号:
  • 规格:
  • 图片:
  • 其他:


  • 纯度:
    >95% as determined by SDS-PAGE.
  • 内毒素:
    Less than 1.0 EU/μg as determined by LAL method.
  • 生物活性:
    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 >3.3x104 IU/mg, in the presence of 15 ng/ml of rHuTWEAK.
  • 基因名:
  • Uniprot No.:
  • 别名:
    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
  • 种属:
    Homo sapiens (Human)
  • 蛋白长度:
  • 来源:
  • 分子量:
    5.6 kDa
  • 表达区域:
  • 氨基酸序列
  • 蛋白标签:
  • 产品提供形式:
    Liquid or Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 缓冲液:
    0.2 μm filtered PBS, pH 7.4 ,lyophilized
  • 储存条件:
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期:
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期:
    5-10 business days
  • Datasheet & COA:
    Please contact us to get it.



  • 功能:
    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.
  • 基因功能参考文献:
    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



  • 亚细胞定位:
    Membrane; Single-pass type I membrane protein.
  • 组织特异性:
    Highly expressed in heart, placenta and kidney. Intermediate expression in lung, skeletal muscle and pancreas.
  • 数据库链接:

    HGNC: 18152

    OMIM: 605914

    KEGG: hsa:51330

    STRING: 9606.ENSP00000326737

    UniGene: Hs.355899