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  4. Recombinant Mouse Tumor necrosis factor ligand superfamily member 12 (Tnfsf12), partial

Recombinant Mouse Tumor necrosis factor ligand superfamily member 12 (Tnfsf12), partial

  • 中文名稱：
    小鼠Tnfsf12重組蛋白
  • 貨號(hào)：
    CSB-YP023987MO1
  • 規(guī)格：
  • 來(lái)源：
    Yeast
  • 其他：
  • 中文名稱：
    小鼠Tnfsf12重組蛋白
  • 貨號(hào)：
    CSB-EP023987MO1
  • 規(guī)格：
  • 來(lái)源：
    E.coli
  • 其他：
  • 中文名稱：
    小鼠Tnfsf12重組蛋白
  • 貨號(hào)：
    CSB-EP023987MO1-B
  • 規(guī)格：
  • 來(lái)源：
    E.coli
  • 共軛：
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他：
  • 中文名稱：
    小鼠Tnfsf12重組蛋白
  • 貨號(hào)：
    CSB-BP023987MO1
  • 規(guī)格：
  • 來(lái)源：
    Baculovirus
  • 其他：
  • 中文名稱：
    小鼠Tnfsf12重組蛋白
  • 貨號(hào)：
    CSB-MP023987MO1
  • 規(guī)格：
  • 來(lái)源：
    Mammalian cell
  • 其他：

產(chǎn)品詳情

  • 純度：
    >85% (SDS-PAGE)
  • 基因名：
    Tnfsf12
  • Uniprot No.：
  • 別名：
    Tnfsf12; Tumor necrosis factor ligand superfamily member 12; TNF-related weak inducer of apoptosis; TWEAK
  • 種屬：
    Mus musculus (Mouse)
  • 蛋白長(zhǎng)度：
    Partial
  • 蛋白標(biāo)簽：
    Tag?type?will?be?determined?during?the?manufacturing?process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 產(chǎn)品提供形式：
    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.
  • 復(fù)溶：
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 儲(chǔ)存條件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保質(zhì)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.
  • 貨期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事項(xiàng)：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet ：
    Please contact us to get it.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

  • 功能：
    Binds to FN14 and possibly also to TNRFSF12/APO3. Weak inducer of apoptosis in some cell types. Mediates NF-kappa-B activation. Promotes angiogenesis and the proliferation of endothelial cells. Also involved in induction of inflammatory cytokines. Promotes IL8 secretion.
  • 基因功能參考文獻(xiàn)：
    1. TWEAK is a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis PMID: 28530223
    2. A Nec-1-sensitive cell death pathway, presumably driven by an inflammatory response involving TWEAK/Fn14 to an initial wave of cell death, appears to be responsible for amplification of the tubular cell death response and for persistence of acute kidney injury PMID: 29588419
    3. Our results illustrate a novel regulatory role of TWEAK, in which its activity positively regulates type I IFN pathway in lupus nephritis (LN) based on preclinical models. Our findings suggest TWEAK could act as a critical target in preventing renal damage in patients with LN. PMID: 29333443
    4. this paper shows that miR-200bc/429 cluster alleviates inflammation in IgA nephropathy by targeting TWEAK/Fn14 PMID: 28910745
    5. TWEAK:Fn14 binding activates non-canonical NF-kappaB signaling in B16 melanoma cells, inhibiting cell invasiveness. PMID: 27821799
    6. TWEAK/Fn14 signalling is important in the pathogenesis of ultraviolet B-induced cutaneous disease manifestations in the MRL/lpr model of lupus. PMID: 27305603
    7. Disruption of the TWEAK/Fn14 pathway affects several interconnected pathways, including those associated with IL-13, IL-33, and IL-13Ralpha2, to attenuate 5-fluorouracil-induced intestinal side effects. PMID: 28428709
    8. TWEAK promotes migration and invasion in murine embryonic fibroblasts through a mechanism dependent on ERKs activation and Fibulin 3 down-regulation. PMID: 28383766
    9. These results implicate TWEAK as a potential molecular target for treatment or prevention of inflammatory arthritis and autoimmune diseases such as rheumatoid arthritis. PMID: 27653285
    10. soluble Fn14 may serve as a potential biomarker for both acute and chronic kidney diseases. PMID: 27171494
    11. Findings suggest that TWEAK may contribute to chronic renal changes and renal fibrosis by activating TGF-beta1 signaling pathway, and phosphorylation of Smad2 and p38 MAPK proteins was also involved in this signaling pathway. PMID: 27365897
    12. TWEAK/Fn14 signaling represses PGC-1alpha expression during acute kidney injury through activation of canonical NF-kappaB pathways and epigenetic mechanisms including histone deacetylation on NF-kappaB-binding sites. PMID: 26535995
    13. These findings suggest that TWEAK signaling might be an aspect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine -mediated neuropathology and be involved in the overall neurodegenerative pathology of Parkinson's disease PMID: 26808775
    14. results revealed that TWEAK and Fn14 are expressed by uterine natural killer cells in pregnant mice PMID: 27040357
    15. studies show that signaling via TWEAK is deleterious to muscle in RNA toxicity and support the demonstrated utility of anti-TWEAK therapeutics. PMID: 26901467
    16. During ischaemia, soluble CD163 functions as a decoy receptor for TWEAK, to regulate TWEAK-induced activation of canonical nuclear factor-kappaB and Notch signalling necessary for myogenic progenitor cell proliferation. PMID: 26242746
    17. TWEAK/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 PMID: 25911200
    18. Tweak regulates astrogliosis, microgliosis and skeletal muscle atrophy in a mouse model of amyotrophic lateral sclerosis PMID: 25765661
    19. The results demonstrated that the expression levels of TWEAK and p-p38 MAPK increased in the periprosthetic interface membrane tissues and the RAW cells stimulated with Ti particles PMID: 25815691
    20. TWEAK/Fn14 signaling is strongly implicated in the pathogenesis of the cutaneous manifestations in the MRL/lpr model of spontaneous lupus in mice. PMID: 25826425
    21. Elevated levels of TWEAK in skeletal muscle promote visceral obesity, insulin resistance, and metabolic dysfunction. PMID: 25466899
    22. TWEAK/Fn14 pathway instrumental in the pathogenesis of spontaneous lupus nephritis PMID: 25270074
    23. our data indicate that anti-TWEAK treatment has the capacity to diminish proinflamatory response associated with atherosclerotic plaque progression and to alter plaque morphology towards a stable phenotype PMID: 24479820
    24. TWEAK and Fn14 are upregulated by high fat diet feeding and by adipocyte death. PMID: 24616441
    25. TWEAK-FN14 signaling is necessary for the healthy adult liver to regenerate normally after acute partial hepatectomy. PMID: 24416188
    26. show that Nrf2 protects SM from TWEAK-induced cell death in vitro and that Nrf2-deficient mice therefore have poorer muscle regeneration PMID: 24406502
    27. Treatment of mice with HSA-Flag-TWEAK induces myocardial healing defects after experimental MI. This is mediated by an exaggerated neutrophil infiltration into the myocardium. PMID: 24244389
    28. study demonstrates that TWEAK induces muscle atrophy through repressing the levels of PGC-1alpha PMID: 24327607
    29. 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
    30. TWEAK transactivation of the epidermal growth factor receptor mediates renal inflammation. PMID: 24037740
    31. TWEAK promotes osteoclastogenesis in rheumatoid arthritis. PMID: 23845567
    32. Notch signaling is significantly elevated in cultured satellite cells and in regenerating myofibers of TWEAK-KO mice. PMID: 24151074
    33. Manifestations of neuropsychiatric lupus, including depression-like behavior and altered cognition, are normalized in MRL/lpr mice lacking Fn14. Results indicate a role for the TWEAK/Fn14 pathway in the pathogenesis of neuropsychiatric lupus. PMID: 23578591
    34. lack of TWEAK reduces renal fibrosis in a model of persistent kidney insult and overexpression of TWEAK led to renal fibrosis PMID: 23748045
    35. Bone marrow injection stimulates hepatic ductular reactions in the absence of injury via macrophage-mediated TWEAK signaling. PMID: 23576749
    36. TWEAK can regulate expression and secretion of HMGB1 in monocytes/macrophages, participating in the inflammatory response associated with atherosclerotic plaque development. PMID: 23288170
    37. TWEAK, cIAP1, and noncanonical NF-kappaB signaling has roles in the regulation of myoblast fusion PMID: 23074266
    38. TWEAK upregulates the expression of the chemokine CXCL16 in tubular epithelium and this may contribute to kidney tubulointerstitial inflammation. PMID: 22278019
    39. Thie results of this study indicated that the interaction between TWEAK and Fn14 triggers the activation of a cell signaling pathway that results in the induction of tolerance to lethal hypoxia and ischemia. PMID: 22394384
    40. The mechanisms of action of TWEAK in the proteolysis of skeletal muscle require the roles of the ubiquitin-proteasome system, autophagy, and caspases in muscle-wasting myotubes. PMID: 21567392
    41. Tweak induces proliferation in renal tubular epithelium, and has a role in uninephrectomy induced renal hyperplasia PMID: 19426154
    42. Data show that TWEAK regulates adult neurogenesis in the subventricular zone by binding to the membrane receptor Fn14 and activating NF-kappaB. PMID: 21040786
    43. the TWEAK-Fn14 axis can regulate activation of TF and PAI-1 expression in vascular cells PMID: 20810696
    44. Genetic ablation of TWEAK augments regeneration and post-injury growth of skeletal muscle. PMID: 20724600
    45. TWEAK acts directly and stimulates liver progenitor cells (LPC) mitosis in an Fn14-dependent and NFkappaB-dependent fashion, and signaling via this pathway mediates the LPC response to CDE-induced injury and regeneration. PMID: 20578156
    46. during cerebral ischemia, the interaction between TWEAK and Fn14 leads to the recruitment of leukocytes into the ischemic tissue. PMID: 20068578
    47. results thus identify TWEAK as a regulator of non-canonical NFkappaB activation and CCL21 expression in tubular cells thus promoting lymphocyte recruitment to the kidney during acute injury PMID: 20126461
    48. results suggest that TWEAK affects the expression of several genes and microRNAs involved in inflammatory response, fibrosis, extracellular matrix remodeling, and proteolytic degradation which might be responsible for TWEAK-induced skeletal muscle loss PMID: 20098732
    49. The novel mediator of skeletal muscle atrophy and indicates that the TWEAK-Fn14 system is an important target for preventing skeletal muscle wasting. PMID: 20308426
    50. TWEAK mediated the differentiation of RAW monocyte/macrophage cells into osteoclasts; propose that the biological effects of TWEAK are mediated by binding to one of at least two receptors that induce differential activation of downstream signal pathways PMID: 12794080

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  • 亞細(xì)胞定位：
    Cell membrane; Single-pass type II membrane protein.; [Tumor necrosis factor ligand superfamily member 12, secreted form]: Secreted.
  • 蛋白家族：
    Tumor necrosis factor family
  • 組織特異性：
    Widely expressed.
  • 數(shù)據(jù)庫(kù)鏈接：