Human TNF α converting enzyme,TACE ELISA Kit

Code CSB-E09315h
Size 96T,5×96T,10×96T
Trial Size 24T ELISA kits trial application
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Product Details


Based on the Sandwich-ELISA principle and enzyme-substrate chromogenic reaction property, the users can measure the content of mouse ADAM17 in serum, plasma, tissue homogenates, and cell culture supernates. This mouse ADAM17 ELISA kit is quality tested with high specificity, excellent sensitivity, the precision of less than 10%, good linearity, and high recovery.

ADAM17, also called TACE, is a type I transmembrane metalloproteinase that is involved in the shedding of the extracellular domain of several transmembrane proteins such as cytokines, growth factors, receptors, and adhesion molecules thus regulating these crucial signaling pathways. It participates in various physiological and pathophysiological processes, including development, regeneration, differentiation, immunity, inflammation, neurodegeneration, fibrosis, and cancer progression. Overexpression of ADAM17 has been linked to invasion and metastasis in a variety of malignancies. Studies have shown that ADAM17 plays a potential role in breast cancer, including cell proliferation, invasion, angiogenesis, apoptosis, and therapy resistance.

Target Name ADAM metallopeptidase domain 17
Alternative Names ADAM17; CSVP; TACE; Disintegrin and metalloproteinase domain-containing protein 17; ADAM 17; Snake venom-like protease; TNF-alpha convertase; TNF-alpha-converting enzyme; CD antigen CD156b
Abbreviation ADAM17
Uniprot No. P78536
Species Homo sapiens (Human)
Sample Types serum, plasma, tissue homogenates, cell lysates
Detection Range 62.5 pg/mL-4000 pg/mL
Sensitivity 15.6 pg/mL
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Signal Transduction
Assay Principle quantitative
Measurement Sandwich
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
To assess the linearity of the assay, samples were spiked with high concentrations of human TACE in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:1Average %84
Range %80-90
1:2Average %97
Range %92-103
1:4Average %92
Range %86-99
1:8Average %93
Range %85-98
The recovery of human TACE spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 9589-100
EDTA plasma (n=4)9790-103
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
40001.931 1.872 1.902 1.770
20001.648 1.596 1.622 1.490
10001.335 1.304 1.320 1.188
5001.082 1.012 1.047 0.915
2500.643 0.609 0.626 0.494
1250.409 0.379 0.394 0.262
62.50.274 0.257 0.266 0.134
00.135 0.128 0.132  
ELISA Data Analysis Watch ELISA data processing video & download Curve Expert if needed
and FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 3-5 working days


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Target Background

(From Uniprot)
Cleaves the membrane-bound precursor of TNF-alpha to its mature soluble form. Responsible for the proteolytical release of soluble JAM3 from endothelial cells surface. Responsible for the proteolytic release of several other cell-surface proteins, including p75 TNF-receptor, interleukin 1 receptor type II, p55 TNF-receptor, transforming growth factor-alpha, L-selectin, growth hormone receptor, MUC1 and the amyloid precursor protein. Acts as an activator of Notch pathway by mediating cleavage of Notch, generating the membrane-associated intermediate fragment called Notch extracellular truncation (NEXT). Plays a role in the proteolytic processing of ACE2. Plays a role in hemostasis through shedding of GP1BA, the platelet glycoprotein Ib alpha chain. Mediates the proteolytic cleavage of LAG3, leading to release the secreted form of LAG3. Mediates the proteolytic cleavage of IL6R, leading to the release of secreted form of IL6R.
Gene References into Functions
  1. High ADAM17 expression is associated with cystic fibrosis. PMID: 29351448
  2. These findings link iNOS to Notch1 signaling in CD24(+)CD133(+) LCSCs through the activation of TACE/ADAM17. PMID: 30297396
  3. ADAM17 activation and secretion in the myeloid cells during HIV infection. PMID: 29331674
  4. A novel ADAM17 inhibitor ZLDI-8 may be a potential chemosensitizer which sensitized CRC cells to 5-fluorouracil or irinotecan by reversing Notch and EMT pathways. PMID: 30069943
  5. The isolated membrane proximal domain (MPD) of ADAM17 binds to phosphatidylserine (PS) but not to phosphatidylcholine liposomes. A cationic PS-binding motif is identified in this domain, replacement of which abrogates liposome-binding and renders the protease incapable of cleaving its substrates in cells. PMID: 27161080
  6. ADAM-17 in inflammatory myopathy was significantly higher than that in healthy control. ADAM-17 in post-treatment with corticosteroid and/or immunosuppressant serum was significantly decreased compared with that in pre-treatment serum. PMID: 29411180
  7. The present research suggests that ADAM17shRNA can inhibit MCF7 cell invasion and proliferation in vitro and inhibit MCF7 xenograft growth in vivo through the EGFR/PI3K/AKT and EGFR/MEK/ERK signaling pathways. PMID: 29393483
  8. Uev1A-Ubc13 complex catalyzes lysine63-linked ubiquitination of RHBDF2 to promote TACE maturation. PMID: 29069608
  9. ADAM17 plays a role in chronic kidney disease-mineral and bone disorder. PMID: 29056164
  10. Insulin-like growth factor-1 activates different catalytic subunits p110 of PI3K in a cell-type-dependent manner to induce lipogenesis-dependent epithelial-mesenchymal transition through the regulation of ADAM10 and ADAM17. PMID: 28819788
  11. ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157. Findings reveal a link between shedding of TREM2 and its regulation during inflammatory conditions or chronic neurodegenerative disease in which activity or expression of sheddases might be altered. PMID: 28923481
  12. Oxidative stress is correlated with hyperactivation of the ADAM17/Notch signaling pathway and a consequent increase in fibrosis in patients with endometriosis. PMID: 28486700
  13. Plasma levels of ADAM17 are increased in Tanzanian children hospitalized with a malaria infection compared with asymptomatic children but similar to children hospitalized with other infectious diseases. The plasma levels of ADAM17 decreased during recovery after an acute malaria episode. PMID: 27784899
  14. Data found that ADAM17 is constitutively internalized by clathrin-coated pits and that physiological stimulators such as GPCR ligands induce ADAM17-mediated shedding, but do not alter the cell-surface abundance of the protease. Also, physiological activation of ADAM17 does not rely on its relocalisation, but that PMA-induced PKC activity drastically dysregulates the localisation of ADAM17. PMID: 27731361
  15. Cullin 3 regulates ADAM17-mediated ectodomain shedding of AREG. PMID: 29550478
  16. ADAM17 may be a key enzyme that regulates the generation of TNF-alpha in oral keratinocytes. PMID: 28637950
  17. therapies against ADAM10 and ADAM17 may promote cancer stem cell migration away from the tumourigenic niche resulting in a differentiated phenotype that is more susceptible to treatment. PMID: 27541285
  18. ADAM10 and ADAM17 are the best characterized members of the ADAM (A Disintegrin and Metalloproteinase) - family of transmembrane proteases. Both are involved diverse physiological and pathophysiological processes.For ADAM17 phosphatidylserine exposure is required to then induce its shedding function. PMID: 28624437
  19. In the present study, the authors show that deletion of a triple serine (3S) motif (Ser-359 to Ser-361) adjacent to the cleavage site is sufficient to prevent IL-6R cleavage by ADAM17, but not ADAM10. We find that the impaired shedding is caused by the reduced distance between the cleavage site and the plasma membrane. PMID: 27151651
  20. ADAM17 is a Western diet-inducible enzyme activated by CXCL12-CXCR4 signaling, suggesting the pathway: Western diet-->CXCL12-->CXCR4-->ADAM17-->TGFalpha-->EGFR. ADAM17 might serve as a druggable target in chemoprevention strategies PMID: 27489286
  21. The regulation of the shedding activity of ADAM17 is multilayered and different regions of the protease are involved. Intriguingly, its extracellular domains play crucial roles in different regulatory mechanisms. We will discuss the role of these domains in the control of ADAM17 activity. PMID: 28571693
  22. We show ADAM17 expression in human dopaminergic neurons derived from induced pluripotent stem cells and we discuss how this state-of-the-art technology can be further exploited to study the function of this important protease in the brain and other tissues. PMID: 28705384
  23. High ADAM17 expression is associated with radioresistance in liver cancer. PMID: 26993601
  24. inhibition of autophagy led to the decrease in stemness, restoration of mitochondrial proteins and reduced expression of CD44, ABCB1 and ADAM17 PMID: 29171106
  25. FoxM1 regulates the expression of ADAM-17, which is upregulated in gastric carcinoma. PMID: 29180185
  26. Glypican-1 was validated as a novel substrate for ADAM17, with important function in adhesion, proliferation and migration of carcinoma cells. PMID: 27576135
  27. the chaperone 78-kDa glucose-regulated protein (GRP78) protects the MPD against PDI-dependent disulfide-bond isomerization by binding to this domain and, thereby, preventing ADAM17 inhibition. PMID: 28949004
  28. The ADAM17 messenger RNA (mRNA) and protein levels were significantly higher in the inferior turbinate than in nasal polyps (p < 0.05). The ADAM10 mRNA and protein levels did not differ significantly between NPs and inferior turbinates (p > 0.05). ADAM10 and ADAM17 were expressed primarily in inflammatory cells, submucosal glandular cells, and lining epithelial cells. PMID: 27012683
  29. The iRhom2 N-terminus stabilizes mature ADAM17 at the cell surface where it cleaves TNF and EGFR in inflammatory and innate immune responses. (Review) PMID: 28815577
  30. inhibition of ADAM17 enhanced the purity of expanded NK cells and the antibody-dependent cellular cytotoxicity activity of these cells against trastuzumab treated breast cancer cell lines. PMID: 28982863
  31. hypoxia instigates the RSK1-dependent C/EBPbeta signaling pathway, which in turn initiates binding of C/EBPbeta to the ADAM 17 promoter and ultimately induces ADAM 17 expression in human lung fibroblasts. PMID: 28646679
  32. TNF-alpha-converting enzyme -mediated cleavage of soluble RANKL from activated lymphocytes, especially B cells, can promote osteoclastogenesis in periodontitis. PMID: 27815441
  33. Cell stimulation can downregulate expression of mature ADAM17 from the cell surface and induce release of exosomal ADAM17, which can then distribute and contribute to substrate shedding on more distant cells. PMID: 27599715
  34. Aging and obesity cooperatively reduce caveolin-1 expression and increase vascular endothelial ADAM17 activity and soluble TNF release in adipose tissue, which may contribute to the development of remote coronary microvascular dysfunction in older obese patients. PMID: 28473444
  35. Our data demonstrated that elevated serum Semaphorin5A (Sema5A) in SLE patients correlated with disease activity and are involved in kidney and blood system damage; ADAM17 might be involved in the release of secreted Sema5A. PMID: 28063160
  36. ADAM17 and ADAM10 cleave Nectin-4 and release soluble Nectin-4 (sN4). PMID: 28232483
  37. ADAM17 promotes epithelial-mesenchymal transition via the TGF-beta/Smad pathway. the present study demonstrates that ADAM17 plays a critical role in the development of gastric cancer and provides a potential therapeutic target for gastric cancer. PMID: 27779657
  38. FHL2 interacts with ADAM-17 in normal, dysplastic and malignant colon epithelial cells. Colocalisation of these proteins is more frequent in malignant than in normal and dysplastic cells, suggesting a role for ADAM-17/FHL2 complex in the development of colorectal cancer. PMID: 28349819
  39. The present study suggests that ADAM17-siRNA inhibits MCF-7 breast cancer and is activated through the EGFR-PI3K-AKT signaling pathway PMID: 27221510
  40. Data show that mononuclear leukocytes (PBMC) AXL receptor tyrosine kinase (Axl) is rescued by combined matrix metalloproteases ADAM10 and TACE (ADAM17) inhibition. PMID: 27237127
  41. the TLR4/Gal-1 signaling pathway regulates lactate-mediated EMT processes through the activation of ADAM10 and ADAM17 in colon cancer cells. PMID: 27837433
  42. The HNE-TACE signalling pathway has an important role in the process of MUC5AC overexpression in chronic rhinosinusitis. PMID: 26881964
  43. The inhibition of cell proliferation and invasion was observed in the ADAM17 knockdown cells, which was associated with modulation of the EGFR signalling pathway. PMID: 27878499
  44. ADAM17 expression was increased in the sepsis patients with the rs12692386 GA/GG genotypes, accompanied by up-regulation of expression of the ADAM17 substrates (TNF-alpha, IL-6R and CX3CL1) and pro-inflammatory cytokines (IL-1beta and IL-6). PMID: 27607600
  45. ADAM17 genetic variants were shown to be associated with KD risk, even when excluding the influence of TGF-beta signaling pathway genes, suggesting that ADAM17 is an important KD susceptibility-related genetic locus. PMID: 26833052
  46. We found that percent body fat was directly associated with TLR4 and TACE expression in skeletal muscle of older adults. PMID: 26988770
  47. Presented genes, especially ADAM17, MMP9, EphA2, TIMP1, ICAM 11, and CD4, may be used as prognostic markers of advanced stages of colorectal cancer, contributing to the development of new lines of therapy focused on reducing metastasis of the primary tumor. PMID: 27110571
  48. We also demonstrated that the cell-surface CA IX level dropped during the death progress due to an increased ECD shedding, which required a functional ADAM17. Inhibitors of metalloproteinases reduced CA IX ECD shedding, but not apoptosis. PMID: 26993100
  49. Case Report: genetic deficiency of ADAM17 altering cytokine secretion and NK cell activity. PMID: 26683521
  50. lower expression levels in the allergic nasal mucosa PMID: 26250527

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Involvement in disease Inflammatory skin and bowel disease, neonatal, 1 (NISBD1)
Subcellular Location Membrane; Single-pass type I membrane protein.
Tissue Specificity Ubiquitously expressed. Expressed at highest levels in adult heart, placenta, skeletal muscle, pancreas, spleen, thymus, prostate, testes, ovary and small intestine, and in fetal brain, lung, liver and kidney.
Database Links

HGNC: 195

OMIM: 603639

KEGG: hsa:6868

STRING: 9606.ENSP00000309968

UniGene: Hs.404914

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