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Validated All-in-One™ qPCR Primer for ADAM17(NM_003183.4) Search again
Product ID:
HQP017866
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADAM18, CD156B, CSVP, NISBD, NISBD1, TACE
Gene Description:
ADAM metallopeptidase domain 17
Target Gene Accession:
NM_003183.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biologic processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. The protein encoded by this gene functions as a tumor necrosis factor-alpha converting enzyme; binds mitotic arrest deficient 2 protein; and also plays a prominent role in the activation of the Notch signaling pathway. [provided by RefSeq].
Gene References into function
- Engineering N-terminal domain of tissue inhibitor of metalloproteinase (TIMP)-3 to be a better inhibitor against tumour necrosis factor-alpha-converting enzyme
- phosphorylated by ERKs; demonstrates a potential role in regulated shedding of membrane proteins
- Data show that tumor necrosis factor-alpha-converting enzyme (TACE)is involved in the shedding of L-selectin by NSAIDS in human neutrophils.
- regulated by protein tyrosine phosphatase PTPH1
- This enzyme mediates MUC1 shedding.
- multiple sclerosis patients found positive for TACE mRNA in PBMCs showed a significantly higher mean number of new lesions
- The results indicate that ADAM9, ADAM10, and ADAM17, members of the disintegrin and metalloprotease family, catalyze alpha-secretory cleavage and therefore act as alpha-secretases in A172 cells.
- Review. The activation of EGFR in response to smoke involves cleavage of amphiregulin by ADAM 17.
- Data show that tumor necrosis factor-alpha converting enzyme (TACE) is required for epidermal growth factor receptor activation in vivo and for the development of tumors in nude mice, indicating a crucial role of TACE in tumorigenesis.
- TACE binds to SAP97, which may have a role in the regulation of TACE shedding activity
- Intracellular maturation and transport of TACE.
- ADAM-17 has a role in stimulation of lung epithelial cells upon exposure to tobacco smoke by cleaving amphiregulin, which binds to EGF receptor
- TACE has a role in protein ectodomain shedding
- under inflammatory conditions, ADAM-10, expressed by perivascular macrophages, and ADAM-17, expressed by invading T cells, may actively contribute to the pathogenesis of inflammatory disorders of the CNS.
- Data show that in squamous cell carcinoma cells, stimulation with G protein-coupled receptor agonists specifically results in cleavage and release of amphiregulin (AR) by TACE.
- Tumor necrosis factor-alpha converting enzyme is processed by proprotein-convertases to its mature form which is degraded upon phorbol ester stimulation
- TACE processes CD40
- cholesterol depletion triggers shedding of the human interleukin-6 receptor by ADAM10 and ADAM17
- TACE (ADAM 17) may not be the ectoprotease involved in the secretion of pro-EGF ectodomain
- role in mucin production by airway epithelial cells by means of a TACE ligand-epidermal growth factor receptor cascade in response to various stimuli
- ADAM-17/TACE and TIMP-3 might play an important role in the pathogenesis of prostate cancer
- TACE controls mast cell survival by regulating shedding and surface expression of c-Kit
- Integrin alpha5beta1 and ADAM-17 interact in vitro and co-localize in migrating HeLa cells
- ADAM-17 IS a potent activator of Vibrio Cholerae pro-cytolysin.
- although there is a seemingly high structural similarity between TACE and MMP-2, these enzymes are significantly diverse in the electronic and chemical properties within their active sites
- ADAM10 is the major alpha-secretase cleaving amyloid precursor protein, with TACE playing a minor role; neither ADAM10 nor TACE is involved in the shedding of angiotensin converting enzyme
- analysis of the molecular basis of the inactivity of tissue inhibitor of metalloproteinase-2 against tumor necrosis factor-alpha-converting enzyme
- Lower mRNA expression of ADAM17 mRNA in solitary large cell hepatocellular carcinoma may be associated with the better molecular pathological features.
- Data show that activation of ADAM-17 results in discrete cellular responses, while G protein-coupled receptor agonists promote activation of the Ras/MAPK pathway and cell proliferation via the epidermal growth factor receptor.
- GPV is cleaved upon agonist-induced platelet activation, with ADAM17 as the major enzyme mediating this process
- the active form of TACE is overexpressed in breast tumors and may indicate that TACE is responsible for Nectin-4 shedding not only in vitro but also in vivo
- ADAM17 is the protease responsible for shedding of the SARS-CoV receptor, ACE2
- Bacteria are physiological activators of TACE expression, which provides a mechanism to regulate inflammatory signaling that is initiated by airway epithelial cells.
- TIMP-3 reactive site mutations disrupt inhibition of matrix metalloproteinases but not TACE
- HNE activates TACE via ROS generation, resulting in cleavage of pro-TGF-alpha, EGFR activation, and MUC5AC mucin expression in airway epithelial cells
- GPIbalpha and GPV are shed through an ADAM17-dependent mechanism after aspirin administration
- the expression, regulation, and catalytic function of TACE in healthy human alveolar macrophages
- These data show that inhibition of TNF-alpha processing by acute ethanol is a direct affect of ethanol on the cell membrane and is reversible upon cessation or metabolism.
- Overexpression of TACE in HEK293 cells increased the release of soluble APLP2 severalfold.
- analysis of how TACE mediates the ectodomain cleavage of ICAM-1
- HAT induces amphiregulin production through the PAR-2 mediated ERK pathway, and then causes amphiregulin release by a TACE-dependent mechanism
- potential role of TACE in the pathogenesis of chorioamnionitis
- Results identify a protein tyrosine phosphatase as a potential substrate of TACE and describe proteolytic processing of PTP-LAR as a means of regulating phosphatase activity downstream and thus under the control of EGFR-mediated signaling pathways.
- results show that TACE undergoes phosphorylation that regulates release of amphiregulin upon GRP treatment; a signaling cascade of GRP-Src-PI3-K-PDK1-TACE-amphiregulin-EGFR with multiple points of interaction, translocation & phosphorylation is suggested
- ADAM9 does not behave as a genuine alpha-secretase but rather acts as an important upstream regulator of ADAM10 activity.
- ADAM-17 expression was associated with the blood vessel endothelium, activated macrophages/microglia and parenchymal astrocytes in multiple sclerosis white matter
- Highly malignant renal carcinoma cancer cells fail to form in vivo tumors in the absence of ADAM17.
- furin enhances alpha-secretase activity via the cleavage of ADAM10 and TACE, and attenuated furin activity is connected to the production of Abeta
- Findings provide evidence of aberrant expression of the proteolytically active ADAM17/TACE in advanced precursor lesions (PanIN-3) and PDAC while identifying its critical involvement in the invasion process.
- Our data support the idea that one of the mechanisms regulating ADAM17 substrate cleavage involves protein partitioning in lipid rafts.
- the EPCR sequence requirement for shedding is amino acids from residue 193 to residue 200. ADAM17 is responsible for EPCR shedding.
- long term treatment with epidermal growth factor (EGF) leads to a marked increase in the levels of ADAM17, which also increases the shedding of several substrates of ADAM17, including the desmosomal cadherin Dsg-2
- The structure, chemistry and lifetime of transient metal-protein reaction intermediates evolving during the substrate turnover reaction of a metalloproteinase, the tumor necrosis factor-alpha converting enzyme (TACE), is reported.
- TNF-alpha seems to be activated (by the converting enzyme TACE) and biologically active through its receptors in human lumbar disc tissue
- The proportion of active to total ADAM-17 increased progressively from normal breast tissue to primary breast cancer to lymph node metastases.
- This review focuses on a subset of soluble proteins , which are cleaved by tumor necrosis factor alpha-converting enzyme (TACE)/ADAM17, and on their role in cancer.
- Type 2 diabetes LDL lipoproteins increasin adhesion molecules by promoting increased expression of ADAM17.
- These data demonstrate that high-density lipoproteins alter the lipid raft structure, which in turn activates the ADAM17-dependent processing of transmembrane substrates.
- TMEFF2 contributes to cell proliferation in an ADAM17-dependent autocrine fashion in cells expressing this protein
- In conclusion, ADAM-17 plays an important role in cancer invasion probably through CD44 cleavage.
- TNFR1 accumulated at the chlamydial inclusion and was shed by the infected cell into the culture supernatant. Receptor shedding depended on the infection-induced activation of the MEK-ERK pathway and the metalloproteinase TACE
- disruption of ALCAM-mediated adhesion is a relevant step in ovarian cancer cell motility, and ADAM17/TACE takes part in this process, which may be relevant to invasive potential
- ADAM-17 is involved in breast cancer progression
- oxygen regulates the expression of TACE and TACE may be important for placental development during human pregnancy.
- These results implicate TACE/ADAM-17 as a promising target of epidermal growth factor receptor axis inhibition in colorectal cancer.
- Nardilysin synergistically enhanced TACE-induced TNF-alpha shedding.
- ADAM10 and ADAM17 were identified as being responsible for the cytokine-induced shedding of CXCL16 in mesangila cells.
- IL-10 further regulates TNF-alpha by modulating TACE activation at early time points and by contributing to the induction of TIMP-3, the natural inhibitor of active TACE, at later time points
- These results suggested that the TNF-alpha gene G-308A polymorphism might be a risk factor for late onset of Alzheimer's disease and dependent on APOE epsilon4 status in Chinese.
- The data presented herein show TACE expression in endocrine cancers and further support a role for TACE in breast cancer apoptosis.
- ADAM17 mediates the EGFR/AKT/cyclin D1 pathway and cell cycle progression to the S phase induced by UVA radiation
- The spike protein of SARS-CoV (SARS-S) induced TNF-alpha-converting enzyme (TACE)-dependent shedding of the ACE2 ectodomain.
- Datas show that transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to trastuzumab.
- The combination of favourable functional epitopes together with a considerable flexibility renders TIMP-3 an efficient TACE inhibitor.
- data show that ADAM10 and ADAM17 are critically involved in the tumor-associated proteolytic release of soluble MICA facilitating tumor immune escape
- the cleavage sites in the extracellular juxtamembrane region of Ptprz by tumor necrosis factor-alpha converting enzyme and matrix metalloproteinase 9.
- VEGF-A stimulates ADAM17-dependent shedding of VEGFR2 and crosstalk between VEGFR2 and ERK signaling.
- lung epithelial cells secrete AMCase via an EGFR-dependent pathway that is activated by ADAM17 and mediates its effects via Ras.
- Src and ADAM-17-mediated shedding of transforming growth factor-alpha is a mechanism of acute resistance to TRAIL.
- cleavage of C4.4A by ADAM10 and ADAM17 contributes to tumor progression
- Data showed that ADAM17 and its specific inhibitor TIMP3 were co-expressed in the human intestinal barrier and ADAM17 inhibition, either physiologically or pharmacologically, amplified TNF-alpha-mediated hyperpermeability.
- ADAM-17 is part of a novel pro-angiogenic pathway leading to MMP-2 activation and vessel formation.
- Removal of cell surface heparan sulfate increased TACE activity and cleavage of ErbB4 receptor.