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anti-Human ADAM17 Anticorps:
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Human Monoclonal ADAM17 Primary Antibody pour CyTOF, FACS - ABIN4900516
Breshears, Schlievert, Peterson: A disintegrin and metalloproteinase 17 (ADAM17) and epidermal growth factor receptor (EGFR) signaling drive the epithelial response to Staphylococcus aureus toxic shock syndrome toxin-1 (TSST-1). dans The Journal of biological chemistry 2012
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Human Monoclonal ADAM17 Primary Antibody pour FACS - ABIN4897863
Moreira-Tabaka, Peluso, Vonesch, Hentsch, Kessler, Reimund, Dumont, Muller: Unlike for human monocytes after LPS activation, release of TNF-α by THP-1 cells is produced by a TACE catalytically different from constitutive TACE. dans PLoS ONE 2012
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Human Polyclonal ADAM17 Primary Antibody pour IHC - ABIN965510
Rabie, Strehl, Ludwig, Nieswandt: Evidence for a role of ADAM17 (TACE) in the regulation of platelet glycoprotein V. dans The Journal of biological chemistry 2005
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Human Polyclonal ADAM17 Primary Antibody pour ELISA, WB - ABIN542853
Tellier, Canault, Poggi, Bonardo, Nicolay, Alessi, Nalbone, Peiretti: HDLs activate ADAM17-dependent shedding. dans Journal of cellular physiology 2007
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Human Polyclonal ADAM17 Primary Antibody pour ELISA, WB - ABIN542854
Takamune, Ikebe, Nagano, Shinohara: Involvement of NF-kappaB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma. dans Biochemical and biophysical research communications 2007
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Human Polyclonal ADAM17 Primary Antibody pour ICC, ELISA - ABIN1003300
Moss, Jin, Milla, Bickett, Burkhart, Carter, Chen, Clay, Didsbury, Hassler, Hoffman, Kost, Lambert, Leesnitzer, McCauley, McGeehan, Mitchell, Moyer, Pahel, Rocque, Overton, Schoenen, Seaton, Su et al.: Cloning of a disintegrin metalloproteinase that processes precursor tumour-necrosis factor-alpha. ... dans Nature 1997
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Human Monoclonal ADAM17 Primary Antibody pour CyTOF, FACS - ABIN4900515
Nishi, Hiraoka, Yoshida, Okawa, Kita: Nardilysin enhances ectodomain shedding of heparin-binding epidermal growth factor-like growth factor through activation of tumor necrosis factor-alpha-converting enzyme. dans The Journal of biological chemistry 2006
Human Polyclonal ADAM17 Primary Antibody pour EIA, IF - ABIN5555290
Wang, Wang, Yin, Zhang, Yu, Kong, Yuan, Fang, Liu, Liu, Shi: Reduced neurotrophic factor level is the early event before the functional neuronal deficiency in high-fat diet induced obese mice. dans Metabolic brain disease 2018
Human Polyclonal ADAM17 Primary Antibody pour ELISA, WB - ABIN1531481
Bilousova, Taylor, Emirzian, Gylys, Frautschy, Cole, Teng: Parallel age-associated changes in brain and plasma neuronal pentraxin receptor levels in a transgenic APP/PS1 rat model of Alzheimer's disease. dans Neurobiology of disease 2015
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Human Polyclonal ADAM17 Primary Antibody pour FACS, WB - ABIN388309
Sun, Jiang, Lu, Chen, Tao, Chen: Therapeutic potential of ADAM17 modulation in gastric cancer through regulation of the EGFR and TNF-α signalling pathways. dans Molecular and cellular biochemistry 2017
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increased ADAM17 expression may have contributed to gastric cancer metastasis and progression, potentially via activation of the Notch or Wnt signaling pathways
These data indicate that ADAM-17 is expressed on rheumatoid arthritis synovial tissues s and plays a role in rheumatoid arthritis inflammation
Membrane-anchored CD40 is processed by the tumor necrosis factor-alpha-converting enzyme. Implications for CD40 signaling.
iTAP (FRMD8) is a novel iRhom2 interactor that controls TNF-alpha secretion by policing the stability of iRhom2/ADAM17 complex.
FRMD8 promotes inflammatory and growth factor signaling by stabilizing the iRhom2/ADAM17 sheddase complex.
Lentivirus mediated ADAM17 RNAi may reverse the acquired resistance of lung adenocarcinoma to gefitinib via inhibiting the upstream of EGFR signal pathway, which may provide a new therapeutic target to solve the acquired resistance to EGFR tyrosine kinase inhibitors in lung adenocarcinoma
High expression of ADAM17 is associated with oxaliplatin chemosensitivity. Down regulation of ADAM17 can enhance sensitivity and reverse resistance to oxaliplatin.
ADAM-17 is an independent prognostic marker for patients with hilar cholangiocarcinoma. FoxM1 regulates the expression of ADAM-17 and then induced TNFa production and cleavage.
High ADAM17 expression is associated with cystic fibrosis.
These findings link iNOS to Notch1 signaling in CD24(+)CD133(+) LCSCs through the activation of TACE/ADAM17.
ADAM17 activation and secretion in the myeloid cells during HIV infection.
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.
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.
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.
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.
Uev1A-Ubc13 complex catalyzes lysine63-linked ubiquitination of RHBDF2 to promote TACE maturation.
ADAM17 plays a role in chronic kidney disease-mineral and bone disorder.
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.
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.
Oxidative stress is correlated with hyperactivation of the ADAM17/Notch signaling pathway and a consequent increase in fibrosis in patients with endometriosis.
DKK3 overexpression substantially alleviated AngII infusion-induced cardiac hypertrophy and fibrosis by regulating ADAM17/ACE2 pathway activity and inhibiting the GSK-3beta/beta-catenin pathway.
Cell surface CSF-1 (csCSF-1) is one of the substrates of ADAM17. We demonstrate that both infiltrated neutrophils and macrophages are major sources of csCSF-1.
ADAM17 is needed for EGF-R-mediated induction of IL-6 synthesis, which via IL-6 trans-signaling induces beta-catenin-dependent tumorigenesis.
The data indicate that hepatic TIMP3 expression can slow the progression of nonalcoholic fatty liver disease and tumorigenesis, at least in part, through the regulation of ADAM17 activity.
suggest that STING activates ADAM17 and that this activation produces soluble proinflammatory SEMA4D independently of the TBK1/IRF3-mediated transcriptional pathway
while Adam17-deficiency suppresses Ang II-induced SMC remodeling in vitro, in vivo Adam17-deficiency provides only a transient protective effect against Ang II-mediated hypertension and end-organ damage.
Report atheroprotective functions of ADAM17 in myeloid cells but atheroprogressive ADAM17 functions in endothelial cells.
results suggest ADAM17/EGFR-driven PLCgamma1 and PKC pathways as important promoters of TG1 expression during terminal keratinocyte differentiation.
iRhom2 controls multiple aspects of TACE biology, including stimulated shedding on the cell surface.
Targeting ADAM17 with a lentiviral vector attenuates endotoxemia in mice.
Addition of a disintegrin and metallopeptidase domain 17 (ADAM17) to the culture supernatant of stimulated splenocytes decreased Interferon-gamma (IFN-gamma) concentration.
Overall, iRhom2 binds to TACE throughout its lifecycle, implying that iRhom2 is a primary regulator of stimulated cytokine and growth factor signalling.
Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR-ligands by differentially activating ADAM17 or ADAM10.
Fhl2 anticipates the emerging inflammation and specifically the development of psoriatic arthritis by impeding the Adam17-mediated release of TNF
most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR
ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms
In a clinically relevant CADASIL mouse model, we show that exogenous ADAM17 or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3-induced deficits.
Conditional ADAM17 knockout mice lacking ADAM17 in all leukocytes had a significant survival advantage during severe polymicrobial sepsis induced by CLP, associated with enhanced neutrophil recruitment at the infectious locus along with decreased bacterial spread and circulating levels of proinflammatory factors. Its induction during sepsis may tip the balance between efficient and impaired neutrophil recruitment.
these findings provide the direct evidence that ADAM17 cleaves porcine TNFalpha, which represents a new view for identifying potential therapeutic targets in anti-porcine reproductive and respiratory syndrome virus therapy
ADAM17 was involved in porcine CD16 shedding in porcine reproductive and respiratory syndrome virus-infected pigs.
Overexpression of ADAM17 induced downregulation of CD163 expression and a reduction in reproductive and respiratory syndrome virus infection.
activation of TACE/ADAM17 via a PKC-induced c-Src-dependent manner mediates proteolytic activation of the EGF-like factors that are involved in the induction of granulosa cell differentiation, cumulus expansion, and meiotic maturation of porcine oocytes
Data indicate that TNF-alpha stimulates Rac, ADAM17/TACE, and RhoA through the guanine nucleotide exchange factor (GEF)-H1.
progesterone-induced TACE/ADAM17 leads to production of soluble EGF domain from cumulus cells, which enhances functional changes of cumulus cells and progresses meiotic maturation of oocytes
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.
ADAM metallopeptidase domain 18
, TNF-alpha convertase
, TNF-alpha converting enzyme
, disintegrin and metalloproteinase domain-containing protein 17
, snake venom-like protease
, tumor necrosis factor, alpha, converting enzyme
, ADAM 17
, TNF-alpha-converting enzyme
, a disintegrin and metalloprotease domain 17; TNF-alpha converting enzyme
, a disintegrin and metalloproteinase domain 17
, a disintegrin and metallopeptidase domain 17
, ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme)
, a disintegrin and metalloproteinase domain 17 (tumor necrosis factor, alpha, converting enzyme)
, tumor necrosis factor alpha converting enzyme
, ADAM metallopeptidase domain 17
, a disintegrin and metalloprotease domain 17
, disintegrin metalloproteinase
, disintegrin and metalloproteinase domain-containing protein 17-like
, ADAM metallopeptidase domain 17a
, a disintegrin and metalloproteinase domain 17a