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anti-Human ADAM17 Antibodies:
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Human Monoclonal ADAM17 Primary Antibody for 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). in The Journal of biological chemistry 2012
Show all 8 Pubmed References
Human Monoclonal ADAM17 Primary Antibody for 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. in PLoS ONE 2012
Show all 5 Pubmed References
Human Polyclonal ADAM17 Primary Antibody for IHC - ABIN965510
Rabie, Strehl, Ludwig, Nieswandt: Evidence for a role of ADAM17 (TACE) in the regulation of platelet glycoprotein V. in The Journal of biological chemistry 2005
Show all 12 Pubmed References
Human Polyclonal ADAM17 Primary Antibody for ELISA, WB - ABIN542853
Tellier, Canault, Poggi, Bonardo, Nicolay, Alessi, Nalbone, Peiretti: HDLs activate ADAM17-dependent shedding. in Journal of cellular physiology 2007
Show all 2 Pubmed References
Human Polyclonal ADAM17 Primary Antibody for ELISA, WB - ABIN542854
Takamune, Ikebe, Nagano, Shinohara: Involvement of NF-kappaB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma. in Biochemical and biophysical research communications 2007
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Human Polyclonal ADAM17 Primary Antibody for 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. ... in Nature 1997
Show all 4 Pubmed References
Human Monoclonal ADAM17 Primary Antibody for 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. in The Journal of biological chemistry 2006
Human Polyclonal ADAM17 Primary Antibody for 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. in Molecular and cellular biochemistry 2017
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Human Polyclonal ADAM17 Primary Antibody for ICC, FACS - ABIN1030720
McGowan, Mullooly, Caiazza, Sukor, Madden, Maguire, Pierce, McDermott, Crown, ODonovan, Duffy: ADAM-17: a novel therapeutic target for triple negative breast cancer. in Annals of oncology : official journal of the European Society for Medical Oncology / ESMO 2013
Human Polyclonal ADAM17 Primary Antibody for FACS, IF (p) - ABIN705671
Li, Xie, He, Wang, Duan, Yang, Wang: Identification of ADAM10 and ADAM17 with potential roles in the spermatogenesis of the Chinese mitten crab, Eriocheir sinensis. in Gene 2015
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.
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.
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.
Cullin 3 regulates ADAM17-mediated ectodomain shedding of AREG.
ADAM17 may be a key enzyme that regulates the generation of TNF-alpha in oral keratinocytes.
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.
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.
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.
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
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 results demonstrate a novel physiologic role for a disintegrin and metalloprotease 17 in regulating murine IL-6 signals during inflammatory processes.
These results show that TACE is a target of, and is downregulated by, soluble TNF-induced AP-2alpha transcription factor in dendritic cells
the critical role of the transmembrane domains of ADAM17 and Rhbdf2 in the regulation of the ADAM17 and EGFR, and ADAM17 and TNFalpha signaling pathways, was examined.
Findings provide evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.
this study shows that the iRhom2/ADAM17 pathway plays an important role in regulating CSF1R expression in the myeloid cell compartment at steady state, and in modulating development of monocytes/macrophages during their repopulation
Suggest an atheroprotective role of ADAM17, which might be mediated by cleaving membrane-bound TNFalpha and TNFR2, thereby preventing overactivation of endogenous TNFR2 signaling in cells of the vasculature.
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.
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