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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 - ABIN4897862
Kermarrec, Selloum, Plantefeve, Chosidow, Paoletti, Lopez, Mantz, Desmonts, Gougerot-Pocidalo, Chollet-Martin: Regulation of peritoneal and systemic neutrophil-derived tumor necrosis factor-alpha release in patients with severe peritonitis: role of tumor necrosis factor-alpha converting enzyme cleavage. in Critical care medicine 2005
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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 4 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
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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
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Human Polyclonal ADAM17 Primary Antibody for 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. in Neurobiology of disease 2015
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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 Monoclonal ADAM17 Primary Antibody for IHC (p), PLA - ABIN563080
Kahlert, Weber, Mogler, Bergmann, Schirmacher, Kenngott, Matterne, Mollberg, Rahbari, Hinz, Koch, Aigner, Weitz: Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse. in British journal of cancer 2009
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
Human Polyclonal ADAM17 Primary Antibody for ELISA, FACS - ABIN4357502
Lemjabbar, Li, Gallup, Sidhu, Drori, Basbaum: Tobacco smoke-induced lung cell proliferation mediated by tumor necrosis factor alpha-converting enzyme and amphiregulin. in The Journal of biological chemistry 2003
iRhom2 (show RHBDF2 Antibodies) 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 (show IFNG Antibodies)) concentration.
Overall, iRhom2 (show RHBDF2 Antibodies) binds to TACE throughout its lifecycle, implying that iRhom2 (show RHBDF2 Antibodies) is a primary regulator of stimulated cytokine and growth factor signalling.
Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR (show EGFR Antibodies)-ligands by differentially activating ADAM17 or ADAM10 (show ADAM10 Antibodies).
Fhl2 (show FHL2 Antibodies) anticipates the emerging inflammation and specifically the development of psoriatic arthritis by impeding the Adam17-mediated release of TNF (show TNF Antibodies)
most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR (show EGFR Antibodies)
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 (show NOTCH3 Antibodies) mouse model, we show that exogenous ADAM17 or HB-EGF (show HBEGF Antibodies) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 Antibodies) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (show TIMP3 Antibodies)-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.
ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 (show TREM2 Antibodies) after Histidine 157. Findings reveal a link between shedding of TREM2 (show TREM2 Antibodies) 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 (show NOTCH1 Antibodies) 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 (show NMUR1 Antibodies) 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 (show PRRT2 Antibodies) activity drastically dysregulates the localisation of ADAM17.
Cullin 3 (show CUL3 Antibodies) regulates ADAM17-mediated ectodomain shedding of AREG (show AREG Antibodies).
ADAM17 may be a key enzyme that regulates the generation of TNF-alpha (show TNF Antibodies) in oral keratinocytes.
therapies against ADAM10 (show ADAM10 Antibodies) 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 (show ADAM10 Antibodies) 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 (show SIGLEC1 Antibodies)-359 to Ser (show SIGLEC1 Antibodies)-361) adjacent to the cleavage site is sufficient to prevent IL-6R cleavage by ADAM17, but not ADAM10 (show ADAM10 Antibodies). 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 (show CXCL12 Antibodies)-CXCR4 (show CXCR4 Antibodies) signaling, suggesting the pathway: Western diet-->CXCL12 (show CXCL12 Antibodies)-->CXCR4 (show CXCR4 Antibodies)-->ADAM17-->TGFalpha-->EGFR (show EGFR Antibodies). ADAM17 might serve as a druggable target in chemoprevention strategies
these findings provide the direct evidence that ADAM17 cleaves porcine TNFalpha (show TNF Antibodies), 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 (show CD16 Antibodies) shedding in porcine reproductive and respiratory syndrome virus-infected pigs.
Overexpression of ADAM17 induced downregulation of CD163 (show CD163 Antibodies) expression and a reduction in reproductive and respiratory syndrome virus infection.
activation of TACE/ADAM17 via a PKC (show FYN Antibodies)-induced c-Src (show SRC Antibodies)-dependent manner mediates proteolytic activation of the EGF (show EGF Antibodies)-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 (show TNF Antibodies) stimulates Rac (show AKT1 Antibodies), ADAM17/TACE, and RhoA (show RHOA Antibodies) through the guanine nucleotide exchange factor (show ARHGEF12 Antibodies) (GEF)-H1 (show ARHGEF2 Antibodies).
progesterone-induced TACE/ADAM17 leads to production of soluble EGF (show EGF Antibodies) 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 17 (tumor necrosis factor, alpha, converting enzyme)
, a disintegrin and metalloproteinase domain 17 (tumor necrosis factor, alpha, converting enzyme)
, disintegrin and metalloproteinase domain-containing protein 17
, tumor necrosis factor alpha converting enzyme
, a disintegrin and metallopeptidase domain 17
, ADAM metallopeptidase domain 17
, a disintegrin and metalloprotease domain 17
, disintegrin metalloproteinase
, disintegrin and metalloproteinase domain-containing protein 17-like
, ADAM 17
, TNF-alpha convertase
, TNF-alpha converting enzyme
, TNF-alpha-converting enzyme
, a disintegrin and metalloprotease domain 17; TNF-alpha converting enzyme
, a disintegrin and metalloproteinase domain 17
, ADAM metallopeptidase domain 18
, snake venom-like protease
, tumor necrosis factor, alpha, converting enzyme