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Cardellini, Menghini, Martelli, Casagrande, Marino, Rizza, Porzio, Mauriello, Solini, Ippoliti, Lauro, Folli, Federici: TIMP3 is reduced in atherosclerotic plaques from subjects with type 2 diabetes and increased by SirT1. in Diabetes 2009
Show all 33 Pubmed References
Human ADAM17 ELISA Kit for Sandwich ELISA - ABIN625253
Lamas, Rodríguez-Rodríguez, Tornero-Esteban, Villafuertes, Hoyas, Abasolo, Varadé, Alvarez-Lafuente, Urcelay, Fernández-Gutiérrez: Alternative splicing and proteolytic rupture contribute to the generation of soluble IL-6 receptors (sIL-6R) in rheumatoid arthritis. in Cytokine 2013
Show all 4 Pubmed References
Human ADAM17 ELISA Kit for Sandwich ELISA - ABIN415265
Serra, Gallelli, Butrico, Buffone, Caliò, De Caridi, Massara, Barbetta, Amato, Labonia, Mimmi, Iaccino, de Franciscis: From varices to venous ulceration: the story of chronic venous disease described by metalloproteinases. in International wound journal 2016
Mouse (Murine) ADAM17 ELISA Kit for Sandwich ELISA - ABIN810367
Lagrange, Li, Fassot, Bourhim, Louis, Nguyen Dinh Cat, Parlakian, Wahl, Lacolley, Jaisser, Regnault: Endothelial mineralocorticoid receptor activation enhances endothelial protein C receptor and decreases vascular thrombosis in mice. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2014
Human ADAM17 ELISA Kit for Sandwich ELISA - ABIN366611
Wang, Ren, Wang, Li, Li, Zheng: Combining detection of Notch1 and tumor necrosis factor-? converting enzyme is a reliable biomarker for the diagnosis of abdominal aortic aneurysms. in Life sciences 2015
Human ADAM17 ELISA Kit for Sandwich ELISA - ABIN2683343
Tatebe, Iwatsuki, Hirata, Oguchi, Tanaka, Urata: Effects of depression and inflammatory factors on chronic conditions of the wrist. in The bone & joint journal 2016
most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR (show EGFR ELISA Kits)
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 ELISA Kits) mouse model, we show that exogenous ADAM17 or HB-EGF (show HBEGF ELISA Kits) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 ELISA Kits) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (show TIMP3 ELISA Kits)-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 (show IL6 ELISA Kits) signals during inflammatory processes.
These results show that TACE is a target of, and is downregulated by, soluble TNF (show TNF ELISA Kits)-induced AP-2alpha (show TFAP2A ELISA Kits) transcription factor in dendritic cells
the critical role of the transmembrane domains of ADAM17 and Rhbdf2 (show RHBDF2 ELISA Kits) in the regulation of the ADAM17 and EGFR (show EGFR ELISA Kits), and ADAM17 and TNFalpha (show TNF ELISA Kits) signaling pathways, was examined.
Findings provide evidence that ADAM10 (show ADAM10 ELISA Kits), and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH (show NOTCH1 ELISA Kits) signaling.
this study shows that the iRhom2 (show RHBDF2 ELISA Kits)/ADAM17 pathway plays an important role in regulating CSF1R (show CSF1R ELISA Kits) 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 (show TNF ELISA Kits) and TNFR2 (show TNFRSF1B ELISA Kits), thereby preventing overactivation of endogenous TNFR2 (show TNFRSF1B ELISA Kits) signaling in cells of the vasculature.
the chaperone 78-kDa glucose-regulated protein (GRP78 (show HSPA5 ELISA Kits)) protects the MPD (show MVD ELISA Kits) against PDI (show PADI1 ELISA Kits)-dependent disulfide-bond isomerization by binding to this domain and, thereby, preventing ADAM17 inhibition.
The ADAM17 messenger RNA (mRNA) and protein levels were significantly higher in the inferior turbinate than in nasal polyps (p < 0.05). The ADAM10 (show ADAM10 ELISA Kits) mRNA and protein levels did not differ significantly between NPs (show NPS ELISA Kits) and inferior turbinates (p > 0.05). ADAM10 (show ADAM10 ELISA Kits) and ADAM17 were expressed primarily in inflammatory cells, submucosal glandular cells, and lining epithelial cells.
The iRhom2 (show RHBDF2 ELISA Kits) N-terminus stabilizes mature ADAM17 at the cell surface where it cleaves TNF (show TNF ELISA Kits) and EGFR (show EGFR ELISA Kits) in inflammatory and innate immune responses. (Review)
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.
hypoxia instigates the RSK1 (show RPS6KA1 ELISA Kits)-dependent C/EBPbeta (show CEBPB ELISA Kits) signaling pathway, which in turn initiates binding of C/EBPbeta (show CEBPB ELISA Kits) to the ADAM 17 promoter and ultimately induces ADAM 17 expression in human lung fibroblasts.
TNF-alpha-converting enzyme -mediated cleavage of soluble RANKL (show TNFSF11 ELISA Kits) from activated lymphocytes, especially B cells, can promote osteoclastogenesis in periodontitis.
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.
Aging and obesity cooperatively reduce caveolin-1 (show CAV1 ELISA Kits) expression and increase vascular endothelial ADAM17 activity and soluble TNF (show TNF ELISA Kits) release in adipose tissue, which may contribute to the development of remote coronary microvascular dysfunction in older obese patients.
Our data demonstrated that elevated serum Semaphorin5A (Sema5A (show SEMA5A ELISA Kits)) 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 (show SEMA5A ELISA Kits).
ADAM17 and ADAM10 (show ADAM10 ELISA Kits) cleave Nectin-4 (show PVRL4 ELISA Kits) and release soluble Nectin-4 (show PVRL4 ELISA Kits) (sN4).
ADAM17 was involved in porcine CD16 (show CD16 ELISA Kits) shedding in porcine reproductive and respiratory syndrome virus-infected pigs.
Overexpression of ADAM17 induced downregulation of CD163 (show CD163 ELISA Kits) expression and a reduction in reproductive and respiratory syndrome virus infection.
activation of TACE/ADAM17 via a PKC (show FYN ELISA Kits)-induced c-Src (show SRC ELISA Kits)-dependent manner mediates proteolytic activation of the EGF (show EGF ELISA Kits)-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 ELISA Kits) stimulates Rac (show AKT1 ELISA Kits), ADAM17/TACE, and RhoA (show RHOA ELISA Kits) through the guanine nucleotide exchange factor (show ARHGEF12 ELISA Kits) (GEF)-H1 (show ARHGEF2 ELISA Kits).
progesterone-induced TACE/ADAM17 leads to production of soluble EGF (show EGF ELISA Kits) 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