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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. dans Diabetes 2009
Show all 33 Pubmed References
Human ADAM17 Kit ELISA pour 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. dans Cytokine 2013
Show all 4 Pubmed References
Human ADAM17 Kit ELISA pour 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. dans Life sciences 2015
Human ADAM17 Kit ELISA pour 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. dans International wound journal 2016
Mouse (Murine) ADAM17 Kit ELISA pour 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. dans FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2014
Human ADAM17 Kit ELISA pour Sandwich ELISA - ABIN2683343
Tatebe, Iwatsuki, Hirata, Oguchi, Tanaka, Urata: Effects of depression and inflammatory factors on chronic conditions of the wrist. dans The bone & joint journal 2016
most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR (Montrer EGFR Kits ELISA)
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 (Montrer NOTCH3 Kits ELISA) mouse model, we show that exogenous ADAM17 or HB-EGF (Montrer HBEGF Kits ELISA) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (Montrer KCNAB2 Kits ELISA) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (Montrer TIMP3 Kits ELISA)-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 (Montrer IL6 Kits ELISA) signals during inflammatory processes.
These results show that TACE is a target of, and is downregulated by, soluble TNF (Montrer TNF Kits ELISA)-induced AP-2alpha (Montrer TFAP2A Kits ELISA) transcription factor in dendritic cells
the critical role of the transmembrane domains of ADAM17 and Rhbdf2 (Montrer RHBDF2 Kits ELISA) in the regulation of the ADAM17 and EGFR (Montrer EGFR Kits ELISA), and ADAM17 and TNFalpha (Montrer TNF Kits ELISA) signaling pathways, was examined.
Findings provide evidence that ADAM10 (Montrer ADAM10 Kits ELISA), and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH (Montrer NOTCH1 Kits ELISA) signaling.
this study shows that the iRhom2 (Montrer RHBDF2 Kits ELISA)/ADAM17 pathway plays an important role in regulating CSF1R (Montrer CSF1R Kits ELISA) 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 (Montrer TNF Kits ELISA) and TNFR2 (Montrer TNFRSF1B Kits ELISA), thereby preventing overactivation of endogenous TNFR2 (Montrer TNFRSF1B Kits ELISA) signaling in cells of the vasculature.
the chaperone 78-kDa glucose-regulated protein (GRP78 (Montrer HSPA5 Kits ELISA)) protects the MPD (Montrer MVD Kits ELISA) against PDI (Montrer PADI1 Kits ELISA)-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 (Montrer ADAM10 Kits ELISA) mRNA and protein levels did not differ significantly between NPs (Montrer NPS Kits ELISA) and inferior turbinates (p > 0.05). ADAM10 (Montrer ADAM10 Kits ELISA) and ADAM17 were expressed primarily in inflammatory cells, submucosal glandular cells, and lining epithelial cells.
The iRhom2 (Montrer RHBDF2 Kits ELISA) N-terminus stabilizes mature ADAM17 at the cell surface where it cleaves TNF (Montrer TNF Kits ELISA) and EGFR (Montrer EGFR Kits ELISA) 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 (Montrer RPS6KA1 Kits ELISA)-dependent C/EBPbeta (Montrer CEBPB Kits ELISA) signaling pathway, which in turn initiates binding of C/EBPbeta (Montrer CEBPB Kits ELISA) to the ADAM 17 promoter and ultimately induces ADAM 17 expression in human lung fibroblasts.
TNF-alpha-converting enzyme -mediated cleavage of soluble RANKL (Montrer TNFSF11 Kits ELISA) 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 (Montrer CAV1 Kits ELISA) expression and increase vascular endothelial ADAM17 activity and soluble TNF (Montrer TNF Kits ELISA) 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 (Montrer SEMA5A Kits ELISA)) 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 (Montrer SEMA5A Kits ELISA).
ADAM17 and ADAM10 (Montrer ADAM10 Kits ELISA) cleave Nectin-4 (Montrer PVRL4 Kits ELISA) and release soluble Nectin-4 (Montrer PVRL4 Kits ELISA) (sN4).
ADAM17 was involved in porcine CD16 (Montrer CD16 Kits ELISA) shedding in porcine reproductive and respiratory syndrome virus-infected pigs.
Overexpression of ADAM17 induced downregulation of CD163 (Montrer CD163 Kits ELISA) expression and a reduction in reproductive and respiratory syndrome virus infection.
activation of TACE/ADAM17 via a PKC (Montrer FYN Kits ELISA)-induced c-Src (Montrer SRC Kits ELISA)-dependent manner mediates proteolytic activation of the EGF (Montrer EGF Kits ELISA)-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 (Montrer TNF Kits ELISA) stimulates Rac (Montrer AKT1 Kits ELISA), ADAM17/TACE, and RhoA (Montrer RHOA Kits ELISA) through the guanine nucleotide exchange factor (Montrer ARHGEF12 Kits ELISA) (GEF)-H1 (Montrer ARHGEF2 Kits ELISA).
progesterone-induced TACE/ADAM17 leads to production of soluble EGF (Montrer EGF Kits ELISA) 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