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Rat (Rattus) ADAM17 Protein expressed in Human Cells - ABIN2009530
Wang, Huang, Nayak, Matthews, Warburton, Shi, Sanchez-Esteban: Strain-induced differentiation of fetal type II epithelial cells is mediated via the integrin ?6?1-ADAM17/tumor necrosis factor-?-converting enzyme (TACE) signaling pathway. in The Journal of biological chemistry 2013
Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR (show EGFR Proteins)-ligands by differentially activating ADAM17 or ADAM10 (show ADAM10 Proteins).
Fhl2 (show FHL2 Proteins) anticipates the emerging inflammation and specifically the development of psoriatic arthritis by impeding the Adam17-mediated release of TNF (show TNF Proteins)
most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR (show EGFR Proteins)
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 Proteins) mouse model, we show that exogenous ADAM17 or HB-EGF (show HBEGF Proteins) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 Proteins) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (show TIMP3 Proteins)-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 Proteins) signals during inflammatory processes.
These results show that TACE is a target of, and is downregulated by, soluble TNF (show TNF Proteins)-induced AP-2alpha (show TFAP2A Proteins) transcription factor in dendritic cells
the critical role of the transmembrane domains of ADAM17 and Rhbdf2 (show RHBDF2 Proteins) in the regulation of the ADAM17 and EGFR (show EGFR Proteins), and ADAM17 and TNFalpha (show TNF Proteins) signaling pathways, was examined.
Findings provide evidence that ADAM10 (show ADAM10 Proteins), and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH (show NOTCH1 Proteins) signaling.
FoxM1 (show FOXM1 Proteins) regulates the expression of ADAM-17, which is upregulated in gastric carcinoma.
Glypican-1 (show GPC1 Proteins) was validated as a novel substrate for ADAM17, with important function in adhesion, proliferation and migration of carcinoma cells.
the chaperone 78-kDa glucose-regulated protein (GRP78 (show HSPA5 Proteins)) protects the MPD (show MVD Proteins) against PDI (show PADI1 Proteins)-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 Proteins) mRNA and protein levels did not differ significantly between NPs (show NPS Proteins) and inferior turbinates (p > 0.05). ADAM10 (show ADAM10 Proteins) and ADAM17 were expressed primarily in inflammatory cells, submucosal glandular cells, and lining epithelial cells.
The iRhom2 (show RHBDF2 Proteins) N-terminus stabilizes mature ADAM17 at the cell surface where it cleaves TNF (show TNF Proteins) and EGFR (show EGFR Proteins) 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 Proteins)-dependent C/EBPbeta (show CEBPB Proteins) signaling pathway, which in turn initiates binding of C/EBPbeta (show CEBPB Proteins) 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 Proteins) 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 Proteins) expression and increase vascular endothelial ADAM17 activity and soluble TNF (show TNF Proteins) 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 (show TNF Proteins), 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 Proteins) shedding in porcine reproductive and respiratory syndrome virus-infected pigs.
Overexpression of ADAM17 induced downregulation of CD163 (show CD163 Proteins) expression and a reduction in reproductive and respiratory syndrome virus infection.
activation of TACE/ADAM17 via a PKC (show FYN Proteins)-induced c-Src (show SRC Proteins)-dependent manner mediates proteolytic activation of the EGF (show EGF Proteins)-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 Proteins) stimulates Rac (show AKT1 Proteins), ADAM17/TACE, and RhoA (show RHOA Proteins) through the guanine nucleotide exchange factor (show ARHGEF12 Proteins) (GEF)-H1 (show ARHGEF2 Proteins).
progesterone-induced TACE/ADAM17 leads to production of soluble EGF (show EGF Proteins) 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