Browse our anti-ADAM17 (ADAM17) Antibodies

Human ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. High expression of ADAM17 is associated with oxaliplatin chemosensitivity. Down regulation of ADAM17 can enhance sensitivity and reverse resistance to oxaliplatin.

2. ADAM-17 is an independent prognostic marker for patients with hilar cholangiocarcinoma. FoxM1 regulates the expression of ADAM-17 and then induced TNFa production and cleavage.

3. High ADAM17 expression is associated with cystic fibrosis.

4. These findings link iNOS to Notch1 signaling in CD24(+)CD133(+) LCSCs through the activation of TACE/ADAM17.

5. ADAM17 activation and secretion in the myeloid cells during HIV infection.

6. 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.

7. 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.

8. 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.

9. 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.

10. Uev1A-Ubc13 complex catalyzes lysine63-linked ubiquitination of RHBDF2 to promote TACE maturation.

11. ADAM17 plays a role in chronic kidney disease-mineral and bone disorder.

12. 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.

13. 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.

14. Oxidative stress is correlated with hyperactivation of the ADAM17/Notch signaling pathway and a consequent increase in fibrosis in patients with endometriosis.

15. 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.

16. 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.

17. Cullin 3 regulates ADAM17-mediated ectodomain shedding of AREG.

18. ADAM17 may be a key enzyme that regulates the generation of TNF-alpha in oral keratinocytes.

19. 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.

20. 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.

Mouse (Murine) ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. suggest that STING activates ADAM17 and that this activation produces soluble proinflammatory SEMA4D independently of the TBK1/IRF3-mediated transcriptional pathway

2. 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.

3. Report atheroprotective functions of ADAM17 in myeloid cells but atheroprogressive ADAM17 functions in endothelial cells.

4. results suggest ADAM17/EGFR-driven PLCgamma1 and PKC pathways as important promoters of TG1 expression during terminal keratinocyte differentiation.

5. iRhom2 controls multiple aspects of TACE biology, including stimulated shedding on the cell surface.

6. Targeting ADAM17 with a lentiviral vector attenuates endotoxemia in mice.

7. Addition of a disintegrin and metallopeptidase domain 17 (ADAM17) to the culture supernatant of stimulated splenocytes decreased Interferon-gamma (IFN-gamma) concentration.

8. Overall, iRhom2 binds to TACE throughout its lifecycle, implying that iRhom2 is a primary regulator of stimulated cytokine and growth factor signalling.

9. Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR-ligands by differentially activating ADAM17 or ADAM10.

10. Fhl2 anticipates the emerging inflammation and specifically the development of psoriatic arthritis by impeding the Adam17-mediated release of TNF

11. most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR

12. 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

13. 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.

14. 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.

15. These results demonstrate a novel physiologic role for a disintegrin and metalloprotease 17 in regulating murine IL-6 signals during inflammatory processes.

16. These results show that TACE is a target of, and is downregulated by, soluble TNF-induced AP-2alpha transcription factor in dendritic cells

17. 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.

18. Findings provide evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.

19. 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

20. 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.

Pig (Porcine) ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. 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

2. ADAM17 was involved in porcine CD16 shedding in porcine reproductive and respiratory syndrome virus-infected pigs.

3. Overexpression of ADAM17 induced downregulation of CD163 expression and a reduction in reproductive and respiratory syndrome virus infection.

4. 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

5. Data indicate that TNF-alpha stimulates Rac, ADAM17/TACE, and RhoA through the guanine nucleotide exchange factor (GEF)-H1.

6. 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