Browse our anti-ADAM17 (ADAM17) Antibodies

Human ADAM Metallopeptidase Domain 17 (ADAM17) interaction partners

1. increased ADAM17 expression may have contributed to gastric cancer metastasis and progression, potentially via activation of the Notch or Wnt signaling pathways

2. These data indicate that ADAM-17 is expressed on rheumatoid arthritis synovial tissues s and plays a role in rheumatoid arthritis inflammation

3. Membrane-anchored CD40 is processed by the tumor necrosis factor-alpha-converting enzyme. Implications for CD40 signaling.

4. iTAP (FRMD8) is a novel iRhom2 interactor that controls TNF-alpha secretion by policing the stability of iRhom2/ADAM17 complex.

5. FRMD8 promotes inflammatory and growth factor signaling by stabilizing the iRhom2/ADAM17 sheddase complex.

6. Lentivirus mediated ADAM17 RNAi may reverse the acquired resistance of lung adenocarcinoma to gefitinib via inhibiting the upstream of EGFR signal pathway, which may provide a new therapeutic target to solve the acquired resistance to EGFR tyrosine kinase inhibitors in lung adenocarcinoma

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

8. 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.

9. High ADAM17 expression is associated with cystic fibrosis.

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

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

12. 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.

13. 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.

14. 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.

15. 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.

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

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

18. 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.

19. 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.

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

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

1. Our study reveals maturation and activity of ADAM17 in a more physiological-immune cell system

2. results suggest that blood entering the joint activates the iRhom2/ADAM17/TNF-alpha pathway, thereby contributing to osteopenia and synovitis in mice.

3. DKK3 overexpression substantially alleviated AngII infusion-induced cardiac hypertrophy and fibrosis by regulating ADAM17/ACE2 pathway activity and inhibiting the GSK-3beta/beta-catenin pathway.

4. Cell surface CSF-1 (csCSF-1) is one of the substrates of ADAM17. We demonstrate that both infiltrated neutrophils and macrophages are major sources of csCSF-1.

5. ADAM17 is needed for EGF-R-mediated induction of IL-6 synthesis, which via IL-6 trans-signaling induces beta-catenin-dependent tumorigenesis.

6. iTAP (FRMD8) is a novel iRhom2 interactor that controls TNF-alpha secretion by policing the stability of iRhom2/ADAM17 complex.

7. FRMD8 promotes inflammatory and growth factor signaling by stabilizing the iRhom2/ADAM17 sheddase complex.

8. The data indicate that hepatic TIMP3 expression can slow the progression of nonalcoholic fatty liver disease and tumorigenesis, at least in part, through the regulation of ADAM17 activity.

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

10. 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.

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

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

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

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

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

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

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

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

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

20. 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

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